New GEO Series

GSE352702 Single-cell RNA sequencing of appendiceal adenocarcinoma reveals a low proportion of epithelial cells and a fibroblast enriched tumor microenvironment

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Betul B Gunes ; Nicholas Hornstein ; Mingshuang Wang ; Mahmoud Yousef ; Mohammad M Fanaeian ; Abdelrahman Yousef ; Saikat Chowdhury ; Mohammad A Zeineddine ; Cara Haymaker ; Beth Helmink ; Keith Fournier ; John P Shen
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Appendiceal adenocarcinoma (AA) is an understudied gastrointestinal malignancy. Treatment is guided by its proximal counterpart, colorectal cancer (CRC), despite recent studies demonstrating AA’s unique mutational landscape and poor response to CRC chemotherapy. As the first application of single-cell technology to AA these data provide insight into the intratumor heterogeneity of AA and highlight the important contribution of the tumor microenvironment in this orphan disease. These results also reinforce multiple observations that AA is a unique disease entity from CRC and targeting the tumor microenvironment should be considered as a therapeutic strategy.

GSE352692 Local chromatin, 3D genome folding and transposon cargo shape Sleeping Beauty transposition

Sat, 31 Oct 2026 00:00:00 -0400

Series Type : Other
Organism : Mus musculus

This SuperSeries is composed of the SubSeries listed below.

GSE352662 Longitudinal spatial mapping of tumor–immune microenvironment following electrochemotherapy of cutaneous melanoma metastases

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Tina Kos ; Sara Milićević ; Gorana Gašljević ; Iva Šantek ; Maša Omerzel ; Gregor Serša ; Barbara Perić ; Maja Čemažar
Series Type : Other
Organism : Homo sapiens

Background: Electrochemotherapy (ECT) utilizes reversible electroporation for localized chemotherapeutic delivery, where beyond local cytotoxicity, ECT acts as an in situ immunomodulator. However, the dynamic spatial orchestration of the TME that translates this localized therapy into potential abscopal-like responses in untreated lesions remains poorly understood. Methods: To uncover the mechanisms of evolving tumor microenvironment (TME) that dictate this immune activation, we applied Xenium spatial transcriptomics to longitudinally sampled in-transit cutaneous melanoma metastases from three patients, capturing baseline immune states and two distinct post-ECT intervals (two-to-three and nine-to-ten days). Furthermore, to explicitly characterize potential abscopal-like effects, biopsies were collected also from non-treated lesions. Following sample integration, we annotated cell types and identified functional subpopulations of key compartments, which we compared across treatment timepoints and patients. Further, we resolved functional spatial niches and identified spatially localized immune front, which we characterized and linked to patients' clinical responses. Results: Our analysis uncovered heterogeneous patient trajectories: a robust local and regional responder, a localized-only responder, and a delayed regional responder. These divergent outcomes were linked to baseline TME heterogeneity that was reflected by diverging proportions of functional spatial niches. While the partial responder exhibited an immune-cold architecture, complete responders were characterized by an immune-permissive TME with a prominent immune front at the interface of malignant and immune-active niches. Molecular profiling of these spatial boundaries exposed patient-specific signatures of activation and suppression within infiltrating T cells, myeloid cells, and fibroblasts. Although the states of malignant cells remained predominantly unchanged in the partial responder, the malignant cells of complete responders transitioned into a unique SOX2-OT-expressing dormant state, sequestered within keratinocyte-rich zones and characterized by an immunosuppressive signature post-treatment. Conclusions: Together, our findings suggest that beside local ablation, ECT might actively instigate regional antitumor immunity, a therapeutic effect that we observed in two patients harboring a permissive TME. Further, our deep spatial TME profiling identifies several exploratory observations on the effects of ECT that should be addressed in future studies.

GSE352630 Local and circulating cytotoxic CD4 T cells are early markers of disease activity in pediatric Crohn’s disease

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Veronika Niederlova
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Inflammatory bowel disease (IBD) requires improved molecular and cellular stratification to guide therapy. In the PREDICT study, we profiled intestinal and blood T cells from treatment-naïve pediatric patients with IBD, disorders of gut–brain interaction controls, and healthy donors using single-cell RNA sequencing. Across 107 participants, we identify a population of clonally expanded cytotoxic CD4 T cells (CD4 CTL) enriched in the inflamed gut of patients with Crohn's disease (CD) and ulcerative colitis. Cell–cell interaction analyses and validation in a mouse model implicate IL-27 in CD4 CTL differentiation. Elevated CD4 CTL frequencies in gut and peripheral blood at diagnosis are associated with subsequent poor outcome of anti-TNF therapy in pediatric CD. Findings in our identification cohort are validated in an independent cohort and through reanalysis of published datasets. Blood CD4⁺CXCR6⁺CD27⁻ T cells displayed a CD4 CTL transcriptional phenotype, supporting CD4 CTLs as a candidate blood-accessible biomarker for treatment stratification.

GSE352613 Cooperative interaction of Foxp3 and STAT5 confers regulatory T cell fitness by tuning IL-2-induced gene expression [ATAC-Seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Michaels Anthony ; Dolsten Gabriel ; Uhl Lion ; Hu Wei ; Dhilon Bahawar ; Ghelani Aazam ; Giovanelli Paolo ; Andretta Emma ; Pritykin Yuri ; Rudensky Alexander
Series Type : Genome binding/occupancy profiling by high throughput sequencing
Organism : Mus musculus

Transcription factor Foxp3, with its singular role in differentiation and function of regulatory T (Treg) cells in physiologic and inflammatory settings, is thought to act by modulating transcriptional responses to activatory extracellular cues including pro-inflammatory cytokines. However, the underlying mechanisms remain largely unknown. After Foxp3 is induced during Treg differentiation upon STAT5 activation downstream of interleukin-2 receptor (IL-2R), sustained STAT5 signaling facilitates fitness and suppressive capacity of mature Treg cells. We found that Foxp3 and phospho-STAT5 (pSTAT5) form a stable transcriptional complex. Upon IL-2 sensing, Foxp3 is recruited in a pSTAT5-dependent manner to GAS-motif-enriched cis-regulatory elements that are developmentally primed by STAT5 in Treg precursors prior to Foxp3 expression. Using chemogenetically and pharmacologically induced protein degradation, we demonstrate that Foxp3 modulates STAT5 signaling in activated Treg cells to selectively modulate their transcriptional response to IL-2, most prominently involving a Myc-dependent gene module. Our studies suggest that direct Foxp3-STAT5 cooperativity fine-tunes STAT5 signaling downstream of IL-2 receptor activation to support functionality of differentiated Treg cells.

GSE352606 Transcriptomic profiling of Gem-miR-15a treatment in parental and drug resistant HCT116 colorectal cancer cells

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Anushka Ojha ; Amartya Pal ; Max Chao ; Ramana V Davuluri ; Jingfang Ju
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Resistance to 5-fluorouracil (5-FU)-based chemotherapy is a major obstacle in colorectal cancer (CRC). Gem-miR-15a, a gemcitabine-modified tumor-suppressor microRNA-15a mimic, was developed to overcome chemoresistance by combining the tumor-suppressive activity of miR-15a with the cytotoxic activity of gemcitabine in a single, vehicle-free molecule. To investigate the transcriptomic basis of its activity and its ability to reverse resistance-associated gene expression, RNA-sequencing was performed on parental and 5-FU-resistant HCT116 CRC cells under untreated and Gem-miR-15a-treated conditions. Analysis of these profiles identified modulation of key oncogenic and stress-response pathways and reversal of resistance-associated expression patterns following Gem-miR-15a treatment.

GSE352602 Cooperative interaction of Foxp3 and STAT5 confers regulatory T cell fitness by tuning IL-2-induced gene expression [Myc_RNA]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Michaels Anthony ; Dolsten Gabriel ; Uhl Lion ; Hu Wei ; Dhillon Bahawar ; Ghelani Aazam ; Giovanelli Paolo ; Andretta Emma ; Pritykin Yuri ; Rudensky Alexander
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

The transcription factor Foxp3, with its singular role in the differentiation and function of regulatory T (Treg) cells, is thought to modulate their responses to activatory extracellular cues. However, the underlying mechanisms remain largely unknown. Beyond its requirement for Foxp3 induction during Treg differentiation, STAT5 activation downstream of interleukin-2 (IL-2) signaling is essential for the fitness, activation, and suppressive capacity of mature Treg cells. Here, we demonstrate that IL-2-induced phospho-STAT5 directly binds Foxp3, endowing Foxp3 with a new binding specificity and enabling its recruitment to a distinct set of GAS motif-enriched cis-regulatory elements. Using acute chemogenetic and pharmacological protein degradation strategies, we show that Foxp3 selectively modulates STAT5-dependent transcriptional responses of activated Treg cells to IL-2, including a Myc-dependent gene module. These results suggest that Foxp3-STAT5 complexes “customize” transcriptional responses of activated Treg cells to IL-2 stimulation to support their fitness and functionality.

GSE352573 Integrated transcriptomic and tissue profiling reveals imprinted-gene dysregulation and PEG10 upregulation in liposarcoma

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Roberta Turiello ; Andrea Bonicelli ; Pietro Carotenuto
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Liposarcoma is a rare cancer, comprising four major histological subtypes with distinct molecular features and limited therapeutic options in advanced disease. We investigated subtype-associated transcriptional programmes, imprinted-gene dysregulation and the expression context of PEG10 in liposarcoma. Bulk RNA sequencing was performed on 16 independent liposarcoma tumours and five adjacent non-tumour tissues. PEG10 was further examined by RT-qPCR, RNA fluorescence in situ hybridisation (RNA-FISH), exploratory TCGA-SARC survival analysis and an external single-cell RNA-sequencing dataset of dedifferentiated liposarcoma. Transcriptomic profiling identified subtype-associated programmes and significant enrichment of imprinted genes in liposarcoma. PEG10 showed tumour-associated upregulation supported by RT-qPCR and RNA-FISH. PEG10 was detectable across all major subtypes, with the highest bulk transcript levels in myxoid liposarcoma, while RNA-FISH signal was higher in G3 than G2 tumours. In TCGA-SARC, higher PEG10 expression was associated with shorter overall survival, whereas DDLPS-specific analyses were not significant. External single-cell data localised PEG10 predominantly to tumour and cycling-cell populations and to angiogenesis- and invasion-associated tumour-cell states. Histological subtype accounted for a substantial component of PEG10-associated pathway variation. These findings identify PEG10 as a tumour-associated imprinted transcript in liposarcoma and provide a framework for further investigation of its biological and clinical relevance in larger, subtype-balanced cohorts.

GSE352557 Circulating microRNA profiles in patients with MASLD-related cirrhosis and hepatic encephalopathy: an exploratory pilot study

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Clelia Asero ; Irene Gasparo ; Francesca Polito ; Silvia Romano ; Annamaria Mirabello ; Cristina Barbagallo ; Selene Drago ; Alba Migliorato ; Laura Licitri ; Vincenzo Macaione ; Marco Ragusa ; Mhammed Aguennouz ; Irene Cacciola
Series Type : Expression profiling by RT-PCR
Organism : Homo sapiens

Background and Aims: Hepatic encephalopathy (HE) is a common complication of cirrhosis, characterized by biochemical alterations in the central nervous system microenvironment. Although the molecular mechanisms underlying HE have been partly characterized at the protein level, their upstream regulation remains poorly understood. This study aimed to characterize circulating microRNA (miRNA) expression in patients with overt HE and identify the biological pathways associated. Materials and methods: Ten patients with MASLD-related cirrhosis and HE and four controls – subjects without chronic liver disease – attending the Liver Unit of the University Hospital of Messina, were enrolled after the exclusion of neurological comorbidities. Blood samples were collected at enrolment, cell-free RNA was isolated from plasma using the miRNeasy Kit, and functional enrichment analysis was performed using DIANA-miRPath v4. Results: Compared with controls, patients with HE showed downregulation of miR-18a and upregulation of miR-150, miR-214, miR-296, miR-320, miR-423-5p, miR-483-5p, miR-484, miR-486, miR-636, miR-92a, miR-10b, miR-1233, miR-1255b, miR-1285, miR-1290, miR-1291, miR-30a-5p, miR-338-5p, and miR-378. Functional enrichment analysis identified pathways and molecular functions related to glycolipid metabolism regulators and neuronal homeostasis signalling. Conclusion: Study results reveal a complex miRNA-associated network involving metabolic dysfunction, neuroinflammation, cellular integrity, and neuronal plasticity, highlighting the biological complexity of MASLD-related cirrhosis with HE. Keywords: Metabolic dysfunction-associated steatotic liver disease, liver cirrhosis, hepatic encephalopathy, microRNAs.

GSE352555 The CRISPR-Cas system functions as a regulatory module in Salmonella enterica serovar Typhi

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Ismael Hernandez Lucas
Series Type : Expression profiling by array
Organism : Salmonella enterica subsp. enterica serovar Typhi ; Salmonella enterica subsp. enterica serovar Typhi str. CT18 ; Salmonella enterica subsp. enterica serovar Typhimurium str. LT2

Transcriptional profile of Salmonella enterica serovar Typhi IMSS-1 mutants lacking individual components of the Type I-E CRISPR-Cas system. Strains carrying deletions of cas1, cas2, cas3, casB (cse2), casD (cas5), casE (cas6e) or the cas3-CRISPR region were compared with the wild-type strain, which was used as control. All strains were grown in N-minimal medium at 37 °C to an OD600 of 0.6. CRISPR-Cas systems are best known as adaptive immune systems of bacteria against phages and plasmids, but they are increasingly recognized as regulators of endogenous gene expression. The aim of the experiment was to learn if the loss of CRISPR-Cas components was able to modify the overall mRNA expression profile of S. Typhi. Here, we demonstrate that the Type I-E CRISPR-Cas system in S. Typhi modulates the expression of the key transcriptional regulator TviA.

GSE352548 Analysis of Sacituzumab Govitecan-Resistant Syngeneic Patient-Derived Xenograft Pairs

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Carson Walker ; Amy L Olex ; Mohammad Mikail I Bala ; J C Harrell
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

This study identifies RNA expression changes in models that have acquired Sacituzumab Govitecan (SG) resistance over extended treatment in triple-negative breast cancer patient-derived xenograft (PDX) models. Patients diagnosed with triple-negative breast cancer do not have many targeted treatment options, yet SG has recently been approved for first-line treatment of these patients. SG is an antibody drug conjugate that binds to TROP2 and delivers a topoisomerase 1 inhibitor, SN-38, as its payload. We have selected three PDX models which were initially sensitive to SG treatment, and treated them with suboptimal doses of SG until the tumors grew through treatment. Previous studies have shown that resistance to SG could be due to inefficient antibody internalization or lack of payload efficacy, however, other genetic or transcriptomic factors may influence drug sensitivity. We hypothesize that individual acquired SG resistance mechanisms will uncover features that can be targeted to extend the duration of response to SG.

GSE352509 Gut microbial equol production associates with cognitive trajectories and suppresses NLRP3 inflammasome activation

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Abigail H Evered ; Jea Woo Kang ; Margo B Heston ; Cassandra J McGill ; Michael L Sande ; Daniel C Shippy ; Rozalyn M Anderson ; Barbara B Bendlin ; Tyler K Ulland
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Many intestinal microbiome-produced metabolites have neuroimmunomodulatory properties. To identify metabolites associated with cognition and neuroinflammation, we measured microbially derived metabolites in the blood serum of 1,206 cognitively normal participants from the Wisconsin Alzheimer’s Disease Research Center (ADRC) and the Wisconsin Registry for Alzheimer’s Prevention (WRAP). We found that serum presence of equol, a microbially-produced metabolite derived from the soy-isoflavone daidzein, was related to preclinical cognition over time in a sex-dependent manner, suggesting that microbe-derived equol may attenuate cognitive decline through sex-specific biological pathways. Additionally, serum equol was associated with slower accumulation of the CSF biomarkers GFAP, S100B, and NfL, suggesting equol may be linked to glial regulation and neuronal integrity. To understand how equol may mediate inflammation systemically to reduce neuroinflammation, we performed bulk RNA-sequencing on bone marrow-derived macrophages (BMDMs) and found S-equol treatment modestly altered pathways associated with the NOD, LRR, and pyrin domain containing (NLRP3) inflammasome, an established driver of neuroinflammation in Alzheimer’s disease. We used ELISAs and caspase-1 immunoblots to show S-equol inhibits NLRP3 activation in BMDMs, evidenced by significantly decreased IL-1β secretion and caspase-1 processing after equol treatment. We confirmed that this effect is directly dependent on equol’s inhibition of potassium efflux. These findings lay a strong foundation for future studies examining the neuroimmunomodulatory action of equol in NLRP3 driven disease and cognitive decline.

GSE352343 Targeting the Alk4 pathway protects against age-related bone loss.

Sat, 31 Oct 2026 00:00:00 -0400

Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Osteoporosis is a chronic age-related condition where imbalanced activities between bone-forming osteoblasts and bone-resorbing osteoclasts result in the progressive loss of bone volume and reduced bone quality. While drugs that target osteoclast activity have been developed, there remains a lack of efficient therapies that increase osteoblast function in aging bones. Here, we showed that in mouse femurs, levels of Activin signaling progressively increased with age and strongly correlated with the loss of trabecular bone. When we removed Alk4, the type I receptor for Activin in osteoblast progenitors, Alk4 cKO mice had increased numbers of osteoblasts, an increased rate of bone formation, and increased trabecular bone acquisition. These results indicate that Activin through Alk4 signaling inhibits bone formation and osteoblast activity and is likely associated with osteoporosis. Furthermore, when we injected 2-year-old male mice with Alk4-Fc to capture circulating Activin, aged mice were protected against loss of trabecular bone in both femurs and L5 vertebrae. Remarkably, Alk4-Fc also prevented the age-related decrease in muscle mass that normally accompanies age-related bone loss, indicating that circulating Activins also play a role in sarcopenia. In summary, our preclinical mouse models reveal that circulating Activins play a primary role in age-related bone and muscle loss and can be efficiently targeted to alleviate osteoporosis and sarcopenia in aging mice.

GSE352331 Baseline immune transcriptional states predict future HIV-1 acquisition in individuals at risk of sexual infection

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Antonio Caruz ; Celia Ruiz-Garcia
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Natural resistance to HIV-1 acquisition in highly exposed seronegative (HESN) individuals suggests the existence of pre-existing host states associated with reduced susceptibility. However, the baseline molecular determinants of susceptibility remain poorly understood. We analyzed PBMC transcriptomes by RNA sequencing in 104 HIV-1-seronegative men who have sex with men (MSM) at high risk of sexual exposure, including 65 HESN and 39 who subsequently seroconverted. Differential expression, functional enrichment, and spatial genomic clustering analyses were integrated with Elastic Net regularized logistic regression. HESN individuals showed enrichment of sensory receptor (p.adj=2×10⁻¹⁶) and cell-adhesion pathways (p.adj=9×10⁻³), together with non-random genomic clustering (p.adj=1×10⁻⁴) of differentially expressed genes at immune-related loci, including TCR, IGH, KIR, and MHC/HLA regions. In contrast, future seroconverters exhibited increased mRNA metabolism (p.adj=1.5×10⁻¹⁴), immune activation (p.adj=0.01), and type I interferon signaling (p.adj=0.02). A 14-gene risk score showed an out-of-fold AUC of 0.888. Cross-cohort transportability was evaluated in an independent ectocervical RNA-seq dataset. Applied without refitting, the signature showed moderate discrimination between long-term HESN and HIV-negative women at high risk of acquisition (AUC=0.689). The out-of-fold molecular risk score was also associated with time to HIV-1 seroconversion in MSM (log-rank p=7.1×10⁻¹¹; score×time interaction p=0.0086). These findings identify distinct pre-infection transcriptional states associated with HIV-1 acquisition and support partially transportable transcriptional architecture across blood and genital mucosal compartments.

GSE352288 Local chromatin, 3D genome folding and transposon cargo shape Sleeping Beauty transposition [tagmap]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Christina J Moene ; Mathias Eder ; Lise Dauban ; J. Omar Yáñez-Cuna ; Acadia A Kocher ; Laurens Eschauzier ; Martijn Verkuilen ; Vinícius H Franceschini-Santos ; Bas van Steensel
Series Type : Other
Organism : Mus musculus

The cut-and-paste DNA transposon Sleeping Beauty (SB) is widely used for genome engineering, mutagenesis and gene delivery. When mobilized from a genomic donor position (“launch site”), SB preferentially reintegrates locally (< 2 Mb), but factors governing its transposition from genomic sites remain incompletely understood. Here we analysed local transposition experiments in mouse embryonic stem cells to determine the influence of chromatin context and transposon cargo on SB transposition. Transposons in launch sites with transcriptionally active, accessible chromatin showed lower transposition efficiency. Large cargo and cargo with higher transcriptional activity also result in reduced transposition efficiency. After excision, local reintegration patterns closely resembled 3D contact frequencies of the launch site. This indicates that chromosome folding is a major determinant of the transposition pattern. Surprisingly, we did not detect any effect of the destination chromatin composition on reintegration efficiency. Cargo sequence modified the reintegration patterns: promoter-containing cargo increased both very proximal (<10kb) and interchromosomal transpositions, while CTCF binding sites in the cargo increased reintegration on the launch chromosome. Together, these results define key determinants of SB transposition in chromosomes and inform the design of SB-based genome engineering strategies.

GSE352286 Local chromatin, 3D genome folding and transposon cargo shape Sleeping Beauty transposition [pADam]

Sat, 31 Oct 2026 00:00:00 -0400

GSE352244 Longitudinal Gene Expression Profiling Reveals Molecular Evolution and Transcriptional Reprogramming During Multiple Myeloma Relapse

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Yan Cheng ; John D Shaughnessy ; Fenghuang Zhan
Series Type : Expression profiling by array
Organism : Homo sapiens

This study aims to characterize gene expression alterations associated with multiple myeloma (MM) relapse by performing longitudinal gene expression profiling (GEP) of CD138+ plasma cells isolated from bone marrow mononuclear cells collected from 35 patients at baseline, first relapse, and second relapse.

GSE352234 Investigating the transcriptional response of PSC2 deletion and overexpression in C. neoformans

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Emma E Blackburn ; Benjamin Chadwick ; Xiaofeng Xie ; Xiaorong Lin
Series Type : Expression profiling by high throughput sequencing
Organism : Cryptococcus neoformans

Adaptation to CO2 is necessary for virulence in Cryptococcus neoformans. The regulation of Ace2p activity and cellular morphogenesis (RAM) pathway is essential for growth under high temperature and high CO2 conditions. We identified PSC2 (CNAG_01335) as a suppressor of the RAM pathway in H99 cbk1 deletion mutant. To investigate the role of Psc2, RNA sequencing was performed on the wild-type H99, PSC2 deletion, and Psc2 over expression strains.

GSE351871 Age-associated hsa_piR_020485 inhibits osteogenic differentiation of bone marrow stromal cells and promotes macrophage migration

Sat, 31 Oct 2026 00:00:00 -0400

Series Type : Expression profiling by high throughput sequencing
Organism : Rattus norvegicus

Age-related decline in bone marrow stromal cell (BMSC) function and inflammatory changes contribute to osteoporosis. We investigated the age-associated PIWI-interacting RNA hsa_piR_020485 and its effects on BMSC function, macrophage responses, and trabecular bone volume fraction.

GSE351755 Proteasomes in extracellular vesicles mediate most transcriptional effects in recipient colorectal cancer cells

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Alexey Morozov ; Alexander Rezvykh ; Elizaveta Starodubova ; Alexander Burov ; Kseniia Kozlova ; Alexey Belogurov Jr ; Vadim Karpov
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Extracellular vesicles (EVs) transmit lipids, proteins and RNA between cells of the organism. Among their cargo, EVs contain different forms of proteasomes - multi-subunit protein complexes responsible for degradation of most intracellular proteins. The transmission of proteasomes by EVs from one cell to another has been recently shown; however the biological significance of the phenomenon is generally unknown. Here we purified EVs from control colorectal adenocarcinoma cells and cells treated with IFN-γ, a cytokine known to activate expression of specific proteasome forms - non-constitutive proteasomes (ncPs). The obtained vesicles were incubated with two different irreversible proteasome inhibitors: carfilzomib and ONX-0914, targeting all forms and specifically ncPs, correspondingly. EVs were then incubated with control or carfilzomib-treated colorectal adenocarcinoma cells and the cellular RNA was obtained, followed by transcriptome acquisition and analysis. Incubation of control and carfilzomib-treated cells with treated or non-treated EVs obtained from control donor cells induced almost no effect on gene expression in recipient cells. However, vesicles obtained from IFN-γ-treated cells modulated expression of 53 genes in control cells and 2 genes in carfilzomib-treated cells. Treatment of vesicles with either one or another proteasome inhibitor affected the expression of 49 genes in control cells. In carfilzomib-treated cells inhibition of proteasomes in EVs affected 21 genes. Importantly, in both cases inhibition of ncPs in vesicles using ONX-0914 induced more pronounced effects on transcription in recipient cells. Most of the genes with differential expression were involved in oxidative phosphorylation. Obtained results indicate that most of the effects mediated in recipient cells by EVs were associated with the activity of proteasomes and specifically non-constitutive proteasomes, highlighting novel insights into EVs mediated proteasome transfer.

GSE351748 Overexpression of IL-1Ra in MSCs Ameliorates Hepatic Injury via GGT5 and Improves Survival of aGVHD Mice

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Yang Jang ; Shunye Wang ; Chengyun Zheng
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

In conclusion, oeIL_x001E_1Ra_x001E_MSCs alleviate aGVHD_x001E_related hepatic lesions through anti_x001E_inflammatory effects and GGT5_x001E_dependent maintenance of redox and mitochondrial homeostasis, offering a promising cell_x001E_therapy strategy and theoretical foundation for targeted treatment of hepatic aGVHD.

GSE351587 Liver Kinase B1 depletion disrupts the pantothenic acid: coenzyme A pathway in astrocytes

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Rebecca Alemani ; Sergey Kalinin ; Douglas L Feinstein
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Previous studies showed conditional knockout of Liver Kinase B1 (LKB1) from astrocytes exacerbated disease severity and glial cell activation in a mouse model of Multiple Sclerosis (MS). A major function of LKB1 is to maintain energy supplies under conditions of metabolic stress, suggesting that loss of LKB1 could alter astrocytic metabolic processes. Following siRNA mediated knockdown (KD) of LKB1 from primary mouse astrocytes, untargeted metabolomic screening identified significant increases in Pantothenic Acid (PA) and related metabolites; and pathway analysis showed the PA:Coenzyme A (PA:CoA) pathway was significantly modified. This pathway was also identified by bulk RNA sequencing. In LKB1 KD cells, relative mRNA levels of enzymes in the PA:CoA pathway were reduced, and PA Kinase 2 (Pank2, which converts PA to phosphoPA) expression was reduced. Deficiencies in Pank2 are known to cause iron accumulation, which we confirmed occurs in LKB1 KD astrocytes. The KD cells also showed increased sensitivity to induction of ferroptosis. Measurement of serum PA levels showed a positive correlation with age at diagnosis in relapsing remitting MS patients harboring a variant in the gene encoding LKB1. Together, these results indicate that metabolic disturbance leads to dysregulation of the PA:CoA pathway in astrocytes and suggest that plasma PA levels could provide a novel biomarker for MS disease.

GSE351179 Twenty-Hour Hypothermic Oxygenated Perfusion Preserves Myocardial Viability and Bioenergetics with No Primary Graft Dysfunction After Porcine Heart Transplantation

Sat, 31 Oct 2026 00:00:00 -0400

Series Type : Expression profiling by high throughput sequencing
Organism : Sus scrofa

Background: Hypothermic oxygenated perfusion (HOPE) may extend donor heart preservation beyond conventional storage durations. We evaluated early graft function and myocardial cellular and metabolic integrity following porcine heart transplantation after 20 hours of HOPE. Methods: Ten donor hearts underwent various preservation conditions: static cold storage (SCS) for 4 hours (n=2), HOPE for 4 hours (n=3), and HOPE for 20 hours (n=5), followed by heart transplantation (HT) in recipient pigs. Following implant and reperfusion, graft function was assessed over 3 hours by serial echocardiography, invasive hemodynamics, optical flow analysis, and vasoactive support scoring; myocardial tissue was analyzed by histopathology, flow cytometry, mitochondrial respirometry, transcriptomics, and proteomics. Results: Ejection fraction, right atrial pressure and systolic blood pressure did not differ significantly between groups, and no graft met criteria for primary graft dysfunction. LV contractility was within normal range with comparable vasoactive support among all groups. Preservation-associated weight gain was greatest after HOPE 20h, and histopathology showed comparable findings with edema present in all cohorts, without fibrosis, thrombosis, or necrosis. Cardiomyocyte viability was preserved across all groups (HOPE 20h, 86%, HOPE 4h, 81%, and SCS 4h, 77%). Maximal oxygen consumption rate was elevated in HOPE 20h versus HOPE 4h and SCS 4h (p<0.01), while basal and non-mitochondrial respiration were similar. Transcriptomics and proteomics revealed minimal differences in gene and pathway expression among groups. Conclusions: HOPE preserves donor heart viability, mitochondrial integrity, and ventricular function after 20 hours of ischemia in a porcine model, without evidence of primary graft dysfunction, supporting extended preservation for heart transplantation. Edema, recovery of function, and metabolic responses warrant further investigation with longer-term monitoring.

GSE351178 Parallel transcriptomics reveals insect developmental shifts and gall-associated host transcriptional differences in Quadrastichus erythrinae and Erythrina variegata

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Serdar Dinç
Series Type : Expression profiling by high throughput sequencing
Organism : Erythrina variegata ; Quadrastichus erythrinae

Gall development involves changes in insect development and host tissue gene expression. This study used separate RNA-seq comparisons of Quadrastichus erythrinae larvae and pupae and of galled and ungalled Erythrina variegata petioles collected from one host tree during one sampling occasion. Insect reads were analyzed against a reference genome, while plant reads were assembled de novo and analyzed using a frozen sequence-provenance exclusion mask. Differential expression and annotation-based candidate analyses were used to describe developmental-stage differences in the insect and gall-associated transcriptional differences in the host. The comparisons support candidate functional themes for further investigation and do not directly test molecular interactions between the organisms.

GSE350895 Spatial transcriptomic analysis of fibroblast therapy with collagen/PMMA in human skin [Xenium]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Lee Sam S. ; Garza Luis A.
Series Type : Other
Organism : Homo sapiens

Xenium spatial transcriptomic analysis was performed to investigate cellular responses and tissue remodeling following fibroblast therapy with or without collagen/PMMA in human skin.

GSE350894 Collagen-PMMA scaffolds induce dermal remodeling and immune recruitment distinct from simple volar fibroblast therapy in human skin [scRNAseq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Sam S. Lee ; Luis A. Garza
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Cellular therapy is promising but requires optimization in human subjects. Volar skin of the palms and soles is adapted to mechanical stress through a thick epidermis and dense extracellular matrix, whereas non-volar skin is vulnerable at high-pressure sites such as prosthetic limb interfaces. Because volar fibroblasts can partially reprogram non-volar skin, we tested whether collagen/polymethyl methacrylate (PMMA) could enhance volar fibroblast therapy. Healthy volunteers received vehicle, scalp fibroblast, or volar fibroblast injections, with or without collagen/PMMA, into non-volar skin. Durometer, optical coherence tomography, histology, and transcriptomic analyses showed volar-like structural changes and activation of skin-development, keratinocyte-differentiation, extracellular-matrix, and morphogenesis pathways. Collagen/PMMA promoted fibroblast, immune, and endothelial cell accumulation, consistent with a scaffold-associated tissue response. These findings distinguish volar fibroblast–associated skin identity changes from collagen/PMMA-induced stromal remodeling with foreign body, inflammatory, and fibrotic/myofibroblast-associated features.

GSE350656 Single-cell analysis reveals sex-specific ERβ regulation of neurovascular protection in the AppNL-G-F mouse model of Alzheimer’s disease

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Heba G Ali ; Ivan Nalvarte
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Alzheimer’s disease (AD) exhibits pronounced sex differences, but the molecular mechanisms underlying this dimorphism remain unclear. To investigate the role of estrogen receptor beta (ERβ; Esr2) in modulating sex-specific amyloid pathology, single-cell RNA sequencing was performed on hippocampal tissue from six-month-old male and female AppNL-G-F and AppNL-G-F/Esr2KO mice. Loss of Esr2 induced sex-dependent alterations in amyloid burden, glial activation states, and endothelial-centered intercellular communication networks, with more pronounced transcriptomic remodeling in males. Transthyretin (Ttr) emerged as a strongly sex-modulated gene associated with increased amyloid pathology in male Esr2-deficient mice. These data provide a sex-stratified transcriptomic resource for understanding ERβ-dependent regulation of cellular programs in AD-related pathology

GSE350588 Tidal ventilation induces divergent repair responses in lung epithelial cells and fibroblasts mediated by IL-6 signaling

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Laura Amado-Rodríguez ; Guillermo M Albaiceta ; Sara M Exojo-Ramírez
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Mechanical ventilation may alter lung repair by differentially regulating epithelial and fibroblast responses. This study investigated transcriptional responses in human bronchial epithelial cells (BEAS-2B) and lung fibroblasts (MRC-5) exposed to bronchoalveolar lavage fluid from patients receiving tidal mechanical ventilation or continuous positive airway pressure (CPAP). Following scratch injury, cells were cultured with bronchoalveolar lavage fluid, with or without the IL-6 receptor inhibitor tocilizumab, and profiled using the Ion AmpliSeq Transcriptome Human Gene Expression Panel on an Ion S5 Prime sequencer. Differential gene expression and pathway analyses identified distinct responses associated with ventilatory condition, including altered inflammatory signaling and epithelial repair programs in BEAS-2B cells and increased extracellular matrix remodeling and profibrotic signaling in MRC-5 fibroblasts. IL-6 receptor blockade attenuated ventilation-associated transcriptional differences in both cell types. These data support a role for IL-6 signaling in the divergent epithelial and fibroblast repair responses associated with mechanical ventilation.

GSE350427 SARS-CoV-2 Nsp2 reprograms host immunity to drive pathogenic inflammation

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Lacasse Émile ; Dubuc Isabelle ; Leclerc Joannie ; Gravel Annie ; Gudimard Leslie ; Joly Beauparlant Charles ; Faure Marion ; Fortin Patrick ; Blanchet Marie-Renée ; Droit Arnaud ; Flamand Louis
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus ; Severe acute respiratory syndrome coronavirus 2

Despite the end of the COVID-19 pandemic, SARS-CoV-2 continues to circulate endemically, highlighting the need to better understand the viral determinants of pathogenesis. Putative functions of the non-structural protein 2 (Nsp2) have been studied in vitro but how Nsp2 affects pathogenesis and overall viral fitness in vivo has yet to be demonstrated. Here, we generated a recombinant SARS-CoV-2 lacking Nsp2 (ΔNsp2) to investigate its role in viral replication and disease. While ΔNsp2 replicated comparably to wild-type virus in vitro and in vivo, its deletion resulted in markedly attenuated disease in K18-hACE2 mice. Wild-type virus infection induced a strong pro-inflammatory response associated with increased recruitment of monocytes and macrophages, whereas ΔNsp2 virus infection promoted a more balanced antiviral response characterized by enhanced lymphocyte and NK cell recruitment. This was accompanied by reduced pulmonary and systemic inflammation and distinct transcriptional programs, including downregulation of pathways related to RNA processing and translation. Mechanistically, CLIP-seq and proximity labeling suggest that Nsp2 interacts with host RNA and components of the translational machinery. Together, our findings identify Nsp2 as a key virulence factor that drives immunopathology by skewing host immune responses, highlighting its role as a regulator of host–pathogen interactions.

GSE349688 Gene Expression in the Glioblastoma Cell Line (GL261) Transcriptome Following Treatment with Magnetic Nanoparticles (MNPQ)

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Yuanyuan Cheng ; Yifan Zhang ; Bin Lan ; Hongbing Lu ; Xinggang Mao ; Yang Liu ; Galong Li
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

GL261 cells are a widely used glioma tumor model system; following in situ transplantation, they stably form glioblastoma and are extensively utilized as a preclinical evaluation model for brain gliomas. Magnetic nanomedicines (MNPQ), with their advantages of magnetically responsive targeted enrichment and locally controlled release, have demonstrated effective antitumor potential against gliomas; however, how they reshape the gene expression profile of tumor cells at the transcriptomic level remains unclear. Our study has one primary objective: to identify differentially expressed genes and their enriched signaling pathways in the GL261 cell transcriptome before and after MNPQ treatment, thereby elucidating the molecular mechanisms underlying its antitumor effects.

GSE349627 RNA-seq of mouse bone marrow mesenchymal stem cells treated with different NPY concentrations

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Yang Chen ; Yuying Yang ; Pengling Yao ; Tingmo Huang ; Jianzhong Hu ; Tao Zhang ; Hongbin Lu
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Mouse bone marrow mesenchymal stem cells (BMSCs) were treated with neuropeptide Y (NPY) at 0, 1e-8, 1e-7, or 1e-6 mM for 7 or 14 days. Twenty-four polyA UID-mRNA-seq paired-end libraries (three biological replicates per treatment and time point) were sequenced to assess transcriptomic changes associated with low versus high NPY intervention.

GSE349461 Gene expression in pericental and periportal hepatocytes

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Rongya Tao ; Baiyu He
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Hepatic metabolic zonation enables periportal (PP) and pericentral (PC) hepatocytes to perform distinct metabolic functions. To characterize spatial differences in hepatic gene expression, we isolated PP and PC hepatocytes from mouse liver and performed RNA sequencing. This dataset provides transcriptomic profiles of PP and PC hepatocytes and enables identification of genes and pathways differentially regulated across the portal-to-central vein axis.

GSE349296 KLF16 and SIN3A facilitate endometrial cancer cell proliferation in association with CTD-2377D24.6

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Ping Wang ; Jiamei Zhu ; Xueli Zha ; Bingyan Li ; Jinhua Zhou ; Hongmei Ding
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Endometrial cancer (EC) is the most common gynecological malignancy in developed countries. Pathogenetically, most cases arise from uncontrolled proliferative expansion of endometrial cells under prolonged estrogen stimulation, ultimately leading to malignant transformation within the glandular epithelium. Identifying key regulators of aberrant endometrial proliferation is therefore critical for developing novel therapeutic modalities against EC. In the present study, we characterized Kruppel-like factor 16 (KLF16), a transcription factor that drives proliferative signaling across multiple cellular components of the endometrium, including endothelial, epithelial, and smooth muscle cell types. Clinicopathological analysis revealed significantly elevated KLF16 expression in human EC tissues, which was positively associated with both advanced tumor stages and high histological grades. Genetic perturbation experiments demonstrated that knockdown of KLF16 robustly inhibited endometrial cancer cell proliferation in vitro and impeded tumor growth in vivo. Given its role as a master regulator controlling broad transcriptomic programs encompassing both protein-coding genes and non-coding RNAs, we performed unbiased screening and identified lncRNA CTD-2377D24.6 as a potential downstream mediator associated with KLF16 signaling. Notably, overexpression of CTD-2377D24.6 effectively counteracted the anti-proliferative effects induced by KLF16 depletion. Mechanistically, single-cell transcriptomics, coimmunoprecipitation, and functional assays demonstrated that SIN3A interacts with KLF16 and may contribute to the association between KLF16 and CTD-2377D24.6 expression, which is linked to enhanced endometrial cancer cell proliferation. Together, these findings established KLF16 contributes to endometrial cancer progression and highlight the KLF16/SIN3A/CTD-2377D24.6-associated regulatory axis as a potential molecular pathway relevant to EC proliferation.

GSE349203 Targeting EGR1 Attenuates CCL2 Expression in Inflammatory Keratinocytes and Allergic Skin Inflammation

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Soon Young Shin ; You Jung Jung ; Euitaek Jung
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Early growth response 1 (EGR1) is a zinc-finger transcription factor involved in inflammatory gene regulation, but the extent to which pharmacological inhibition of EGR1 DNA-binding activity influences inflammatory transcriptional responses in keratinocytes remains incompletely understood. Here, we explored the transcriptional effects of pharmacological EGR1 inhibition in tumor necrosis factor-α (TNFα)-stimulated HaCaT keratinocytes. RNA sequencing was employed as an exploratory, hypothesis-generating screen using three structurally related EGR1 inhibitors (IT21, IT23, and IT25) to identify candidate genes showing concordant expression patterns across the three pharmacological perturbations. This analysis suggested broader changes in inflammation-associated transcriptional programs and identified several leukocyte-recruiting chemokines among the candidate genes. CCL2 was selected as a representative candidate for independent biological and mechanistic validation. IT25 treatment and EGR1 knockdown attenuated TNFα-induced CCL2 expression, while promoter-reporter analysis, EGR1-binding site mutagenesis, EGR1 overexpression, and chromatin immunoprecipitation supported EGR1-dependent transcriptional regulation of CCL2 in keratinocytes. Furthermore, topical IT25 treatment attenuated house dust mite-induced atopic dermatitis-like skin inflammation and was associated with reduced epidermal CCL2 expression and inflammatory cell infiltration in vivo. Collectively, these findings establish EGR1-dependent regulation of CCL2 in inflammatory keratinocytes and support further investigation of EGR1 DNA-binding activity as a pharmacological target in cutaneous inflammation.

GSE348913 HNRNPH2-R114W remodels RNA splicing and neurodevelopmental gene programs in isogenic cerebral organoids

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Carlo D Caiaffa ; Neda Ghousifam ; Rodney A Bowling Jr. ; Richard H Finnell ; Robert M Cabrera
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Autism spectrum disorder has been linked to disrupted RNA processing during corticogenesis, yet variant-specific mechanisms remain difficult to resolve. Isogenic cerebral organoids derived from a patient-derived induced pluripotent stem cell (iPSC) line carrying the HNRNPH2-R114W variant and its CRISPR-corrected counterpart serve as a human developmental model to investigate variant-associated RNA dysregulation. Imaging quantification and exploratory bulk RNA sequencing, performed at a single developmental time point using one pooled organoid RNA sample from each genotype, identify coordinated remodeling of neuronal and metabolic programs, along with junction-centered splicing dysregulation involving 6,310 differentially used junctions. Computational structural docking situates HNRNPH2 RNA recognition motifs (RRMs) 1-3 within a spliceosomal context and locates residue R114 near a predicted RNA-contact interface, indicating that the R114W substitution may alter RNA engagement. Integration of differential expression with event- and isoform-level analyses identifies regulatory hubs enriched for axon guidance and synaptic signaling pathways. Single-cell-reference-based deconvolution suggests modest compositional shifts that are unlikely to account for the extent of transcriptional and splicing alterations observed. Collectively, these findings implicate HNRNPH2-R114W in widespread RNA rewiring and define candidate isoform-level endpoints for mechanistic and therapeutic investigation in human cortical organoids. These molecular signatures open new avenues to examine how HNRNPH2-associated RNA dysregulation evolves across developmental time and recurs across independent biological contexts, providing a foundation for further mechanistic studies of this rare neurodevelopmental disorder.

GSE348876 PERSIST-On enables heritable and fine-tunable human gene activation [RNA-seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Y. Esther Tak ; Jonathan Y Hsu ; Justine Y Shih ; Hayley T Schultz ; Ivy T Nguyen ; Kin Chung Lam ; Keagan M Hesse ; Rui Dong ; Miguel N Rivera ; Martin J Aryee ; Luca Pinello ; J. Keith Joung
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

PERSIST-On uses CRISPR prime editing to insert an endogenous transcription-factor binding motif (ELF2X) into target gene promoters, driving heritable, fine-tunable gene activation with only transient editor expression. To assess transcriptome-wide effects and specificity of ELF2X insertion, we performed mRNA-seq on cells with ELF2X inserted into the EPCAM, HER2, or IL2RA promoter and on matched non-targeting editor controls.

GSE348793 KIF1A p.T258M Impairs Neural Progenitor Differentiation and Axonal Transport Through Dysregulated Wnt/β-Catenin–BDNF Signaling

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Yong Liu ; Jiayuan Wang ; Ruonan Duan ; Wenjie Sun
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Human neural stem cells were derived from KIF1A p.T258M-mutant induced pluripotent stem cells and CRISPR-Cas9-corrected isogenic control cells. RNA sequencing was performed to compare global gene expression profiles between KIF1A-mutant and control neural stem cells. Differentially expressed genes were identified and used for downstream GO and KEGG pathway enrichment analyses to explore molecular pathways associated with KIF1A mutation-induced neural developmental defects.

GSE348705 Sleep-dependent DNA methylation remodeling in basolateral amygdala fear engrams [PIP-Seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Xinyue Chen ; Fanwei Ruan ; Yueqing Peng ; X Shawn Liu
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

How memory consolidates via DNA methylation mechanisms during sleep in the basolateral amygdala (BLA), a critical brain region for fear memory, remains unknown. We performed whole-genome bisulfite sequencing (WGBS) on fear conditioning (FC)-activated cells from the BLAs of adult male mice experiencing either sleep or sleep deprivation following FC learning, evaluated at Day 7 and Day 28 timepoints. Additionally, Day 7 samples include paired single-nucleus RNA sequencing (snRNA-seq) using PIPseq technology. This dataset enables the integration of multi-omics (methylome and transcriptome) to understand learning-induced epigenomic programming in the BLA.

GSE348542 Sleep-dependent DNA methylation remodeling in basolateral amygdala fear engrams

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Xinyue Chen ; Yueqing Peng ; X Shawn Liu
Series Type : Methylation profiling by high throughput sequencing
Organism : Mus musculus

How memory consolidates via DNA methylation mechanisms during sleep in the basolateral amygdala (BLA), a critical brain region for fear memory, remains unknown. Here, we performed whole-genome bisulfite sequencing (WGBS) on fear conditioning (FC)-activated cells from the BLAs of adult male mice experiencing sleep or sleep deprivation following FC learning, at a week (day 7) and a month (day 28) timepoints. This dataset enables the investigation of cytosine methylation changes (CG and non-CG contexts) associated with learning-induced epigenomic programming in the BLA.

GSE348509 Single-cell regulatory genomics reveals coordinated myeloid and T-cell reprogramming in liver cirrhosis

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Chenxuan Li
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

We performed single-cell RNA sequencing (scRNA-seq) on liver tissues from 3 cirrhotic patients and 3 non-cirrhotic controls, analyzing 43,745 high-quality cells. We investigated cellular composition, SCENIC regulon activity, pseudotime trajectories, and CellChat communication. Cirrhosis was associated with Mono1 depletion, expansion of inflammatory macrophages and regulatory T cells, dysregulated YY1/ETV6 regulons in myeloid cells, altered EOMES/KLF6 programs in cytotoxic T cells, and increased EP300/SP3 in Tregs, along with fibrosis-biased ligand-receptor signaling. Note: Raw sequencing data are not available because the sequencing company routinely clears data after two years; only processed expression matrices are provided.

GSE348488 Sleep-dependent DNA methylation remodeling in basolateral amygdala fear engrams [batch 1 WGBS]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Xinyue Chen ; Yueqing Peng ; X Shawn Liu
Series Type : Methylation profiling by high throughput sequencing
Organism : Mus musculus

GSE348480 Sleep-dependent DNA methylation remodeling in basolateral amygdala fear engrams [batch 2 WGBS]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Xinyue Chen ; Yueqing Peng ; X Shawn Liu
Series Type : Methylation profiling by high throughput sequencing
Organism : Mus musculus

GSE348103 Pericytes modulate brain vascular integrity in social stress in mice and human depression [cultured cells RNA-Seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Laurence Dion-Albert ; Caroline Menard
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Major depressive disorder (MDD) is a leading cause of disease burden with low therapeutic efficacy. Chronic social stress, MDD’s main risk factor, is associated with neurovascular pathology in mood-regulating brain regions. Pericytes ensheathe endothelial cells and modulate blood-brain barrier (BBB) functions, but contribution of these mural cells to stress responses or psychiatric conditions is unknown. Here, we show sex-specific transcriptomic, morphological and functional alterations in pericytes in the prefrontal cortex (PFC) following stress exposure in female mice and women with MDD. Endothelial cell-to-pericyte crosstalk via PDGFB:PDGFRB signaling is important for BBB dynamics. Reduction of Pdgfrb+ pericyte coverage in the PFC induces anxiety- and depression-like behaviours in female, but not male mice, while viral-mediated increased pericyte-endothelial communication promotes stress coping. RNA-seq of human endothelial cells and pericytes exposed to MDD serum reveals changes in extracellular matrix-related genes and cell-cell communication. PDGF-BB serum level correlates with depressive symptoms and diagnosis. Altogether, our findings shed light on a mechanism underlying PFC dysfunction in MDD, a therapeutic target and blood biomarker. Our work provides tools to manipulate pericytes applicable for vascular, neurodegenerative, or inflammatory diseases all characterized by high rates of depression.

GSE347657 Functional landscape of enhancers that control the blood-brain barrier

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Zhongming Li ; Philip M Smallwood ; Yanshu Wang ; Jeremy Nathans
Series Type : Genome binding/occupancy profiling by high throughput sequencing ; Expression profiling by high throughput sequencing
Organism : Mus musculus

Cis-regulatory elements (CREs) that control of the blood-brain barrier (BBB) transcriptional program have been studied by transducing candidate CREs together with a GFP reporter into mouse brain endothelial cells (ECs) in vivo using recombinant Adeno-Associated Viruses (rAAVs). Approximately one-quarter of DNA segments encompassing regions of accessible chromatin (ATACseq peaks) in or near 16 genes that are highly expressed in CNS ECs confer brain EC gene expression when transduced using rAAVs. For six active CREs, site-directed mutagenesis showed that ERG/ETS and LEF/TCF motifs are consistently important for CRE activity, while FOX and ZIC motifs are variably important for CRE activity. Transcription factor (TF) occupancy maps, determined by the CUT&RUN method for ERG, LEF1, KLF4, and ZIC3 in and near the same 16 genes in acutely isolated mouse brain ECs, showed that one or more of these TFs occupied binding sites in nearly all of the 55 candidate CREs, with a modestly higher occupancy level among the 14 candidate CREs that were active in vivo in the rAAV assay compared to the 41 candidate CREs that were inactive in vivo in the rAAV assay. As observed previously for ERG and LEF1 (Li et al., 2026), chromatin occupancy by KLF4 and ZIC3 is highly enriched in open chromatin that is brain EC-specific, regions that represent the strongest candidates for brain EC-specific CREs. These studies provide foundational information for research aimed at generating endothelial cells with BBB properties in vitro.

GSE347378 Transcriptomic profiling of human lymphocytes treated with 2'-deoxyinosine reveals immunomodulatory mechanisms relevant to multiple sclerosis

Sat, 31 Oct 2026 00:00:00 -0400

Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

2'-Deoxyinosine (2'-DI) is an endogenous nucleoside formed by the deamination of deoxyadenosine by adenosine deaminase, and nucleoside metabolism pathways are involved in the initiation and progression of Multiple Sclerosis (MS). Our previous study indicated that 2'-DI treatment alleviates disease severity in an MS mouse model. To explore the potential preventive therapeutic mechanism of 2'-DI, we performed RNA sequencing on human lymphocytes isolated from MS patients. Cells were stimulated with OKT3 and treated with 0, 0.5, or 1 mM 2'-DI. Results showed that 2'-DI exposure induced dose-dependent transcriptomic changes. Differentially expressed genes were significantly enriched in immune-related pathways, including chemokine signaling pathway, cytokine-cytokine receptor interaction, and IL-17 signaling pathway, suggesting that 2'-DI may exert a protective effect in MS by finely regulating inflammatory immune responses.

GSE347183 Pericytes modulate brain vascular integrity in social stress in mice and human depression

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Dion-Albert Laurence ; Menard Caroline
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

GSE346858 GR signaling impairs osteoblast differentiation via Map7d2

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Christoph Kölbl ; Amelie Eckert ; Sandra Nungeß ; Sooyeon Lee ; Jan Tuckermann ; Anita Ignatius ; Mubashir Ahmad
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

The glucocorticoid receptor (GR) is an important regulator of skeletal homeostasis; however, the molecular mechanisms through which it regulates osteogenic differentiation remain incompletely understood. Here, we investigated the role of GR using two complementary primary murine osteogenic cell models, bone marrow stromal cells (BMSCs) and bone-derived primary osteoblasts (pOs), together with comparative transcriptomic analyses. RNA sequencing (RNAseq) revealed extensive transcriptional changes following GR knockdown. Despite substantial differences in gene expression profiles of the two osteogenic cell models, pathway enrichment analyses revealed common biological processes, including MAPK signaling and cell migration. Comparative transcriptomic analysis further identified only 17 genes that were consistently regulated in the same direction in both cell preparations, among which Map7d2 emerged as a previously unrecognized GR-responsive candidate. Co-depletion of Map7d2 partially rescued the impairment of osteogenic differentiation caused by GR depletion.Taken together, our study reveals common molecular responses to GR depletion across two primary murine osteogenic cell models and provides new insights into the transcriptional and signaling networks underlying GR-regulated osteogenic differentiation.

GSE346184 Transcription directs the migration of meiotic recombination intermediates [CC-Seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : William H Gittens ; Matthew J Neale
Series Type : Other
Organism : Saccharomyces cerevisiae

During meiosis, genetic diversity arises from the resolution of branched DNA intermediates called Holliday junctions to create crossovers—sites of reciprocal exchange between parental chromosomes. Holliday junctions arise during the repair of Spo11-induced DNA breaks, yet the principles linking break formation, repair, and chromosome architecture remain unclear. Top3, a type IA topoisomerase, acts on Holliday junction-containing recombination intermediates, but its spatiotemporal dynamics are unknown. Here, we map Top3 catalytic activity throughout meiotic prophase with strand specificity and nucleotide resolution. We identify a DNA sequence motif associated with catalysis and a pattern of activity around Spo11 hotspots that requires ongoing repair and Top3’s helicase partner, Sgs1. Strikingly, Top3 activity shifts over time, influenced by transcription, cohesin, and the crossover factors Msh5 and Mer3, redistributing toward sites of convergent transcription—known locations of enhanced meiotic cohesin association. Upon prophase exit, as crossovers are resolved, Top3 activity subsides. Remarkably, maps of genome-wide recombination reveal that crossover frequency is elevated at these same regions of convergent transcription. Collectively, we propose that Top3 tracks the transcription-directed migration of Holliday junction-containing meiotic recombination intermediates from Spo11 hotspots towards cohesin-associated axis sites, where crossover resolution occurs, promoting accurate meiotic chromosome segregation.

GSE346163 Transcription directs the migration of meiotic recombination intermediates

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : William H Gittens ; Matthew J Neale
Series Type : Expression profiling by high throughput sequencing
Organism : Saccharomyces cerevisiae SK1

GSE345114 Gene transcription and chromatin packing domains form a self-organizing system [RIP-Seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Lucas Carter ; Vadim Backman ; Luay Almassalha
Series Type : Other
Organism : Homo sapiens

The human genome organizes into several thousand chromatin packing domains that couple euchromatin and heterochromatin into unified nanoscale volumes. Prior work suggested these domains form by transcriptionally driven loops that guide packing domain assembly. Here, we study the process of transcriptionally driven domain formation and maintenance. By pairing auxin-inducible degron technology with nanoscopic imaging, transcriptomics, and Hi-C, we show that Pol-II regulates conformationally defined interphase chromatin packing domains. Pol-II facilitates nascent domain generation and maintains mature domain integrity through the process of generating transcriptional loops. Mechanistically, Pol-II maintains the packing of intronic and intergenic chromatin within domains by transcribing exons within gene bodies. Consequently, polymerase loss disrupts genome connectivity, in situ packing domains, and gene expression, genome-wide. Our findings suggest chromatin packing domains and RNA synthesis are tightly coupled to optimize transcriptional responses in human cells.

GSE345113 Gene transcription and chromatin packing domains form a self-organizing system [EU-Seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Lucas Carter ; Vadim Backman ; Luay Almassalha
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

GSE345111 Gene transcription and chromatin packing domains form a self-organizing system [CUT&Tag]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Lucas Carter ; Vadim Backman ; Luay Almassalha
Series Type : Genome binding/occupancy profiling by high throughput sequencing
Organism : Homo sapiens

GSE344612 Id2 orchestrates IL-33-driven metabolic reprogramming in pathogenic Th2 cells (RNA-seq)

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Xiaojuan Han ; Huarong Huang ; Xi Wang ; Ping Gao ; Xiangwen Liu ; Chao Li ; Xiaoyu Zhai ; Xuyu Zhou ; Jianwei Wang ; Jian Song ; Fuping Zhang
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

The transcription factor Id2 licenses the transition of stem‑like Th2 cells to pathogenic ST2⁺ Tpath2 cells by orchestrating IL‑33‑ST2 signaling to drive glycolytic reprogramming. Id2 transcriptionally represses Pten by sequestering E proteins at its promoter, amplifying PI3K‑AKT signaling and glycolytic flux, which supports histone acetylation at Il1rl1 and Il5. Id2‑deficient Th2 cells fail to establish this epigenetic state; pyruvate supplementation rescues the defect. Pharmacological Id2 inhibition attenuates Tpath2 responses and airway inflammation in vivo, and cross‑species analysis confirms conserved PTEN dynamics in human asthma. Thus, the IL‑33–Id2–PI3K‑AKT axis represents a metabolic–epigenetic checkpoint and therapeutic target for allergic airway disease.

GSE344609 Immune activation during broadly neutralizing antibody-mediated HIV suppression prior to post-intervention control

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Julia A Wagner ; Ravi K Patel ; Gabriela K Fragiadakis ; Rachel L Rutishauser
Series Type : Other ; Expression profiling by high throughput sequencing
Organism : Homo sapiens

Broadly neutralizing antibodies (bNAbs) have been associated with enhancement of HIV-specific T or B cell responses and sustained partial control of HIV replication in some people with HIV (PWH). The mechanisms through which bNAbs may potentiate host immunity in this context are not known. We previously reported the outcomes of a clinical trial in which ten PWH on antiretroviral therapy (ART) received a combination of immunotherapies including two bNAbs administered immediately preceding an analytic treatment interruption (ATI). After bNAb levels waned, seven participants exhibited varying degrees of post-intervention control of HIV linked to a robust expansion of activated CD8+ T cells in response to rebounding virus. To investigate the role of the bNAbs in enhancing endogenous immune responses, we looked for evidence of HIV-specific or broader immune activation during the period after ART was paused and prior to rebound when bNAbs were controlling HIV replication. At a timepoint early post-ART interruption and at least one month before virus emerged in plasma, we detected an increase in levels of plasma inflammatory proteins as well as phenotypic and transcriptional activation of innate and adaptive immune cells. Compared to non-controllers, post-intervention controllers demonstrated unique transcriptional activation patterns as well as differential longitudinal plasma inflammatory protein trends. No enhancement of HIV-specific T cell or antibody responses was observed in this window. This study identifies activated cell types and inflammatory pathways that are recruited early during bNAb-mediated HIV suppression and that may play a role in potentiating long-lasting HIV immune control after bNAb therapy.

GSE344504 Tissue Nano-Transfection Promotes Vascularization to Enhance Acellular Nerve Allograft–Mediated Nerve Repair

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Ana I Salazar-Puerta ; Megumi Fukuda ; Sara Kheirkhah ; Hallie Harris ; Carlos A Vasquez-Martinez ; Carolina Velasquez-Quintero ; Charlie Wendt ; Nada Khattab ; Hamid Malekzadeh ; Mary Gilsenan ; Reade Otto-Moudry ; Manami Fukuda ; Tiam M Saffari ; Kavya Dathathreya ; William D Arnold ; Daniel Gallego-Perez ; Amy M Moore
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Peripheral nerves possess an inherent capacity for regeneration, yet functional recovery following an injury remains inconsistent despite advances in microsurgical repair. Autologous nerve grafts are the gold standard for complex peripheral nerve injuries (PNI) but are constrained by limited donor availability, donor-site morbidity, and size mismatches. Acellular nerve allografts (ANAs) offer off-the-shelf availability and can bridge longer defects, but their performance is hindered by the lack of intrinsic Schwann cells and vascular structures, essential for axonal regeneration. Here, we report on the use of Tissue Nanotransfection (TNT), a novel non-viral platform that allows the delivery of nucleic acids into solid tissues in combination with ANAs. We used TNT to reprogram resident nerve cells toward a vasculogenic phenotype to locally increase vascularization and improve outcomes following PNI reconstruction. We show that vasculogenic transcription factors (Etv2, Fli1, and Foxc2; EFF) drive transcriptomic changes in vitro. In vivo, vasculogenic TNT increases the number of endothelial cells within ANAs as early as 5 weeks post-treatment. Mice receiving ANAs combined with vasculogenic TNT exhibited superior functional recovery, including enhanced muscle strength and progressive restoration outperforming ANAs only controls. Region-specific transcriptomics reveal that the site of the TNT application along the host nerve critically influences the regenerative response. Together, these findings identify vasculogenic TNT as a potent, non-viral strategy to enhance ANA-mediated repair by promoting localized vasculogenesis and supporting improved functional recovery and muscle protection.

GSE344220 Local effect of Ixodes scapularia TNFBP gene silence on transcriptome of bitten skin of mouse

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Yingjun Cui
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

To explore their potential role in tick-host interactions, RNA-seq was performed on the skin of mice bitten by TNFBP1 and TNFBP2 silenced ticks. The transcriptome was altered after feeding on gene silenced ticks compared with control ticks, and defined pathways including legionellosis, HIF-1TNF, IL-17 signaling pathway, phagosome were significantly enriched in the downregulated genes.

GSE342465 PODXL regulates the neuronal entry of α-Synuclein aggregates

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Sandesh Neupane
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

The spread of pathogenic α-synuclein assemblies between cells is thought to contribute to the progression of Parkinson’s disease, but the neuronal surface factors that control their uptake are still incompletely understood. To address this question, we established an arrayed CRISPR activation platform in human iPSC-derived cortical neurons and quantified the internalization of fluorescent α-synuclein preformed fibrils by high-throughput flow cytometry. Screening Parkinson’s disease genetics-prioritized surface proteins revealed podocalyxin-like protein 1 (PODXL) as a prominent negative regulator of fibril uptake.

GSE342135 RNA‑seq analysis of leaf transcriptomes in wild‑type and slzf3 mutant tomato under normal and cold temperatures.

Sat, 31 Oct 2026 00:00:00 -0400

Series Type : Expression profiling by high throughput sequencing
Organism : Solanum lycopersicum

SlZF3, a C2H2‑type zinc finger protein, plays a pivotal role in tomato cold tolerance. To elucidate the underlying molecular mechanisms and identify its potential target genes under cold stress, we performed transcriptome profiling of wild‑type and slzf3 mutant leaves under normal and low‑temperature conditions. Integrated multi‑omics analysis enabled the identification of downstream target genes involved in SlZF3‑regulated metabolic pathways, providing a comprehensive view of the SlZF3‑mediated cold regulatory network.

GSE342123 Specification of bone marrow sinusoids requires TIE2-mediated positive feedback involving COUP-TFII and VEGFR3 [Nr2f2_ecko P5bm]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Xiao Li ; Xiwen Jia ; Yulong He
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

The bone marrow (BM) vascular network drives bone development and supports hematopoiesis, yet the mechanisms governing its specialized sinusoidal architecture remain poorly characterized. Here, we show that the angiopoietin receptor TIE2 is highly expressed by BM sinusoidal endothelial cells (BM_SECs), and its endothelial deletion triggers sinusoidal capillarization, characterized by reduced vessel diameter and aberrant mural cell coverage. Mechanistically, TIE2 insufficiency drives a downregulation of VEGFR3 in BM_SECs, while leaving hepatic sinusoidal VEGFR3 unaffected. Notably, BM sinusoidal VEGFR3 downregulation occurred within 48 hours of induced endothelial Tek deletion. RNA-sequencing revealed that TIE2 insufficiency downregulated pathways related to sinusoidal development, alongside an aberrant upregulation of arterial and angiogenic genes. We validated this phenotype using inducible Tek deletion specifically within VEGFR3+ SECs, or in mutant mice with the insufficiency of TIE2 ligand ANGPT1. Furthermore, endothelial deletion of the transcription factor Nr2f2 (COUP-TFII) recapitulated these defects, yielding reductions in BM sinusoidal TIE2 and VEGFR3 expression. Finally, induced endothelial deletion of Flt4 produced a similar phenotype of defective BM sinusoidal formation. Together, our findings demonstrate that ANGPT1/TIE2 and COUP-TFII form a reciprocal regulatory loop essential for coordinating BM sinusoidal specification by sustaining VEGFR3 expression.

GSE342122 Specification of bone marrow sinusoids requires TIE2-mediated positive feedback involving COUP-TFII and VEGFR3 [Tek_ecko P3bm]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Xiao Li ; Xiwen Jia ; Yulong He
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

GSE342121 Specification of bone marrow sinusoids requires TIE2-mediated positive feedback involving COUP-TFII and VEGFR3 [Tek_ecko P11bm]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Xiao Li ; Xiwen Jia ; Yulong He
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

GSE341759 A Viral Replication Level-Dependent Continuum of Transcriptional and MicroRNA Reprogramming in HIV-1-Infected Microglia Links Productive Infection to Neurocognitive-Associated Gene Networks [RNA-seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Zahra Vahdat ; Suman Sharma ; Khanghy Truong ; Dilshan Adhikari ; Jason T Kimata ; Cristian Coarfa ; Andrew P Rice
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Microglia are major targets of HIV-1 in the brain. Despite the effectiveness of antiviral therapy, infected microglia, including those containing a replication-defective provirus, can express viral RNA and proteins that contribute to neuroinflammation. However, the degree to which productive infection shapes the host response in microglia remains poorly defined. Using single cell RNA-seq of HIV-1-infected C20 microglia, we stratified cells by counts of HIV-1 reads with splice junctions into low- and high-infection groups, enabling us to resolve a graded rather than binary host transcriptional response. A core set of immune and cell-cycle pathways was induced regardless of infection level, but several programs reversed direction with increasing viral burden: interferon-α/γ and EMT/hypoxia signatures peaked at low infection, while high infection was marked by suppression of these signatures alongside induction of mTORC1/MYC signaling, ribosome biogenesis, RNA processing, and mitotic activity, accompanied by progressive loss of cytoskeletal, motility, and developmental gene programs. This pattern was reproduced in iPSC-derived microglia, supporting its generalizability beyond an immortalized line. Integration of differentially expressed miRNAs with differentially expressed genes from the low- and high-infection groups showing the canonical inverse miRNA-target relationship revealed miRNA/mRNA networks with strong representation of miRNAs previously implicated in HIV-1 replication (e.g., miR-33a-5p, miR-3065-3p) and in neurodegenerative and psychiatric disease (e.g., miR-107, let-7c-5p). These findings define a productive-infection-level continuum in microglial transcription, miRNA reprogramming, and identify candidate miRNA-mediated mechanisms, independent of the canonical Env/Nef/Tat pathway, by which HIV-1-infected microglia may contribute to neuroinflammation and neurocognitive impairment in people with HIV-1.

GSE341758 A Viral Replication Level-Dependent Continuum of Transcriptional and MicroRNA Reprogramming in HIV-1-Infected Microglia Links Productive Infection to Neurocognitive-Associated Gene Networks [scRNA-seq]

Sat, 31 Oct 2026 00:00:00 -0400

GSE341757 A Viral Replication Level-Dependent Continuum of Transcriptional and MicroRNA Reprogramming in HIV-1-Infected Microglia Links Productive Infection to Neurocognitive-Associated Gene Networks [miRNA-seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Zahra Vahdat ; Suman Sharma ; Khanghy Truong ; Dilshan Adhikari ; Jason T Kimata ; Cristian Coarfa ; Andrew P Rice
Series Type : Non-coding RNA profiling by high throughput sequencing
Organism : Homo sapiens

GSE341541 Paternal methylphenidate exposure alters sperm miRNAs and induces intergenerational behavioral and transcriptional changes that are largely reversed by washout

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Kanata Akaike ; Asuka Kaizaki-Mitsumoto ; Satoshi Numazawa
Series Type : Non-coding RNA profiling by high throughput sequencing
Organism : Mus musculus

To determine whether paternal methylphenidate exposure alters sperm small noncoding RNA profiles and whether these changes are reversible after drug withdrawal, male BALB/c mice were administered methylphenidate (15 mg/kg) or saline (10 mL/kg) for 28 days. Cauda epididymal sperm were collected immediately after treatment or after a 40-day washout period and analyzed by small RNA sequencing.

GSE341398 GOLDEN: Gene expression and allele-informed decomposition for genetic heterogeneity in spatial transcriptomic data

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Hyojung Paik ; Sangjeong Lee ; Tae Lyun Ko ; Sung Ki Lee
Series Type : Other
Organism : Homo sapiens

Spatial transcriptomics (ST) enables exploration of cellular interactions, but current methods rely on pathologist annotation and face limitations in addressing genetic heterogeneity, where niches harbor non-clonal cells, as in placental or allograft tissues. To decipher such inter-individual heterogeneity in ST, we developed GOLDEN (Gene expression and allele-informed decomposition for genetic heterogeneity), an allele-aware multi-task network that encodes spot-level expression into shared latent representations. Incorporating allele features, it uses dual heads to classify spot identity (target, non-target, or mixed) and to estimate target fractions. For evaluation, we generated synthetic ST data via a Gamma-distribution model using semi-allogeneic single-cell profiles. On these synthetic benchmarks, GOLDEN achieved reliable deconvolution (Pearson's r = 0.977; MAE = 0.045) while maintaining consistent predictions across real-world STs, which were validated through genetic evidence.

GSE338826 The transcriptomic profile of wild-type HGC-27 cells treated with conditioned media from ANGPTL4-overexpressing or control HGC-27 cells

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Shanshan Qin ; Dandan Li
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Given that ANGPTL4 is a secreted protein, we combined conditioned medium treatment with transcriptomic analysis to determine whether the activation of downstream signaling pathways by ANGPTL4 overexpression is dependent on its secretion.

GSE338308 NLRP3 inflammasome-mediated pyroptosis exacerbates insulin resistance upon exposure to nanoplastics with different surface chemistries

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Xinxin Yao
Series Type : Expression profiling by high throughput sequencing
Organism : Danio rerio

The surface chemical properties of nanoplastics (NPs), such as surface charge and functional groups, can markedly influence their toxicological effects. Recent studies have shown that NPs can disrupt glucose homeostasis. However, under metabolically susceptible conditions, such as hyperglycemia and metabolic dysfunction, differences in metabolic toxicity and the underlying mechanisms among surface-modified NPs remain unclea

GSE337796 Targeting ERO1α Triggers Tumor Immunosurveillance in Triple-Negative Breast Cancer

Sat, 31 Oct 2026 00:00:00 -0400

Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

This SuperSeries is composed of the SubSeries listed below.

GSE337795 Targeting ERO1α Triggers Tumor Immunosurveillance in Triple-Negative Breast Cancer [RNA-seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Ester Zito
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Triple-negative breast cancer (TNBC) remains a highly aggressive malignancy with limited responsiveness to immune checkpoint blockade. Here, we identify endoplasmic reticulum oxidoreductase 1 alpha, a key regulator of oxidative protein folding, as a determinant of tumor immunogenicity and immunotherapy response in TNBC. Unbiased proteomic profiling demonstrated that ERO1α deficiency remodels the TNBC glycoproteome, leading to enrichment of pathways associated with innate immune signaling. Although ERO1α loss did not affect tumor cell growth, it reshaped the immune tumor microenvironment, enhancing antigen presentation, altering myeloid-cell composition, and modulating PD-1/PD-L1–associated signaling. Functionally, ERO1α deficiency sensitized otherwise refractory TNBC tumors to PD-1 blockade, resulting in durable tumor regression in immunocompetent hosts. In contrast, ERO1α deletion in bone marrow–derived immune cells had minimal effects on tumor growth or therapeutic response, supporting an ERO1α tumor-intrinsic mechanism. Pharmacologic inhibition of ERO1α with the novel small-molecule inhibitor I29 phenocopied ERO1α genetic deletion and enhanced the efficacy of anti–PD-1 therapy. Together, these findings identify ERO1α-dependent glycoproteome remodeling as a regulator of antitumor immunity and a therapeutically actionable mechanism of immune checkpoint responsiveness in TNBC.

GSE336881 Targeting ERO1α Triggers Tumor Immunosurveillance in Triple-Negative Breast Cancer [scRNA-seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Ester Zito
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

GSE335728 MicroRNA annotations from the parasitic plant Cuscuta saururi

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Michael J Axtell
Series Type : Non-coding RNA profiling by high throughput sequencing
Organism : Cuscuta saururi

The Cuscuta genus of parasitic plants is widespread and can impact agricultural productivity. Previous studies of C. campestris have described the existence of a special type of microRNA that functions to enter host tissues and regulate host mRNAs. These "interface-induced" microRNAs are uniquely transcribed by RNA polymerase III, have a common promoter element, and specifically accumulate in haustorial tissues of the parasite. Here, we investigate the existence of such "interface-induced" microRNAs in a second Cuscuta species, C. saururi. C. saururi is a recently resurrected species that forms part of the C. gronovii species complex. We used a highly contiguous genome assembly of C. saururi, along with small RNA-seq, to annotate both the interface-induced and canonical microRNA genes of C. saururi.

GSE335170 MORC2A is required for DNA methylation and H3K9me3 at retrotransposons in the male germline

Sat, 31 Oct 2026 00:00:00 -0400

Series Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencing ; Methylation profiling by high throughput sequencing ; Non-coding RNA profiling by high throughput sequencing
Organism : Mus musculus

This SuperSeries is composed of the SubSeries listed below.

GSE335167 MORC2A is required for DNA methylation and H3K9me3 at retrotransposons in the male germline [smallRNA-seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Nazareno Bona ; Niek Wit ; Paul Joseph Lehner ; Ben Nicholson ; Hui Li ; Jeff Gui
Series Type : Non-coding RNA profiling by high throughput sequencing
Organism : Mus musculus

Transposable elements pose a particular threat to the germline, where their activation can compromise fertility and generate heritable mutations. In male germ cells, transposon silencing depends on repressive epigenetic states, including CpG methylation and H3K9me3. Here, we identify MORC2A as an essential regulator of transposon repression in the mouse male germline. Conditional deletion of Morc2a in primordial germ cells caused complete male infertility, testicular atrophy, germ cell loss and meiotic arrest. MORC2A-deficient testes displayed derepression of evolutionarily young retrotransposons, accompanied by DNA damage and apoptosis. Genome-wide profiling revealed loss of CpG methylation and H3K9me3 at these elements. Small RNA sequencing showed that piRNA biogenesis and ping-pong amplification remain largely intact. Together, these datasets identify MORC2A as a male germline chromatin regulator required for epigenetic silencing of young transposable elements.

GSE335166 MORC2A is required for DNA methylation and H3K9me3 at retrotransposons in the male germline [RNA-seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Nazareno Bona ; Niek Wit ; Paul Joseph Lehner ; Ben Nicholson
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

GSE335165 MORC2A is required for DNA methylation and H3K9me3 at retrotransposons in the male germline [EM-seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Nazareno Bona ; Niek Wit ; Paul Joseph Lehner ; Ben Nicholson ; Hui Li
Series Type : Methylation profiling by high throughput sequencing
Organism : Mus musculus

GSE335164 MORC2A is required for DNA methylation and H3K9me3 at retrotransposons in the male germline [CUT&RUN]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Nazareno Bona ; Niek Wit ; Paul Joseph Lehner ; Ben Nicholson
Series Type : Genome binding/occupancy profiling by high throughput sequencing
Organism : Mus musculus

GSE334899 TREX1 limits anti-tumor immunity by degrading short cytosolic DNA molecules

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Philippe Pasero ; Yea-Lih Lin
Series Type : Other
Organism : Mus musculus

TREX1 has recently emerged as a promising therapeutic target in cancer owing to its role in degrading cytosolic DNA and suppressing type I interferon signaling. However, the nature of the immunostimulatory DNA species degraded by TREX1 remains elusive. Here, we show that TREX1 deficiency in murine lung and melanoma tumor cells leads to a substantial, MRE11-dependent increase in short cytosolic DNA fragments that originate preferentially from transcriptionally active regions of the genome, without a corresponding increase in micronuclei. These fragments robustly activate interferon-stimulated genes and drive differentiation of pro-inflammatory macrophages. In syngeneic mice, tumors derived from Trex1-knockout cells exhibit delayed growth, increased sensitivity to anti-PD-1 immune checkpoint blockade, and extended survival. These effects depend on an intact immune system and foster durable anti-tumor memory. Together, our results reveal that short, transcription-derived cytosolic DNA fragments are key TREX1 substrates mediating immune activation in cancer, establishing TREX1 inhibition as a compelling strategy to enhance tumor immunogenicity.

GSE333790 Transcriptomic characterization of macrophage subtype and behavior in early stage myocardial infarction

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Jonathan Yap ; William A Boisvert ; Jason Irei ; Selena Vanapruks
Series Type : Expression profiling by array
Organism : Mus musculus

Elucidate the spatiotemporal behavior of specific macrophage subtypes during AMI and identify novel genes with prospective therapeutic potential.

GSE333450 EZH2 inactivation drives MAPK-dependent vulnerability to MEK inhibition in RAS-mutant CMML

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Armin Zebisch ; Eva Gruden
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Chronic myelomonocytic leukemia (CMML) is a heterogeneous hematologic malignancy with limited therapeutic options. Although RAS and RAS-modifying mutations (RASmut) are common and associated with poor prognosis, targeting RAS signaling has shown limited clinical success. Here, we define co-occurrence of RASmut and EZH2 inactivation (EZH2inact) as a distinct molecular subgroup of CMML characterized by aggressive disease biology. Mechanistically, RASmutEZH2inact drives selective MAPK/ERK hyperactivation in mature myeloid cells and hematopoietic stem and progenitor compartments. Transcriptomic analysis of a large independent myeloid neoplasm cohort (Beat-AML) further supports this finding, demonstrating selective activation of gene signatures of MAPK/ERK activation in RASmutEZH2inact cases. Functionally, this signaling activation promotes proliferation and myelomonocytic differentiation in human and murine models. Therapeutically, this MAPK/ERK upregulation confers increased sensitivity to MEK inhibition (MEKi). In a murine RasmutEzh2inact-driven CMML model, MEKi suppresses MAPK/ERK activity and reduces leukemic burden by impairing proliferation and myelomonocytic differentiation without inducing cell death. In primary human CMML samples ex vivo, MEKi shows stronger anti-proliferative effects in RASmutEZH2inact specimens compared with RASmut samples. Drug-sensitivity data from the Beat-AML cohort further supported this. Ultimately, these findings were confirmed in a patient-derived xenograft model, where MEKi reduced the leukemic burden by selectively inhibiting the proliferation of transplanted human RASmutEZH2inact leukemic cells. In summary, our data define RASmutEZH2inact CMML as a clinically relevant subgroup with selective MAPK/ERK hyperactivation and increased sensitivity to MEKi. They provide a mechanistic explanation for the limited efficacy of MEK inhibitors in unselected CMML and support molecularly guided use of MEK-targeted therapy in this patient population.

GSE332913 Sarm1 Gates the Transition from Protective to Repair Schwann Cell States Following Nerve Injury [snRNA-Seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Ekaterina Stepanova ; Sarah Hunter-Chang ; John Lee ; Anika Tripathi ; Caitlin Pavelec ; Carol Cho ; Tanvika Vegiraju ; Jingxuan Guo ; Charlene Kim-Aun ; Sarah Kucenas ; Norbert Leitinger ; Jaeda Coutinho-Budd ; John Campbell ; Christopher Deppmann
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Schwann cells (SCs) transition into a Repair state after peripheral nerve injury; however, the early SC injury response preceding this transition remains poorly understood. We demonstrate that Sarm1, a key regulator of axon degeneration, is expressed and upregulated in SCs after nerve injury. Cell-type-specific Sarm1 knockout SCs exhibit enhanced axon protection in vitro, and SC- and glia-specific Sarm1 deletion confers axon protection in mouse sciatic nerve and Drosophila wing injury models. Single-nucleus RNA sequencing revealed that Sarm1-deficient SCs are enriched in a distinct cluster expressing genes with developmental roles in axon and myelin protection, with increased oxidative phosphorylation gene expression across all injured SC states. We propose that Sarm1 gates the transition from a Protection-Associated Schwann Cell (PASC) state to a Repair SC state, establishing Sarm1 as a multi-functional regulator with implications for peripheral neuropathies and neurodegenerative diseases.

GSE332854 Sarm1 Gates the Transition from Protective to Repair Schwann Cell States Following Nerve Injury [RNA-seq]

Sat, 31 Oct 2026 00:00:00 -0400

GSE332811 Single cell transcriptomic sequencing in common mouse models of atherosclerosis

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Eng Leng Saw ; Heming Zhang ; Shu Ye
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

A single cell analysis of mice aorta to perform comprehensive comparison among common mouse models of atherosclerosis

GSE331239 Stereo-seq of aortic atherosclerotic lesions in common mouse models

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Eng Leng Saw ; Heming Zhang ; Shu Ye
Series Type : Other
Organism : Mus musculus

A spatial transcriptomic analysis of aortic root atherosclerotic lesions for a comparison between common mouse models of atherosclerosis

GSE331089 Single-cell analysis reveals transcriptomic patterns in active macrophage activation syndrome and therapeutic potential of albumin-fused interleukin-10 in a mouse model

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Wataru Fujii ; Kevin Bassler
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Hemophagocytic lymphohistiocytosis (HLH) and macrophage activation syndrome (MAS) are life-threatening hyperinflammatory conditions characterized by excessive immune activation and cytokine production. To clarify immune cell characteristics and identify potential therapeutic targets in MAS, we performed single-cell RNA sequencing (scRNA-seq) on bone marrow and peripheral blood samples from patients with newly developed MAS caused by diverse etiologies. To broaden the current knowledge of the immune landscape in the bone marrow, we performed scRNA-Seq of bone marrow cells and isolated blood leukocytes obtained from MAS patients using the Seq-Well.

GSE330926 Microglia modulate concussion biomarkers and recovery in male mice

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Erin D Anderson ; Daunel V Augustin ; Anastasia P Georges ; Taehwan Kim ; David A Issadore ; David F Meaney
Series Type : Non-coding RNA profiling by high throughput sequencing ; Expression profiling by high throughput sequencing
Organism : Mus musculus

There is a critical unmet need for concussion biomarkers that predict cognitive recovery. Existing TBI biomarkers largely capture acute cellular damage rather than the multicellular repair processes that determine long-term outcome, and whether microglia causally shape divergent trajectories remains unclear. Here, we used PLX5622 to deplete microglia and other CSF1R-dependent myeloid cells in a male mouse model comparing concussion alone to concussion preconditioned by prior subconcussive impacts. Microglial depletion had no effect on cognitive outcome after concussion alone, but introduced a significant novel object recognition deficit specifically when concussion was preconditioned, revealing a history-dependent role for microglia in recovery. To identify the molecular substrates of this divergence, we profiled brain-derived GluA1/2 + extracellular vesicle (EV) miRNAs and single-nuclei transcriptomes from the injured brain. Diagnostic and injury-history EV miRNA biomarkers discriminated between concussion subtypes in microglia-intact animals but lost this discriminative power after depletion, indicating that these neuron-enriched biomarkers are influenced by microglia-dependent biology rather than injury alone. snRNA-seq further revealed that microglial depletion selectively induced transcriptional programs related to oligodendrocyte maturation after unconditioned concussion, a candidate substrate for this microglia-dependence. Finally, we identified a serum EV miRNA panel that estimated cognitive recovery across injury conditions. Together, these findings identify a history-dependent role for microglia in concussion outcome and characterize brain-derived EVs as a potentially promising tool for surveilling the neuroinflammatory processes influencing recovery.

GSE330582 Exposure to perfluorooctanoic acid perturbs serotonin signaling in maternal pancreatic islets and induces gestational diabetes in mice

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Knickole L Bergman ; Mary Jerred ; Cameron Baker ; Madeline O'Connell ; Clementina Mesaros ; Martha Susiarjo
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

[working abstract for manuscript, in style of how is required for EHP] Background: Perfluorooctanoic acid (PFOA) has been linked to gestational diabetes and other adverse pregnancy outcomes in humans. Despite the association, the mechanisms by which PFOA contributes to GDM have not been studied. The present study investigated whether PFOA exposure resulted in lower pancreatic islet serotonin abundance and β-cell proliferation, glucose intolerance, impaired insulin secretion, insulin resistance, and robust transcriptional changes underlying pancreatic islet adaptation, which provided evidence for a mechanism of PFOA-induced GDM. Objectives: The purpose of this study was to assess whether PFOA exposure impairs pancreatic islet serotonin-driven β-cell proliferation and causes GDM in a C57BL/6J mouse model. Methods: Analysis of pancreatic islet serotonin abundance and β-cell proliferation were measured by immunofluorescence. Metabolic assays, including glucose tolerance test, glucose-stimulated insulin secretion, and insulin tolerance test were used to characterize GDM phenotypes. Bulk RNA sequencing was used to analyze differentially expressed genes and gene set enrichment in pancreatic islets isolated from control and PFOA-exposed mice. Results: PFOA exposure lowered islet serotonin abundance and β-cell proliferation in gestational day (GD) 12.5 pregnant dams. PFOA exposure was associated with glucose intolerance, impaired insulin secretion, and insulin resistance in GD16.5 pregnant dams. β-cell proliferation at GD12.5 and glucose tolerance at GD16.5 was improved in PFOA-exposed dams treated with a serotonin receptor 2B agonist (BW-732C86). RNAseq uncovered four differentially expressed genes and a broad reduction in coordinated transcriptional pathway activity in maternal pancreatic islets of PFOA-exposed GD12.5 dams. Discussion: PFOA-induced glucose intolerance was associated with perturbed pancreatic islet serotonin abundance.

GSE329876 MUC13 enhances IL-17 signaling pathway activity in nasal epithelial cells

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Jiewen Zhou ; Nianzhen Zheng ; Xinyu Zhang
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

MUC13 is a membrane-bound mucin involved in epithelial protection and barrier maintenance, but its role in nasal epithelial inflammation remains unclear. This study aimed to investigate the function of MUC13 in nasal epithelial cells (NECs) and its potential involvement in inflammatory signaling. Primary NECs were isolated from patient-derived inferior turbinate mucosa, and MUC13 overexpression was established by direct transfection of human MUC13 mRNA. RNA sequencing and bioinformatics analyses were performed to characterize transcriptomic changes.

GSE329506 GPR124 upregulation protects AML blasts from lipotoxicity

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Emmanouil Kyrloglou ; Dominique Sternadt ; Albertus T J Wierenga ; Diego A Pereira-Martins ; Vincent van den Boom ; Gerwin Huls ; Jan Jacob Schuringa
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

GPR124 (ADGRA2), a member of the Adhesion G Protein-Coupled Receptor family, has an established role in the embryonic development of the central nervous system vasculature. However, its function in the context of acute myeloid leukemia (AML) remains unexplored. Transcriptome studies revealed upregulation of GPR124 in AML CD34+ blasts compared to healthy counterparts. Lentiviral overexpression of an GPR124-EGFP fusion protein indicated both plasma membrane and intracellular localization. Immunoprecipitation followed by LC-MS/MS showed strong enrichment of intracellular proteins associated with vesicles and vesicle transport, focal adhesion, actin cytoskeleton, and lipid droplets (LDs). In murine bone marrow mesenchymal stromal cells stimulated towards adipocytic differentiation, CRISPR-Cas9 mediated knockout of Gpr124 (Gpr124KO) reduced LD size, while total neutral lipid accumulation showed an increasing trend. In AML cells, lipidomic studies revealed increased baseline triacylglycerol (TG) levels in GPR124KO cells, suggesting altered LD metabolism. Since TGs are key components of LDs and its accumulation is a known response to lipid peroxidation, we next assessed ferroptosis sensitivity. Indeed, GPR124KO cells were significantly more sensitive to ferroptosis induction by GPX4 inhibition, accompanied by increased reactive oxygen species (ROS) and accumulation of lipid peroxidation. Additionally, GPR124KO cells were more sensitive to DGAT1 inhibition, a key enzyme in LD formation, and combination with the ferroptosis inducer RSL3 was synergistic in GPR124KO cells. Together, our findings indicate that GPR124 is essential for maintaining stable lipid homeostasis in AML and identify GPR124 and LD metabolism as potential therapeutic targets for inducing ferroptosis-mediated cell death.

GSE327909 Single-cell atlas reveals shared early microenvironmental remodeling in colorectal polypogenesis

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Zhenling Zhang ; Wang Zhao ; Jiangnan Ren
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Colorectal polyps are the earliest precancerous lesions in colorectal carcinogenesis, but their common microenvironmental drivers remain incompletely defined. We performed single-cell RNA sequencing on paired normal mucosal and colorectal polyp tissues from 3 patients with unselected lesions, including hyperplastic polyps and tubular adenomas. After quality control, 31,147 high-quality cells were obtained. Comparative analysis revealed four conserved hallmarks of colorectal polyps relative to normal mucosa: disrupted epithelial homeostasis characterized by stem cell expansion, Paneth cell reduction, and Wnt pathway activation; pro-inflammatory polarization of CD4+ T cells with increased Th17 cells and activation of NF-kB/IL-17-related pathways; functional reprogramming of CD8+ T cell subsets, especially decreased IELs with specialized immune functions; and extensive remodeling of immune-epithelial intercellular communication, including CD55-ADGRE5, MIF-CD74, and GZMA-PARD3 signaling axes. These data provide a single-cell atlas of shared microenvironmental changes in early colorectal polypogenesis.

GSE327337 A Single-Cell Atlas of Human Periodontal Ligament During Orthodontic Tooth Movement

Sat, 31 Oct 2026 00:00:00 -0400

Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Orthodontic tooth movement (OTM) requires coordinated remodeling of the periodontal ligament (PDL) and alveolar bone, yet the cellular architecture underlying this process in human tissues remains incompletely understood. Here, we generated the first single-cell transcriptomic atlas of the human PDL during OTM by profiling cells from the pressure and tension sides of teeth collected at day 3 and day 7 following force application. This atlas reveals the major stromal and immune cell populations and highlights spatial and temporal heterogeneity across force conditions and remodeling stages.

GSE326633 Endogenous PD-L1-Blocking Antibodies Drive Potent Anti-Tumor Immunity

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Fernanda T Frozza ; Rodrigo B Gassen ; Veridiane M Pscheidt ; Deise de Freitas ; Anelise Baptista da Silva ; Claudia Paiva Nunes ; Millena Scherer ; Gabriel F Mattos ; Julia C Fontoura ; José Eduardo Sacconi Nunes ; Valdir C Barth ; Caio Marques ; Athos Brandielli Schuck ; Marvin P Lins ; Giuliano Rizzotto Guimarães ; Luis E Caldeira ; Pedro H Filipin ; Maurício Rigo ; Camila Diehl ; Solon A da Rosa ; Antonio Kalil ; Stephan A Soder ; Cristina Bonorino
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Checkpoint blockade therapy, though transformative, remains ineffective in 70-80% of patients, with autoimmune adverse effects. Here, we provide the first evidence of a naturally occurring form of immune checkpoint blockade mediated by endogenous antibodies that functionally replicate the effects of therapeutic checkpoint inhibitors, without autoimmune symptoms. Through cloning and reconstructing patient-derived monoclonal antibodies, we show that certain cancer patients produce PD-L1-blocking antibodies that can restore T cell function and induce potent anti-tumor immunity. Broad polyreactive responses to multiple checkpoints confer no survival advantage. However, patients who are selectively positive for PD-L1 antibodies exhibit prolonged survival, tumors enriched with memory T cells, and activated circulating T cells. Mechanistically, these PD-L1 antibodies block PD-1/PD-L1 interactions and restore T cell function, in vitro and in vivo, revealing a naturally regulated form of checkpoint inhibition. Our data reveal that key principles of successful immunotherapy can emerge endogenously in a subset of patients, redefining our understanding of immune competence, tolerance, and therapeutic responsiveness in cancer, offering a mechanistic framework to explain how certain patients mount more effective anti-tumor immunity.

GSE326551 Upregulated TRPM1 is associated with apoptosis in Rs1 knockout mice and in ARPE19 cells through increased intracellular calcium

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Weiping Wang ; Jingyang Liu ; Xiuxiu Jin
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

The pathological mechanism underlying retinal apoptosis in X-linked retinoschisis (XLRS), a disease caused by retinoschisin 1 (RS1) deficiency, remains incompletely understood. This study aimed to investigate the role of transient receptor potential melastatin 1 (TRPM1) in retinal tissues and cells. Retinal function and structure were assessed by electroretinography (ERG) and optical coherence tomography (OCT). Protein expression was evaluated by immunofluorescence staining and western blotting (WB). Retinal morphology was examined by hematoxylin and eosin (H&E) staining. Apoptotic retinal cells were detected by TUNEL staining. Key proteins were screened using proteomics data obtained by mass spectrometry. Intracellular calcium levels were measured using Rhod-2 AM. TRPM1 expression in Rs1-KO mice was 1.3-fold higher than that in wild-type mice (p < 0.05), whereas TRPM1-overexpressing ARPE19 cells exhibited approximately twofold higher expression than the empty vector control group. Mechanistically, TRPM1-mediated calcium influx promoted calcium/calmodulin-dependent protein kinase II (CAMKII) phosphorylation. Concomitantly, the accumulation of the autophagy-related proteins P62 and LC3B, increased BAX expression, and decreased BCL2 expression were observed in both Rs1-KO retinal tissues and TRPM1-overexpressing ARPE19 cells. These findings collectively suggest that TRPM1 may contribute to cell’s apoptosis. Our study provides new insight into the mechanism of retinal apoptosis in XLRS.

GSE326149 Small RNA sequencing of fibrotic intestinal tissues from TNBS-induced mice

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Xintong Wang ; Zhen Huang ; Jiangning Chen
Series Type : Non-coding RNA profiling by high throughput sequencing
Organism : Mus musculus

To investigate miRNA expression changes associated with intestinal fibrosis, we performed small RNA sequencing on colon tissues from TNBS-induced fibrotic mice and control mice. This dataset was generated to identify fibrosis-associated miRNAs and provide a basis for subsequent functional and mechanistic studies of intestinal fibrosis.

GSE326147 mRNA expression profiling of intestinal fibrosis in TNBS-induced mice

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Xintong Wang ; Zhen Huang ; Jiangning Chen
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

To characterize transcriptomic alterations associated with intestinal fibrosis, we performed mRNA sequencing on colon tissues from TNBS-induced fibrotic mice and control mice. This dataset was generated to identify differentially expressed genes and signaling pathways involved in intestinal fibrosis.

GSE325408 Comparative study of the osseointegration capacity of porous tantalum, titanium, and HA/PA66

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Caiping Yan ; Yuanyuan Yi ; Dianming Jiang ; Zhengxue Quan ; Kai Li ; Ai Guo
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Obtaining long-term and stable osseointegration of biomaterials in vivo remains a significant challenge. In recent years, pure titanium, HA/PA66, and porous tantalum have been widely used in the field of orthopedic implants. However, there is no comparative study of these three materials in the field of osseointegration. In this study, the physical properties, biosafety, osteogenic differentiation, and osseointegration of these three materials were comparatively investigated through material characterization, in vitro experiments, and in vivo experiments. In vitro experiments showed that porous tantalum has the roughest surface and better hydrophilicity, which is more conducive to osteoblast adhesion, proliferation, and differentiation. In vivo experiments confirmed that porous tantalum has the best osseointegration effect after implantation in vivo, with more surrounding new bone tissue and higher bonding strength. The results of this study are of great significance in guiding the improvement of biomaterials and promoting the selection of materials for practical clinical applications.

GSE324592 Somatic TP53 Mutations Drive T and NK Cell Dysfunction and Create an Inflammatory Immune Niche in Acute Myeloid Leukemia

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Li Li ; Muharrem Muftuoglu ; Edward Ayoub
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

TP53-mutant acute myeloid leukemia (AML) is characterized by poor prognosis and limited response to immunotherapy, yet the mechanisms underlying immune failure in this setting remain unclear. Here, we integrate single-cell DNA sequencing with surface proteomics to demonstrate that somatic TP53 mutations arise not only in leukemic blasts but also in T and NK cells from patients with TP53-mutant AML. TP53-mutant T cells exhibit enhanced exhaustion phenotypes, impaired cytotoxic function, and altered clonal architecture. Mechanistically, mutant p53 reprograms T cells toward a pro-inflammatory yet dysfunctional state, reshaping cytokine networks and promoting a niche enriched in inflammatory and myeloid-supportive signals. These mutant T cells impair both intrinsic effector function and the functionality of surrounding immune cells. Introduction of TP53 mutations into healthy donor T cells recapitulates exhaustion and impaired tumor control, whereas elimination of mutant p53 restores effector function, normalizes cytokine programs, and improves disease control in a TP53-mutant AML xenograft model.

GSE324316 Priapulids polarize the recurrent genomic evolution of ecdysozoans

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Ferdinand Marlétaz ; Bruno C Vellutini ; Carmen Andrikou ; Luke Sarre ; Alex de Mendoza ; Jose Maria Martin-Duran ; Daniel S Rokhsar ; Andreas Hejnol ; Maximilian J Telford
Series Type : Methylation profiling by high throughput sequencing ; Expression profiling by high throughput sequencing
Organism : Halicryptus spinulosus ; Priapulus caudatus

Priapulids constitute a key lineage for understanding the early ecdysozoan evolution, as their phylogenetic position, slow rates of evolution, and rich Cambrian fossil record contrasts with the highly derived nature of arthropods and nematodes. Here, we report chromosome-scale genomes for two priapulids and show that they did not experience the accelerated genomic evolution prevalent in other ecdysozoans suggesting this acceleration occurred recurrently across multiple branches rather than once. suggesting it did not arise once but occurred recurrently in multiple lineages. This recurrent trend involves the dislocation and rearrangement of ancestral chromosomal units and extensive gene loss, repeatedly affecting essential functions such as ciliary motility and cell division. We further uncover an ancestral whole genome duplication in priapulids; preferential expression of retained paralogues during introvert formation suggests this duplication contributed to priapulid emergence and radiation during the Cambrian. Recurrent loss of ancestral genomic characters during the evolution of Ecdysozoa parallels convergent morphological simplification, such as miniaturisation

GSE323388 RNA-seq of Mus musculus 2-cell embryos (WT vs Tcl1 KO) with CDCA treatment

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Siyu Du ; Yu He ; Xiaojing Hou
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

This study includes paired-end bulk RNA-seq data generated from Mus musculus embryos at the 2-cell stage. Samples comprise wild-type (WT) and Tcl1 knockout (KO) embryos, with and without CDCA treatment, with biological replicates. Raw sequencing data are available in SRA and linked here via SRA Run accessions.

GSE320323 Enhanced plasmin generation due to PAI-1 deficiency impairs regulated vascular endothelial cell motility.

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Hideto Sano ; Masahiko Ito ; Tetsuro Suzuki ; Tetsumei Urano ; Yuko Suzuki
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Background: Plasminogen activator inhibitor-1 (PAI-1) plays a crucial role in the plasminogen activation system and fibrinolysis. Congenital PAI-1 deficiency in humans is characterized by severe bleeding and delayed wound healing, which is consistent with the altered regulation of the fibrinolytic regulation. Although plasmin influences various cellular processes, the mechanisms by which PAI-1-mediated control of plasminogen activation and regulates endothelial cell (EC) behavior, especially at the pericellular level, are not well understood. The aim of this study was to elucidate the specific cellular effects of enhanced plasminogen activator (PA) activity caused by PAI-1 deficiency in human ECs. Methods: PAI-1 deficient human ECs (PAIKO-ECs) were generated using CRISPR/Cas9-mediated gene editing and compared them with wild-type ECs (WT-ECs). We investigated the impact of plasminogen-induced pericellular plasmin activity and its impact on endothelial migration and angiogenic tube formation, conducting additional transcriptomic analysis. Results: PAIKO-ECs exhibited markedly increased PA activity, as demonstrated by elevated plasmin generation in the presence of plasminogen. In scratch assays, PAIKO-ECs exhibited increased overall uncoordinated motility with multidirectional migration trajectories and impaired directional wound closure in the presence of plasminogen; however, cell proliferation remained unaffected. This aberrant migratory phenotype was reversed by aprotinin, recombinant active PAI-1, or the lysine analog epsilon-aminocaproic acid (EACA). EACA notably reduced plasminogen accumulation on the cell surface while preserving fluid-phase plasmin generation. This indicates that enhanced EC motility is driven by pericellular rather than fluid-phase plasmin activity. In tube formation assays, PAIKO-ECs formed a higher number of extremities and branches, a phenotype that was reversed to the level of WT-ECs by EACA or aprotinin. Transcriptome analyses revealed differential gene expression related to fibrinolysis, angiogenesis, and endothelial-mesenchymal transition. Conclusions: These findings reveal that pericellular plasmin activity is essential for EC motility and angiogenic behavior under PAI-1-deficient conditions. This provides novel mechanistic insight into the spatial plasminogen activation systems in vascular remodeling.

GSE318452 A PolyQ Repeat in PIF7 acts as a tunable thermosensor in Arabidopsis [RNA-seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Maolin Peng ; Katja E Jaeger
Series Type : Expression profiling by high throughput sequencing
Organism : Arabidopsis thaliana

Plant growth is a highly plastic response requiring the integration of endogenous and environmental signals. Organisms from different climates must adapt to different temperature ranges, but the mechanisms by which proteins can alter their temperature response profile are not well understood. Central regulators of growth are the PHYTOCHROME INTERACTING FACTOR (PIF) family of bHLH transcription factors that activate the transcription of genes encoding auxin biosynthesis enzymes in response to temperature (thermomorphogenesis). Enhanced auxin levels direct cell elongation and growth. PIF7 is necessary for thermomorphogenesis, but it is not known how temperature activates PIF7. We have identified a critical role for a polyglutamine (polyQ) sequence in PIF7 that is necessary for PIF7 dimerization and DNA binding in response to temperature. We show that higher temperatures directly increase dimerization of PIF7 via the polyQ and thermal responsiveness is proportional to the polyQ length. We are able to use this thermosensory module to create synthetic transcription factors and confer temperature dependency on independent developmental decisions such as the specification of stomata. Extensive variation in the polyQ repeat length in different species suggests a mechanism to tune responsiveness to climate.

GSE318393 A PolyQ Repeat in PIF7 acts as a tunable thermosensor in Arabidopsis

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Maolin Peng ; Katja E Jaeger
Series Type : Genome binding/occupancy profiling by high throughput sequencing
Organism : Arabidopsis thaliana

GSE318110 Comparative profiling of SARS-CoV-2 variant infections reveals diverse impacts on host cell RNA and RNA binding protein distribution and regulation

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : De Bisschop Grégoire ; Pham Tram ; Jacques-De Vries Nicolas ; N Monford Paul Abishek ; Boulais Jonathan ; Deschamps-Francoeur Gabrielle ; Kwon Eunjeong ; Cohen Eric ; Lécuyer Eric
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

RNA viruses perturb cellular RNA metabolism to promote viral transcript expression and genome replication. However, the extent of host cell RNA reprogramming and the consequences on RNA binding protein (RBP) expression and localization remain poorly understood. Here, we utilized an integrated set of transcriptomics, proteomics, and high-content imaging approaches to compare the impact of different SARS-CoV-2 variants, including an early viral isolate and later emerging variants of concern (Alpha, Delta and Omicron) on the host cellular RNA and RBP landscapes. While all variants deeply remodelled the host transcriptome in a subcellular compartment-specific manner, we found that Omicron variants express lower levels of viral RNA products compared to earlier variants, while still driving efficient production of viral proteins. The surge in viral RNA expression correlated with altered subcellular RNA biotype distribution, cytoplasmic mRNA exclusion, the selective disruption of the localization of polyA-tail interacting proteins, and the nuclear accumulation of non-coding transcripts such as RN7SL family members and MALAT-1. Unexpectedly, we found many RBPs that exhibiting altered subcellular localization following abiotic innate immune stimulation with poly(I:C) but remained unaltered in cells infected with SARS-CoV-2 variants, revealing a capacity for these viruses to limit the overall impact on the RBP subcellular distribution. Our results further indicate that Omicron infection sustains higher expression levels of proteins components of the signal recognition particle and translation factors, which may enable a more effective production of immune response and viral components. Altogether, this work highlights the deep impact of SARS-CoV-2 infection on host cell RNA regulatory landscape and provides new insights to explain the differential impact of Omicron compared to early SARS-CoV-2 variants.

GSE317284 Regenerative macrophages from human iPSCs promoted vascular remodeling in human atherosclerotic organoid model

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Seunguk Lee ; Minseon Park ; Hyun-Ji Park
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Recent studies have revealed that macrophages exhibit greater phenotypic diversity than the traditional M1/M2 classification, enabling them to display distinct functional properties depending on the surrounding microenvironment. Accordingly, it has become increasingly important to more finely characterize and evaluate macrophage subtypes that may operate within specific disease microenvironments. In this study, we aimed to identify a macrophage phenotype with therapeutic potential for atherosclerosis using an atherosclerosis-induced blood vessel organoid (BVO) model. To assess the effects of diverse macrophage phenotypes on the atherosclerosis, iPSC-derived macrophages (iMac) were generated and polarized into multiple phenotypic states. The polarized iMac populations displayed distinct gene expression profiles and exhibited functional differences in angiogenesis and regeneration related assays. For therapeutic evaluation, iPSC-derived BVOs were established and then induced to develop atherosclerotic features. During co-culture with the atherosclerotic BVO model, iPSC-derived regenerative macrophages (iMac R) showed active interactions with the organoids and produced therapeutic benefits on lipid clearance, anti-inflammatory responses, and regenerative effects. Notably, iMac R demonstrated superior therapeutic efficacy compared with other polarized macrophage phenotypes, highlighting their potential as a novel cell-based therapeutic strategy for atherosclerosis.

GSE315875 ReprogRAM nanoplatform for direct conversion of fibroblasts into reprogrammed osteoblasts for bone regeneration

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Kiho Jeong ; Wijin Kim ; Ju-Hyun Park
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

mRNA-based direct conversion offers an integration-free route for osteogenic cell-fate reprogramming, yet efficient reprogramming typically requires sustained expression of reprogramming factors. Here, we develop ReprogRAMs (Reprogrammable RNA Assemblies for Multi-factor expression), a self-assembled concatemeric mRNA nanoparticles synthesized by rolling-circle transcription and engineered for cap-independent translation. A single delivery of ReprogRAM to human dermal fibroblasts enabled cytosolic expression that persisted over time with minimal cytokine induction. By leveraging this long-acting expression profile, we encoded the osteogenic reprogramming factors Oct4 and Cbfβ and implemented a hybridized delivery strategy to enforce co-expression of both factors. ReprogRAM induced robust osteogenic conversion, as evidenced by increased mineralized matrix deposition, induction of osteoblast markers, and transcriptomic remodeling toward osteoblasts. Finally, transplantation of ReprogRAM-derived reprogrammed osteoblasts (rOBs) embedded in a gelatin scaffolds promoted bone repair in a critical-sized mouse calvarial defect model. Together, ReprogRAM provides a long-acting, integration-free mRNA modality for in situ cell-fate engineering and bone regeneration.

GSE315602 Complement C3-Mediated Hippocampal CA2 Synaptic Impairments Underlie Social Deficits by Srpx2 Deficiency in Maternal Immune Activation

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Anran Huo ; Qifei Cong
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Social behavior deficits are hallmark features of neurodevelopmental disorders. The hippocampal CA2 region and complement system are critical for social function and neurodevelopment. Here, we show SRPX2 interacts with complement protein C1Q and regulates complement-coagulation pathways, specifically downregulating C3 in astrocytes. Srpx2 deficiency induces transient C3 upregulation and selective excitatory synapse loss in hippocampal CA2 during adolescence. Moreover, Srpx2 deficiency and prenatal maternal immune activation interact to disrupt social behavior, accompanied by enhanced C3 expression and excitatory synapse loss in CA2. Our findings identify SRPX2 as a key regulator of complement-mediated synaptic function in CA2, providing insights into the molecular mechanisms underlying neurodevelopmental disorder-related social deficits.

GSE314297 CRISPR screen after venetoclax and azacitidine treatment in AML cells

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Ahmed Mamdouh ; Fang Qi Lim ; Karanpreet S Bhatia ; Xiao Xian Lin ; Shruti Bhatt
Series Type : Other
Organism : Homo sapiens

CRISPR screen was performed in three isogenic MOLM-13 acute myeloid leukemia (AML) cell lines (p53 WT/p53 R248Q/p53 KO) to analyze gene dependencies changes after treatment with venetoclax and azacitidine.

GSE312640 Transciptomics analysis: the role of chronic ethanol feeding in promoting dysfunction of stromal vascular cells from rat viceral adipose tissue

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Saraswathi Viswanathan ; Weilun Ai
Series Type : Expression profiling by high throughput sequencing
Organism : Rattus norvegicus

Chronic ethanol exposure induces adipose tissue dysfunction. Rats are divided into 2 groups: CONT and ET. The study aim to determine the role of stromal vacular cells (SVC) in mediating viceral adipose tissue (VAT) dysfunction in alcohol-associated liver disease.

GSE312413 Nuclear Argonaute HRDE-1 Maintains Chromatin-Independent Transcriptional Silencing through a Transgenerational Small RNA Feedback Loop

Sat, 31 Oct 2026 00:00:00 -0400

Series Type : Expression profiling by high throughput sequencing ; Other ; Non-coding RNA profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencing
Organism : Caenorhabditis elegans

This SuperSeries is composed of the SubSeries listed below.

GSE311921 Nuclear Argonaute HRDE-1 Maintains Chromatin-Independent Transcriptional Silencing through a Transgenerational Small RNA Feedback Loop [nuclear CUT&Tag]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Arantxa M. L. Rojas ; Almira Chervova ; Loan Bourdon ; Jagannath Jayaraj ; Ana Karina Morao ; Olivier Feudjio ; Sofija Illic ; Sara Capurso ; Piergiuseppe Quarato ; Julie Ovieve ; Germano Cecere
Series Type : Genome binding/occupancy profiling by high throughput sequencing
Organism : Caenorhabditis elegans

Epigenetic inheritance of transcriptional silencing is traditionally attributed to chromatin-based mechanisms in which Argonaute–small RNA complexes recruit histone-modifying enzymes. Here we show that, in Caenorhabditis elegans, the nuclear Argonaute HRDE-1 maintains germline transcriptional repression independently of canonical heterochromatin marks. Using inducible, germline-specific HRDE-1 depletion combined with nuclear sorting, CUT&Tag, and nascent transcription profiling, we identify a functionally defined subset of endogenous genes, pseudogenes, and repetitive elements that become transcriptionally activated upon loss of HRDE-1 despite retaining H3K9me3, H3K23me3, and H3K27me3. HRDE-1 directly restrains RNA polymerase II (Pol II) while simultaneously promoting polyUG-dependent amplification of antisense 22G-RNAs in perinuclear condensates, thereby coupling nuclear transcriptional repression to small RNA biogenesis. HRDE-1 loss causes progressive erosion of 22G-RNAs and delays silencing re-establishment, revealing a transgenerational feedback loop in which small RNAs, and not chromatin modifications, constitute the primary heritable signal. These findings redefine nuclear Argonautes as active drivers of RNA-based epigenetic inheritance and broaden our understanding of how small RNA pathways maintain transcriptional silencing across generations.

GSE311918 Nuclear Argonaute HRDE-1 Maintains Chromatin-Independent Transcriptional Silencing through a Transgenerational Small RNA Feedback Loop [Whole worm CUT&Tag]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Arantxa M Rojas ; Almira Chervova ; Loan Bourdon ; Jagannath Jayaraj ; Ana Karina Morao ; Olivier Feudjio ; Sofija Illic ; Sara Capurso ; Piergiuseppe Quarato ; Julie Ovieve ; Germano Cecere
Series Type : Genome binding/occupancy profiling by high throughput sequencing
Organism : Caenorhabditis elegans

GSE311555 Nuclear Argonaute HRDE-1 Maintains Chromatin-Independent Transcriptional Silencing through a Transgenerational Small RNA Feedback Loop [small RNA-seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Arantxa M. L. Rojas ; Almira Chervova ; Loan Bourdon ; Jagannath Jayaraj ; Ana Karina Morao ; Olivier Feudjio ; Sofija Illic ; Sara Capurso ; Piergiuseppe Quarato ; Julie Ovieve ; Germano Cecere
Series Type : Non-coding RNA profiling by high throughput sequencing
Organism : Caenorhabditis elegans

GSE311554 Nuclear Argonaute HRDE-1 Maintains Chromatin-Independent Transcriptional Silencing through a Transgenerational Small RNA Feedback Loop [nuclear GRO-seq]

Sat, 31 Oct 2026 00:00:00 -0400

GSE311553 Nuclear Argonaute HRDE-1 Maintains Chromatin-Independent Transcriptional Silencing through a Transgenerational Small RNA Feedback Loop [nuclear RNA-seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Arantxa M. L. Rojas ; Almira Chervova ; Loan Bourdon ; Jagannath Jayaraj ; Ana Karina Morao ; Olivier Feudjio ; Sofija Illic ; Sara Capurso ; Piergiuseppe Quarato ; Julie Ovieve ; Germano Cecere
Series Type : Expression profiling by high throughput sequencing
Organism : Caenorhabditis elegans

GSE311522 Nuclear Argonaute HRDE-1 Maintains Chromatin-Independent Transcriptional Silencing through a Transgenerational Small RNA Feedback Loop [bulk RNA-seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Arantxa M. L. Rojas ; Almira Chervova ; Loan Bourdon ; Jagannath Jayaraj ; Ana Karina Morao ; Olivier Feudjio ; Sofija Illic ; Sara Capurso ; Piergiuseppe Quarato ; Julie Ovieve ; Germano Cecere
Series Type : Expression profiling by high throughput sequencing
Organism : Caenorhabditis elegans

GSE311192 Cooperative interaction of Foxp3 and STAT5 confers regulatory T cell fitness by tuning IL-2 induced gene expression

Sat, 31 Oct 2026 00:00:00 -0400

Series Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencing
Organism : Mus musculus

This SuperSeries is composed of the SubSeries listed below.

GSE311187 Cooperative interaction of Foxp3 and STAT5 confers regulatory T cell fitness by tuning IL-2 induced gene expression [Cut & Run]

Sat, 31 Oct 2026 00:00:00 -0400

GSE311182 Cooperative interaction of Foxp3 and STAT5 confers regulatory T cell fitness by tuning IL-2 induced gene expression [RNA-Seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Michaels Anthony ; Dolsten Gabriel ; Uhl Lion ; Hu Wei ; Dhilon Bahawar ; Ghelani Aazam ; Giovanelli Paolo ; Andretta Emma ; Pritykin Yuri ; Rudensky Alexander
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

GSE309777 RNA sequencing to compare SAIPS-PAI0 group with VIPS-PAI group

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Peng Yu ; Yanlin Wu ; Liuyan Huang
Series Type : Expression profiling by high throughput sequencing
Organism : Rattus norvegicus

14 days after the VIPS-PAI and SAIPS-PAI0 scaffolds were implanted in the rat femoral defect models, tissues surrounding and within the scaffolds were harvested from both groups for RNA sequencing to analyze the gene expression profiles.

GSE307757 Accurate In Vitro Recapitulation of Bile and Blood Partitioning of Drug Metabolites Using a hepatocyte culture system with induced open-form bile canaliculus icHep

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Hiroshi Arakawa ; Yuya Nakazono ; Takashi Watanabe ; Atsuo Kobayashi ; Yoshiki Mochizuki ; Yukihide Momozawa
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Systemically circulating drug metabolites can cause organ damage, and there are species differences in the both the types of metabolites formed and their partitioning into bile and blood. Thus, it is necessary to evaluate the formation and biliary excretion of hepatic drug metabolites using in vitro evaluation system using human hepatocytes. Conventional sandwich-cultured hepatocytes (SCHs), however, form closed bile canaliculi that preclude direct collection of biliary excreted metabolites. Here, we assessed whether primary cultured hepatocytes with induced open-form bile canaliculus (icHep) provide a suitable system for evaluating the partitioning of drug metabolites produced in hepatocytes between bile and blood. Human hepatocytes derived from human liver–chimeric mice were cultured on claudin-1–coated plates, which facilitated the formation of open bile canalicular lumina, confirmed by co-immunostaining for MRP2 and ZO-1. RNA-seq analysis revealed that the expression levels of representative pharmacokinetics-related genes in icHep were comparable to those in SCHs. Following the addition of parent drugs to the blood-side chamber, metabolites were successfully collected from both blood- and bile-side chambers. Ziprasidone sulfoxide and mycophenolic acid glucuronide were predominantly recovered on the blood side, whereas celecoxib carboxylic acid and SN-38 glucuronide were preferentially excreted into bile. The metabolite partitioning observed in icHep was consistent with human in vivo data. In conclusion, icHep enables a quantitative evaluation of the hepatic disposition of drug metabolites including partitioning into bile and blood in human and represents a physiologically relevant in vitro system for human pharmacokinetic studies.

GSE307647 Geometric inference of cross-species transcriptome correspondence

Sat, 31 Oct 2026 00:00:00 -0400

Series Type : Expression profiling by high throughput sequencing
Organism : Gorilla gorilla ; Homo sapiens ; Macaca fascicularis ; Mus musculus ; Pan troglodytes ; Pongo abelii

This SuperSeries is composed of the SubSeries listed below.

GSE307646 Geometric inference of cross-species transcriptome correspondence [RNA-Seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Yuya Tokuta ; Tomonori Nakamura ; Kohei Fujiwara ; Masanori Imamura ; Masahiro Nagano ; Mitinori Saitou ; Yusuke Imoto ; Yasuaki Hiraoka
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens ; Macaca fascicularis

Sequence homology underpins cross-species analysis but cannot identify evolutionarily distinct genes that play analogous regulatory roles. Furthermore, ethical restrictions on human experiments necessitate analytical frameworks that translate insights from other animals to humans. To address these challenges, we develop Species-OT, a cross-species transcriptome analysis framework based on Gromov-Wasserstein optimal transport, which quantitatively compares the geometry of transcriptome distributions. Given a pair of bulk or single-cell RNA-sequencing datasets, Species-OT returns a gene-to-gene correspondence capturing probabilistic alignments of regulatory roles, and a transcriptomic distance quantifying overall divergence. Applied pair wise, Species-OT yields a transcriptomic discrepancy array and a hierarchical clustering tree analogous to a phylogenetic tree. We validate Species-OT using bulk RNA-seq data from human, mouse, and macaque germ cell specification as well as scRNA-seq data from pluripotent stem cells of six mammalian species. Species-OT identifies evolutionarily related and distinct gene correspondences including biologically unexplored candidates, while transcriptomic discrepancies recapitulate expected species relationships.

GSE307645 Geometric inference of cross-species transcriptome correspondence [scRNA-Seq]

Sat, 31 Oct 2026 00:00:00 -0400

GSE306251 Transcriptomic changes from resulting from treatment of SVG-A with drugs of abuse

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Sarah Storr
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

SVG-A cells were treated with drugs of abuse (ethanol, cocaine, morphine, THC, and psilocin) prior to RNA sequencing. A bioinformatics pipeline of Trim Galore, Kallisto, DESeq2 and Qiagen Ingenuity Pathway Analysis was used for pathway analysis.

GSE305361 Disruption of nucleolar integrity triggers cellular quiescence through organelle rewiring and secretion

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Prashant Rawat ; Tabea Quaderer ; Ino Karemaker ; Sung Sik Lee ; Federico Ulliana ; Zacharias Kontarakis ; Jacob Corn ; Matthias Peter
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Intrinsic cellular stress responses are often mis regulated in complex human diseases such as cancer and neurodegeneration. To investigate how cellular homeostasis is balanced upon loss of key membraneless organelle – Nucleolus, we performed unbiased systems approach including cellular and temporal characterization of activated cellular stress signaling, associated sub-cellular changes and changes in cellular states and behavior. We report that transient loss of nucleolar architecture and defective ribosome biogenesis is well tolerated by cells as they undergo prolonged cell cycle arrest and rely on buffering capacity of cytoplasmic translation machinery. Cells immediately mount a comprehensive stress response predominantly mediated by TP53 and its downstream effector proteins. This mounted stress response is distinct from other acute stresses altering nucleolar morphology or function such as Pol I inhibition by ActD, heat shock or chemicals like Arsenate and CPT. Cells show a robust transcriptional reprogramming showing upregulation of structural and signaling genes of organelles such as Golgi apparatus and Endo-lysosomal vesicles. This leads to translation and microscopically evident tubular-vesicular expansion of Golgi and increase in number and size of endo-lysosomes. Cells become secretory, pro-metastatic and alter their cell-to-cell communication behavior. Taken together, these stress response pathways show an adaptive quiescent program and acquired partial EMT, allowing cells to resist loss of ribosome biogenesis, nucleolar architecture and ensure survival and restore homeostasis upon recovery. Correlatively, similar stress adaptions are seen to be contributing to progression of different cancer types especially in breast cancer and AML originating in the later stages of ribosomopathies.

GSE302039 Determination of transcriptomic changes associated with salt stress in ethanol-treated control plants and TRB3-SRDX mutants.

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Kota Urushihara ; Akihiro Matsui ; Maho Tanaka ; Sumire Fujiwara ; Nobutaka Mitsuda ; Masaru Ohme-Takagi ; Atsushi J Nagano ; Motoaki Seki ; Kaori Sako
Series Type : Expression profiling by high throughput sequencing
Organism : Arabidopsis thaliana

Soil salinization severely threatens crop productivity. We previously revealed that ethanol treatment enhances abiotic stress tolerance, including salt stress, in plants. Ethanol up-regulated the transcription and activity of ascorbate peroxidase (APX1/2), key ROS detoxifing enzymes, thereby reducing ROS accumulation and improving salt stress tolerance. However, the transcriptional regulation underlying ethanol-mediated stress tolerance remains unclear. In this study, we identified Telomere repeat binding (TRB) proteins as transcription factors involved in ethanol-mediated salt stress tolerance. Transcriptome analysis revealed that copper/zinc superoxide dismutase (CSD) genes were down-regulated in TRB3-SRDX mutant. We further demonstrated that SOD activity was reduced in trb1/2/3 mutantm and csd mutant showed salt stress sensitivity even presence with ethanol, indicating that CSD are essential for ethanol-mediated salt stress tolerance. ChIP assays confirmed that TRB3 directly binds to CSD genes. Furthermore, ethanol treatment promoted H4K5 acetylation at CSD loci. These findings suggests that ethanol metabolism contributes to histone acetylation, and TRB3 facilitates its deposition at CSD loci, leading to enhanced CSD activation and improved salt stress tolerance.

GSE299141 scRNA-seq of skin and PBMC samples of systemic sclerosis patients and healthy controls

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Wei Guo ; Zhaohua Li ; Dan Xu ; Ting Li ; Dan Fang ; Xiaoying Zhang ; Yuebo Jin ; Dan Xing ; Zhaoyu Chen ; Xiandun Yuan ; Zhixin Wang ; Chen Dong ; Huji Xu ; John Varga ; Jinlin Wang ; Jing Ge ; Rong Mu
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Skin and blood samples from systemic sclerosis (SSc) patients and healthy donors were analyzed using single-cell transcriptomics (scRNA-seq). CCL19+ fibroblast was upregulated in the dermis of patients with SSc, and exhibited high expression of immuno-regulatory genes, including CCL19. CCL19 expression correlated with the severity of dermal fibrosis in SSc. The most significant ligand-receptor interaction from CCL19+ fibroblast to T cells in SSc skin was CCL19-CCR7. Furthermore, CCR7+ T cells in the fibrotic skin, particularly CCR7+CD8+ T cells, displayed enhanced stemness and cytotoxicity, actively interacting with extracellular matrix (ECM)-producing fibroblasts in SSc.

GSE291637 Transcriptomic responses of zebrafish following dietary exposure to the short chain PFAS perfluorohexanoic acid (PFHxA)

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Chris Martyniuk ; Jessica Donaldson ; Amany Sultan ; Joseph Bisesi
Series Type : Expression profiling by high throughput sequencing
Organism : Danio rerio

Per- and polyfluoroalkyl substances (PFAS) have garnered tremendous concern due to the widespread contamination and environmental persistence as PFAS and their heavy use in commercial products. While the properties of PFAS are useful for various consumer goods, the same properties result in high persistence of PFAS in the environment as well as an increased risk of exposure and deleterious effects for humans and ecosystems. To address data gaps for less studied PFAS, the use of molecular tools is essential to identify novel toxicity pathways that help to reduce additional animal testing for this large chemical class. In our current study, we exposed a model species (zebrafish) to a short chain PFAS, perfluorohexanoic acid (PFHxA), via the diet, which is an understudied exposure route in fish. Fish were exposed over 28 days to a measured low dietary dose (57.6 ng/g) as well as a higher dose (60.7 ng/g). At the end of the exposure, liver tissues were processed for mRNA and libraries were prepared for RNA-seq analysis. In addition to the transcriptome, qPCR will be performed to further assess changes in gene expression due to PFHxA dietary exposure. This study will be the first to examine sub-chronic dietary exposures to PFHxA and the resulting impacts on the transcriptome.

GSE290169 RNA Immunoprecipitation Sequencing (RIP-seq) of RNAs associated in vivo with the FopA protein performed in Escherichia coli J53 or CFT073

Sat, 31 Oct 2026 00:00:00 -0400

Series Type : Other
Organism : Escherichia coli CFT073 ; Escherichia coli J53

This SuperSeries is composed of the SubSeries listed below.

GSE290168 Identification of RNAs interacting with protein FopA in Escherichia coli [RIP-Seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Hoa Q Pham ; Miaomiao Tan ; Peng Y Xie ; Xin Deng ; Xin Wang ; Terrence Lau
Series Type : Other
Organism : Escherichia coli CFT073 ; Escherichia coli J53

The goal of this analysis was to identify the RNAs interacting with protein FopA which is encoded on IncI1 plasmid in two E. coli strains J53 and CFT073

GSE287634 Social Stress Differentially Affects the Behavior and the Transcriptome of the adBNST between Male and Female Mice.

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Thomas J Degroat ; Sarah E Paladino ; Katherine Denney ; Benjamin A Samuels ; Troy A Roepke
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Stress can be broken down into systemic and processive stressors with processive stressors requiring higher limbic processing. These are also often called social stressors as they require an understanding of social dynamics as opposed to physical based stressors. This differing of processing necessitates we study both phenomena. Additionally, sex is an important aspect of stress research as men and women show differing responses to stress and mood disorder development. To study this, we used a chronic social instability stress (CSIS) paradigm to stress male and female mice. This paradigm is approximately 7-weeks long and involves changing the cage mates of a mouse every 3 days so stable social dynamics cannot form. Afterwards, one cohort was used for avoidance behavior testing using the open field test, the elevated plus maze, the light/dark box emergence test, and the novelty suppressed feeding test. A second cohort was used for bulk RNA-Sequencing of the anterodorsal bed nucleus of the stria terminalis which is a limbic structure known to be related to chronic stress signaling. In the behavior assays, CSIS caused the females to be less avoidant, while the males became more avoidant. Additionally, we found that a low estrogen state in the females caused them to be less avoidant than in a high estrogen state. In the transcriptome, we found major differences between the males and females with the males expressing more genes related to transcription whereas the females expressed more genes related to synaptic transmission. We also found that the transcriptome in the males is more sensitive to the stress than the females. In summary, we have found how social stress is differentially regulated between males and females and how this may be related to the development of stress-related behavioral changes.

GSE287560 Comparative analysis of RLR-specific RNA ligands during influenza virus infection

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Deniz Uresin ; Rachel Legendre ; Sinem Caglar ; Camille Cassonnet ; Valérie Najburg ; Yannis Rahou ; Aleksandr Barinov ; Virginie Marchand ; Régis Grailhe ; Marcel Hollenstein ; Yuri Motorin ; Caroline Demeret ; Sylvie van der Werf ; Anastassia Komarova
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens ; Influenza A virus (A/Guangdong-Maonan/51/2009(H1N1))

RIG-I-like receptors (RLRs) play a critical role in detecting RNA virus infections and initiating antiviral immune responses. This study examined the roles of three RLRs—RIG-I, MDA5, and LGP2—in recognizing wild-type (WT) influenza virus infections and characterized their RNA ligands at both the nucleotide sequence and post-transcriptional modification levels. Our findings indicate that RIG-I and MDA5 are essential for sensing influenza A (IAV) and influenza B (IBV) viruses. RNA ligands isolated from RIG-I and LGP2 demonstrated immunostimulatory activity in type I interferon (IFN) reporter assays. Specifically, RIG-I bound to RNA sequences within the negative-sense NS and M segments of the influenza virus, while LGP2 interacted exclusively with the negative-sense 5′ and 3′ ends of the M segment. Notably, the viral segments were more potent in activating type I IFN signaling than their positive-sense counterparts, which aligns with the IC50 values of the NS and M segments binding to RIG-I. Additionally, in IAV-infected cells, RIG-I selectively recognized RNA polymerase III transcripts, which exhibited decreased 5-methylcytosine (m5C) modification levels upon infection. These results highlight the contributions of both viral and host RLR ligands to anti-influenza virus immunity, emphasizing their specific sequences and the NSUN2-mediated post-transcriptional modification profile. Overall, this study provides a comprehensive view of RLR-mediated sensing mechanisms that regulate antiviral responses to influenza virus infections.

GSE284774 Nephrin-associated phospho-protein network necessary for filtration at the slit-diaphragm and podocyte adhesion.

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Eul Carolin ; Bertgen Luisa ; Stöveken Laura ; Dlugos Christopher ; Beci Blanda ; Van Marck Veerle ; Heitplatz Barbara ; Vollenbröker Beate ; Weide Thomas ; Drexler Hannes ; Pavenstädt Hermann ; George Britta ; Sridhar Sucheta ; Bödecker Sarah
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Minimal Change Disease (MCD) is characterized by nephrotic syndrome. In a subgroup of patients, pathogenic antibodies against the slit-diaphragm (SD) protein Nephrin encoded by the gene NPSH1 were identified in blood and biopsy samples. Nephrin is essential for the SD as specific NPHS1 variants result in congenital nephrotic syndrome. Intact Nephrin is a structural component of the SD, but also transmits signals to the actin cytoskeleton of podocyte foot processes (FP) thereby presumably stabilizing podocyte FP morphology. Thus, analyzing the Nephrin signalosome is attractive to identify potential targets for therapeutic intervention in MCD. We employed a model of MCD with antibody-mediated clustering of Nephrin leading to tyrosine phosphorylation-dependent signal transduction in podocyte culture. Phospho-proteome analysis after antibody-mediated Nephrin clustering revealed approx. 180 differentially phosphorylated peptides. Gene set analysis showed that among others the biological process ‘cell matrix adhesion’ was enriched. We verified that two thirds of the identified proteins were necessary for filtration in vivo employing a knockdown approach with consecutive analysis by an in-vivo filtration assay in Drosophila melanogaster nephrocytes. One of the phosphorylated proteins following Nephrin activation in the phospho-proteome analysis was the activating factor of the small GTPase Rap1 – Rapgef1. The significance of this Nephrin effector Rapgef1 for SD and focal adhesion integrity was exemplary studied generating a Rapgef1 knockout (Rapgef1KO) in the metanephric mesenchyme of mice. We confirmed that an early Rapgef1 knockout in podocytes - like transgenic Nephrin mice deficient in tyrosine-dependent signaling – resulted in nephrotic syndrome and an MCD/focal segmental glomerulosclerosis (FSGS) phenotype. RNA sequencing of Rapgef1 knockout mice glomeruli revealed significant regulation of genes involved in cell signaling, cell adhesion, and extracellular matrix organization. Changes in glomerular basement membrane (GBM), focal adhesion (FA) composition, and significant podocyte loss were confirmed by immunofluorescence analysis in Rapgef1 knockout mice glomeruli. Altogether, we identified a Nephrin-associated phospho-protein network necessary for filtration at the slit-diaphragm and podocyte adhesion.

GSE281560 SUMOylation of SND1 promotes degradation of novel tumor suppressive miRNAs in cancer cells

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Yingting Cao ; Jianxiu Yu
Series Type : Expression profiling by high throughput sequencing ; Non-coding RNA profiling by high throughput sequencing
Organism : Homo sapiens

Endonuclease Staphylococcal nuclease domain-containing protein 1 (SND1) was reported mediate miRNA decay of both protein-free and AGO2-loaded miRNAs. We recently found that SUMOylation of SND1 is involved in the regulation of the mature miRNA decay. The in vivo and in vitro SUMOylation assay have proven that SND1 can be modified by SUMO1 at the major site K513, and this modification can be enhanced upon the sodium arsenite and heat shock. Mutation K513R of SND1 inhibits cell proliferation and colony formation of H1299 cells under both normal and sodium arsenite stimulated conditions. Our data demonstrate that miRNA metabolism is connected to cellular stress response and tumorigenesis through the reversible SUMOylation of SND1. The stress-induced SND1 SUMOylation can degrade miRNA to regulate mRNA homeostasis, which may be a key node in the stress survival strategy.

GSE280503 Deciphering the diversities of CTCF and CTCF-s in human embryonic stem cells

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Hongxin Zhong ; Yuli Lu ; Hongjie Yao
Series Type : Other
Organism : Homo sapiens

In this study, transient transcriptome sequencing (TT-seq) was performed to dectect the impact of the overexpression of CTCF-s on nascent RNA and antisense RNA.

GSE280419 BL-Hi-C, Deciphering the diversities of CTCF and CTCF-s in human embryonic stem cells

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Hongxin Zhong ; Yuli Lu ; Hongjie Yao
Series Type : Genome binding/occupancy profiling by high throughput sequencing
Organism : Homo sapiens

In this study, we performed BL-Hi-C to investigate the influence of the expression of CTCF/CTCF-s on higher-order chromatin structures.

GSE280302 Deciphering the diversities of CTCF and CTCF-s in human embryonic stem cells [ChIP-seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Hongxin Zhong ; Yuli Lu ; Hongjie Yao
Series Type : Genome binding/occupancy profiling by high throughput sequencing
Organism : Homo sapiens

In this study, Biotin ChIP-seq was performed to obtain the independent genome binding sites of CTCF-s or CTCF. CTCF ChIP-seq was performed to investigate the influence of the overexpression of CTCF-s on the binding of CTCF in hESCs.

GSE280233 Habitual betel nut chewing promotes oral squamous cell carcinoma tumorigenesis by inhibiting global methylation in normal oral mucosa

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Suzhen Ma ; Danling Wang
Series Type : Methylation profiling by genome tiling array
Organism : Homo sapiens

Oral squamous cell carcinoma (OSCC) is a major oral-maxillofacial tumor with marked effects on facial appearance and high recurrence rate. In addition to tobacco and alcohol consumption, betel nut chewing plays a significant role in promoting the occurrence of OSCC, highlighted by the prevalence of oral cancer in East Asia, Southeast Asia, and South Asia. However, the specific underlying mechanisms are unclear. By analyzing clinical data, we first noted that habitual betel nut chewing only affect occurrence of second primary tumors, indicated that it induces tumorigenic changes in the normal tumor-adjacent mucosa tissues. Tumorigenesis relies on the combined effect of genetic and environmental changes, with epigenetic changes, primarily methylation, serving as a key link connecting genetics and the environment. Herein, we analyzed global DNA methylation in the oral mucosa and found that habitual betel nut chewing leads to significant hypomethylation in the normal tumor-adjacent mucosa. This change makes the normal mucosa more similar to OSCC tissues than other normal tissues at the molecular pathological level. Our multiomics analysis revealed that habitual betel nut chewing may facilitate tumorigenesis by reducing the global DNA methylation level of normal mucosa, suppressing antitumor immunity, and promoting abnormal cell proliferation. Through experimental verification and screening, we identified five key genes involved in this process: DEPDC1B, ANLN, ECT2, SPC25, and PLK1. Our study revealed that habitual betel nut chewing can promote OSCC tumorigenesis by regulating global DNA methylation. Early detection of global DNA methylation and key gene markers may reveal potential targets for assessing OSCC risk.

GSE280112 Joint profiling of 5-methylcytosine, 5-hydroxymethylcytosine, and the transcriptome in single cells identifies factors responsible for genome-wide DNA methylation erasure in human primordial germ cell maturation

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Alex Chiralastri ; Kellie A Heom ; Siddharth S Dey
Series Type : Genome binding/occupancy profiling by high throughput sequencing ; Other ; Expression profiling by high throughput sequencing
Organism : Homo sapiens

Reprogramming of DNA methylation plays a vital role in the establishment of cell identity during early mammalian development. To gain deeper mechanistic insights into this process requires capturing the entire dynamics of DNA methylation – both 5-methylcytosine (5mC) and its downstream oxidation product 5-hydroxymethylcytosine (5hmC) – in individual cells. Therefore, in this work, we report a new single-cell genome-wide strand-specific sequencing method, scMHT-seq, to jointly profile 5mC, 5hmC, and the transcriptome from individual cells. Using human embryonic stem cells (hESCs), we first show that scMHT-seq can accurately detect both 5mC and 5hmC from the same cell with minimal crosstalk in quantifying these two DNA modifications, and that the multi-modal measurements are in close agreement with individual measurements of 5mC and 5hmC in single cells. After establishing scMHT-seq, we next applied scMHT-seq to gain insights into human primordial germ cell (hPGC) maturation. After specification, hPGCs undergo rapid global demethylation as they mature, and this reprogramming is critical for normal development of gametes. However, it has not been possible to overcome this key epigenetic barrier in a dish, thereby limiting our ability to generate mature hPGC-like cells (hPGCLCs) and accomplish in vitro gametogenesis. To gain a deeper understanding of the molecular factors involved in germ cell maturation, we applied scMHT-seq to an extended in vitro culture system for generating hPGCLCs and observed partial and heterogeneous erasure of the methylome across single cells that is mechanistically predominantly driven by passive demethylation due to reduced DNMT1-mediated maintenance methylation activity. Notably, we discover that hPGCLCs in extended culture can be transcriptionally classified into two distinct states, with one population enriched for more mature hPGCLCs exhibiting genome-wide loss of the methylome. Moreover, we identify DND1 and SOX15 as two critical factors that are potentially key drivers of hPGCLC maturation. Overall, we demonstrate that scMHT-seq is a robust and high-throughput technology that can provide insights into the mechanisms driving DNA methylation dynamics and their effect on cellular states during hPGCLC maturation, thereby providing a platform to advance in vitro gametogenesis in humans.

GSE280089 Chronic Inflammatory Responses in Diabetic Lung and its’ Implications for Tuberculosis Infection.

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Ranjan K Nanda ; Shweta Chaudhary
Series Type : Expression profiling by high throughput sequencing ; Other
Organism : Mus musculus

Diabetes mellitus (DM) increases (~3.11-fold) the risk of tuberculosis (TB), leading to worse disease outcomes and higher relapse rates. scRNAseq revealed compromised adaptive and innate immunity in DM-TB mice, with decreased Th1 and M1 macrophage populations. Further analysis showed hyperinflammation in DM and dampened immune responses in DM-TB, marked by increased IL-16 signaling and reduced TNF and IFN-II responses.

GSE279685 Type I regulatory T cells have overlapping phenotypes with circulating Tfh and Th1 in P. falciparum

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Mayimuna Nalubega ; Megan Soon ; Dean Andrew ; Damian Oyong ; Zuleima Pava ; Jessica R Loughland ; Nicholas L Dooley ; Nankya F Namirimu ; Kenneth Musinguzi ; Abel Kakuru ; John Rek ; Emmanuel Arinaitwe ; Isaaac Ssewanyana ; Moses Kamya ; Prassanna Jagannathan ; Margaret Feeney ; Bridget Barber ; Chris Engwerda ; Michelle J Boyle
Series Type : Expression profiling by high throughput sequencing ; Other
Organism : Homo sapiens

Immunity to P. falciparum malaria develops slowly, requiring repeated infection in areas of high transmission, and wanes rapidly in the absence of parasite exposure. Key to this immunity, is the development of antibodies which is supported by CD4⁺ T follicular helper (Tfh) cells that drive robust germinal centre responses. However, in malaria, the malaria-specific CD4⁺ T cell compartment in peripheral blood is dominated by Type 1 regulatory T cells (Tr1), which produce high levels of IL-10 in response to parasites. Tr1-like Tfh cells (Tfh10) have been reported in several settings of repeated antigen stimulation but have not been investigated in malaria. Here we used single-cell RNA sequencing and multiparameter flow cytometry to characterise malaria-specific Tfh and Tr1 cells in a longitudinal cohort of highly exposed individuals and assessed their persistence after transmission interruption. Malaria-specific Tfh and Tr1 cells shared overlapping profiles, and Tr1 cell-like transcriptional signatures and phenotypes were detectable within the Tfh cell compartment. Tfh10 cell subsets were the dominant phenotype of malaria-specific Tfh cells. Following disruption of malaria transmission, the frequencies of malaria-specific Tr1 and Tfh10 cells declined. These findings highlight a close relationship between Tfh and Tr1 cells and show that the Tfh cell compartment in malaria is dominated by Tfh10 cells. The rapid waning of these cells in the absence of continuous exposure is consistent with requirements of persistent antigen in maintaining regulatory CD4 T cell phenotypes.

GSE279425 Krüppel-like factor 5 remodels lipid metabolism in exercised skeletal muscle

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Konstantin Schneider-Heieck ; Joaquin Perez Schindler ; Jonas Blatter ; Laura M. de Smalen ; Wandrille Duchemin ; Stefan Steurer ; Bettina Karrer-Cardel ; Danilo Ritz ; Christoph Handschin
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Regular physical activity induces a variety of health benefits, preventing and counteracting diseases caused by a sedentary lifestyle. However, the molecular underpinnings of skeletal muscle plasticity in exercise remain poorly understood. We identified a role of the Krüppel-Like Factor 5 (Klf5) in this process, in particular in the regulation of lipid homeostasis. Surprisingly, gain- and loss-of-function studies in muscle in vivo revealed seemingly opposite functions of Klf5 in the response to an acute exercise bout and chronic training, modulating lipid oxidation and synthesis, respectively. Thus, even though only transiently induced, the function of Klf5 is complex and integral for a normal long-term training response. These findings highlight the importance of this mediator of external stress response to adaptive remodeling of skeletal muscle tissue.

GSE276213 Spatial genome and transcriptome co-mapping reveals clonal heterogeneity in tumor tissue

Sat, 31 Oct 2026 00:00:00 -0400

Series Type : Expression profiling by high throughput sequencing ; Other
Organism : Homo sapiens ; Mus musculus

This SuperSeries is composed of the SubSeries listed below.

GSE276212 Spatial genome and transcriptome co-mapping reveals clonal heterogeneity in tumor tissue [DNA-Seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Yang Liu ; Dejiang Wang ; Xiangjun Di ; Shenjie Wang
Series Type : Other
Organism : Homo sapiens ; Mus musculus

Tumor heterogeneity arises from the sequential acquisition of somatic mutations and the selection of fitter clones, leading to distinct genotypes and phenotypes. Joint mapping of genome and transcriptome in the same tumor tissue can directly link clonoal relation to transcriptional state enabling a more in-depth understanding of intrinsic and extrinct tumor heterogeneity in the tissue context. Here, we introduce Spatial-GT-seq, a spatial multi-omic technology capable of genome-wide co-profiling of the genome and transcriptome at near single-cell resolution. We demonstrated in situ identification of tumor subclones in a mouse model of lung metastasis, with parallel transcriptomic profiles indicating that the gene expression profile of the same tumor clone is altered by the tumor microenvironment. Furthermore, analysis of primary and recurrent human pancreatic neuroendocrine tumors reveals both persistent and newly emerging tumor subclones, exhibiting transcriptional changes in both the original and recurrence sites. These findings highlight Spatial-GT-seq as a valuable platform for studying genotype-phenotype-microenvironment associations, providing new insights into cancer evolution and heterogeneity.

GSE276211 Spatial genome and transcriptome co-mapping reveals clonal heterogeneity in tumor tissue [RNA-Seq]

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Yang Liu ; Dejiang Wang ; Xiangjun Di ; Shenjie Wang
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens ; Mus musculus

GSE271191 Collection of CRC cell line grown in vitro

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Claudio Isella ; Alexandra Ambra Ulla ; Anna Cassisa ; Consalvo Petti
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Recent studies revealed the presence of an aggressive subgroup of colorectal cancer (CRC) that exhibits a distinct tumor growth pattern, characterized by high abundance of cancer-associated fibroblasts (CAFs). To identify cancer cells-intrinsic traits underlie this phenotype and to characterize its stromal features, we generated mouse xenografts from 19 CRC cell lines, where normal mouse stroma cells are recruited and educated by epithelial cancer cells. The in vivo xenograft growth rate showed high variability between cell lines, revealing a subgroup of slow-paced tumors. Cancer cells of this subgroup display distinctive transcriptional features, only partially captured by previously described CRC molecular subtypes, involving epithelial-mesenchymal transition and cooperation with a specific CAF population in remodeling the extracellular matrix. We therefore called the cancer cell signature “epithelial matrix remodeling” (EMR), and the CAF signature “matrix remodeling CAF” (mrCAF). In pan-cancer analysis, the EMR and mrCAF signatures were co-detected and associated with poor prognosis in multiple tumor types. Altogether, these results highlight the intrinsic capability of cancer cells to recruit, educate and cooperate with CAFs, indicating route toward tumor progression involving the interaction between tumor and its microenvironment.

GSE267353 Collection of CRC cell line grown in vivo

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Claudio Isella ; Alexandra A Ulla ; Anna Cassisa ; Consalvo Petti
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

GSE255578 TAF1-dependent transcriptional dysregulation underlies multiple sclerosis

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Claudia Rodríguez-López ; Ivo H Hernández ; José Terrón-Bautista ; Eneritz Agirre ; David Lozano-Muñoz ; Julia Pose-Utrilla ; Cristina García-Ortiz ; Miriam Lucas ; Irene Ruiz-Blas ; María González-Bermejo ; Cristina Ortega ; Juan C Chara ; Nina L Fransen ; Miriam Martínez ; Irene B Sancho ; Mukund Kabbe ; Chao Zheng ; Carlos Casado-Barbero ; María Santos-Galindo ; Aldo Borroto ; Balbino Alarcón ; J M Hoozemans ; Diego Clemente ; Claudia Toma ; Carlos Matute ; Felipe Cortés-Ledesma ; Gonçalo Castelo-Branco ; José L Lucas
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

In the search for new targets for therapeutic intervention, MS-associated common variants provide clues about etiology-relevant molecular mechanisms, but the individual effect of each variant is minimal. A current priority to better understand the molecular basis of MS and to identify targets for designing progression-modifying therapies, is therefore to detect in the CNS of MS patients specific biochemical alterations -likely related to environmental factors and/or GWAS-identified molecular mechanisms- that per se would suffice to cause MS progression.

GSE246989 Transcriptomic changes from resulting from treatment of KNS42 with drugs of abuse

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Sarah Storr
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

KNS42 cells were treated with drugs of abuse (ethanol, cocaine, morphine, THC, and psilocin) prior to RNA sequencing. A bioinformatics pipeline of Trim Galore, Kallisto, DESeq2 and Qiagen Ingenuity Pathway Analysis was used for pathway analysis.

GSE246718 Deciphering the interaction between Twist1 and PPARγ during adipocyte differentiation

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Leilei Sun ; Shaoping Ji ; Yang An ; Jian Yang
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Obesity, a worldwide epidemic in recent years, is mainly due to the uncontrolled development of adipose tissues, which includes adipocyte hypertrophy and hyperplasia. Adipocyte differentiation is a process involving multiple transcription factor cascades, and the exact mechanism has not yet been defined. As a bHLH transcription factor, Twist1 exerts its activity by forming homo- or heterodimers with other factors. In this study, we showed Twist1 restricts adipogenesis through PPARγ. Expression of various differentiation markers (including PPARγ and adiponectin) and triglyceride-containing lipid droplets were decreased with overexpression of Twist1. Pathway enrichment analysis of RNA-seq data showed that differentially expressed genes (DEGs) caused by Twist1 overexpression were significantly related to lipolysis and PPARγ signaling. This implicates that Twist1 plays important regulatory roles in these processes. ChIP and dual luciferase assays showed that Twist1 could bind either PPARγ or adiponectin promoter to repress their respective transcription or directly to PPARγ protein to regulate its transcriptional activity. Furthermore, Twist1 directly interacted RXRα, which usually forms heterodimer with PPARγ to regulate adipogenesis. Taken together, our results suggest that Twist1 is an inhibitory modulator of adipogenesis and its function is likely through direct interaction with PPARγ protein or its gene promoter.

GSE246329 ISL1 and AQP5 complement each other to enhance gastric cancer cell stemness by regulating CD44 expression

Sat, 31 Oct 2026 00:00:00 -0400

Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Gastric cancer, a prevalent and life-threatening malignancy, is believed to involve cancer stem cells as a contributing factor to tumor progression. This study delves into the influence of ISL1 on the stem-like properties of human gastric cancer cells. In human gastric cancer samples, there is an observed elevation in ISL1 expression, which correlates with the expression of stem cell markers, notably LGR5. Functionally, ISL1 fosters the self-renewal, cell proliferation, migration, and the clonogenic potential of gastric cancer cells in vitro. Furthermore, it enhances the ability of these cells to form tumors and metastasize in vivo. Additionally, ISL1 collaborates with AQP5, collectively intensifying the tumorigenicity of gastric cancer cells. Mechanistically, transcriptomic analysis of cells overexpressing ISL1 unveils a notable activation of the FOXO pathway. This activation leads to increased nuclear expression of FOXO3, subsequently resulting in elevated expression of the stemness-associated gene CD44 in gastric cancer cells. These findings shed light on the role of ISL1 in promoting the stem-like characteristics of gastric cancer cells and emphasize the connection between ISL1 and AQP5 as a novel therapeutic target for individuals with gastric cancer.

GSE234102 Identification of RNAs interacting with protein FovB in Escherichia coli

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Hoa Q Pham ; Miaomiao Tan ; Peng Y Xie ; Xin Deng ; Xin Wang ; Terrence C Lau
Series Type : Other
Organism : Escherichia coli CFT073 ; Escherichia coli J53

The goal of this analysis was to identify the RNAs interacting with protein FovB which is encoded on IncI1 plasmid in two E. coli strains J53 and CFT073

GSE186488 zebrafish retina m6A epitranscriptome

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Shuyi Chen
Series Type : Methylation profiling by high throughput sequencing
Organism : Danio rerio

m6A epitranscriptome of the retinas of adult zebrafish was sequenced using MeRIP-seq

GSE185777 Microglia Secrete MiR-146a-5p-Containing Exosomes to Regulate Neurogenesis in Depression

Sat, 31 Oct 2026 00:00:00 -0400

Contributors : Cuiqin Fan ; Ye Li ; Tian Lan ; Wenjing Wang ; Yifei Long ; Shu Y Yu
Series Type : Non-coding RNA profiling by high throughput sequencing
Organism : Rattus norvegicus

Enhancing neurogenesis within the hippocampal dentate gyrus is critical for maintaining brain development and function in many neurological diseases. However, the neural mechanisms underlying neurogenesis in depression remain unclear. Here, we show that microglia transfer a microglia-enriched microRNA, miR-146a-5p, via secreting exosomes to inhibit neurogenesis in depression. Overexpression of miR-146a-5p in hippocampal dentate gyrus (DG) suppresses neurogenesis and spontaneous discharge of excitatory neurons by directly targeting Krüppel-like factor 4 (KLF4). Down-regulation of miR-146a-5p expression, ameliorates adult neurogenesis deﬁcits in DG regions and depression-like behaviors in rats. Intriguingly, circular-RNA ANKS1B acts as a miRNA sequester for miR-146a-5p to mediate posttranscriptional regulation of KLF4 expression. Collectively, these results indicate that miR-146a-5p can function as a critical factor regulating neurogenesis under conditions of pathological processes resulting from depression and suggest that microglial exosomes generate new cross-talk channels between glial cells and neurons.

GSE161992 mouse B16-F10 melanoma cells vs. Runx3 expressing B16-F10 cells

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Wenguang Liu
Series Type : Expression profiling by array
Organism : Mus musculus

Transcriptional profiling of the mock control mouse B16-F10 melanoma cells compares with that of the B16-F10 cells retrovirally expressing Runx3.
Runx3 reduced the lung metastasis potential of the B16-F10 melanoma cells. This transcriptional profiling was used to uncover the differentially expressed genes that were regulated by Runx3.

GSE161991 mouse B16-F0 melanoma cells vs. B16-F10 melanoma cells

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Wenguang Liu
Series Type : Expression profiling by array
Organism : Mus musculus

Transcriptional profiling of the mouse B16-F0 melanoma cells compares with that of mouse B16-F10 melanoma cells.
B16-F10 melanoma cell line has very strong lung metastasis potential. B16-F10 melanoma cell line origninates from B16-F0, the later of which has very weak lung metastis potential. This transcriptional profiling was used to uncover the differentially expressed genes that may be associated with the acquirement of lung metastasis potential of B16-F10 cells.

GSE159670 Genome-wide DNA methylation analysis in colorectal tumor and normal tissues

Sat, 31 Oct 2026 00:00:00 -0400

Contributor : Huichuan Yu
Series Type : Methylation profiling by array
Organism : Homo sapiens

The current risk stratification system defined by clinicopathological features do not accurately identify the risk of disease recurrence in patients with stage I-II colorectal cancer (CRC). We aimed to investigate whether the CpG sites from newly established genome-wide methylation profiles could serve as biomarkers to improve prognosis prediction.