New GEO Series

GSE328681 Neonatal Roselovirus Infection Induces Predisposition to Systemic Autoimmunity

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Nillu Ghosh ; Francisco Victorino ; Kaarunya Nachimuthu ; Tarin M Bigley
Series Type : Other ; Expression profiling by high throughput sequencing
Organism : Mus musculus

Autoimmune diseases are characterized by immune dysregulation that begins years prior to the onset of overt disease. Viral infections have been proposed to be a contributing factor to the development of autoimmunity, but in the case of herpesviruses, the onset of autoimmune disease typically occurs years after the initial, acute infection. In this study, we found that adult mice that had been neonatally infected with MRV were predisposed to systemic autoimmunity with features of lupus-like disease after additional immune perturbation with TLR7 stimulation. Single-cell RNA sequencing demonstrated a transcriptional signature and TCR repertoire shift in response to TLR7 stimulation that was unique to prior neonatal infection. .

GSE328676 Chromatin insulators homie and nhomie can interact with distant copies either together or separately, with distinct outcomes for enhancer-promoter interactions

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Fujioka Miki ; Ke Wenfan ; Schedl Paul ; Jaynes James
Series Type : Other
Organism : Drosophila melanogaster

Chromatin insulators, a.k.a. boundary elements, separate regions of the chromosome with distinct chromatin characteristics, including distinct histone modifications. This activity affects gene expression by allowing chromatin domains to be stably regulated and maintained. Insulators also block enhancer-promoter interactions and, somewhat paradoxically, facilitate other interactions, particularly when they stitch together distant regions of the chromosome by pairing with specific partners. Here we explore how long-range interactions facilitated by insulator pairing are affected by the presence of two potentially competing partners. Our results show that when two partners are present, they can reduce each other's effects on distant gene expression, suggesting that enhancer-promoter interactions are best facilitated by pairwise insulator interactions. When a distant copy of an eve insulator (homie or nhomie) is present, it can interact with either or both endogenous insulators. But when one endogenous insulator is removed, the remaining one interacts more strongly with the transgenic copy, biasing the induced enhancer-promoter interactions toward those nearest the remaining endogenous insulator. On the other hand, physical interaction data suggest that strictly pairwise interactions are not the rule, suggesting a more complex model involving tripartite interactions. We further show that removing one or both endogenous eve insulators significantly reduces endogenous eve function at a critical early stage of development, and that the eve Polycomb domain expands in both directions when its insulator boundaries are removed, showing that insulators in their native context are required for each of the main functions that have been ascribed to them based on transgene assays.

GSE328448 Spatiotemporal transcriptomics characterizes immune microenvironment during mouse liver aging [Spatial Transcriptomics]

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Jiahua Lu ; Yuqian Wang ; Wenxue Zhao ; Zihao Zhao ; Zhaoya Gao ; Jin Gu ; Cheng Li ; Jie Cheng
Series Type : Other
Organism : Mus musculus

The liver is a major metabolic organ, responsible for synthesizing and breaking down diverse metabolites. Recently, the liver's immunological functions have gradually been unveiled: combating pathogens and maintaining tissue homeostasis. Age-related functional alterations in these immune cells emerge as potential drivers of hepatic dysfunction and age-associated pathologies. However, systematic investigations into spatiotemporal immune cell dynamics during liver aging remain limited. To address this gap, we analyzed young and old mouse livers using single-cell/nuclei and spatial transcriptomics, revealing T cells as the immune cell population with the most pronounced transcriptomic alterations, marked by enrichment of exhausted CD8+ T cells in aged livers. Spatial mapping showed exhausted CD8+ T cells accumulating in portal vein (PV) zone, co-localizing with periportal hepatocytes (PP hepatocytes). Up-regulation of LPIN1 in PP hepatocyte promoted T cell exhaustion. CD8+ T cell exhaustion was tightly associated with disease progression. Therefore, our findings suggest that targeting LPIN1 may alleviate T cell exhaustion, offering potential therapeutic strategies for age-related liver diseases.

GSE328334 Forming a Precise and Reproducible Hypoxic Tumor Microenvironment in Glioblastoma by High Cell Density Bioprinting

Tue, 21 Apr 2026 00:00:00 -0400

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

Glioblastoma (GBM) is the most common and malignant brain tumor, characterized by its highly aggressive and rapidly proliferative behavior. In this study, we created a high throughput GBM model with a cell density modulated hypoxic niche to investigate the important role of hypoxia in an in vitro model in shaping GBM progression and therapeutic response.

GSE328312 Stable global repertoire architecture masks short- term clonal remodeling in intratumoral TCR repertoires

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Pernille G Pedersen ; Odd L Gammelgaard ; Sofie Traynor ; Christina Ruhlmann ; Aida S Hansen ; Henrik J Ditzel ; Morten F Gjerstorff ; Mikkel G Terp
Series Type : Other
Organism : Mus musculus

Background: Tumor-in ltrating T cell receptor repertoires are increasingly pro led to assess intratumoral T cell dynamics and inform prognosis and treatment response. Most analyzes rely on aggregate diversity metrics, such as Shannon index or clonality, which describe overall repertoire structure but do not resolve changes in clonotype identity over time. Thus, intrinsic temporal dynamics of intratumoral T cell receptor repertoires during tumor progression remain incompletely de ned. Methods: In a bilateral murine cancer model, one tumor was surgically removed, and the paired tumor was collected 11 days later. The T cell receptor repertoires of these tumors, and of synchronously harvested bilateral tumors from separate control animals, were analyzed using diversity metrics, Morisita–Horn similarity, and clonal tracking approaches. Results: Time-matched bilateral tumors exhibited highly similar clonotype composition and abundance. In contrast, time-separated tumors showed reduced clonal overlap, increased fractions of private clonotypes, and redistribution of dominant clones. These changes occurred despite preserved global repertoire metrics, including clonotype number, Shannon diversity, and Gini coef cient. Conclusion: Short-term tumor progression is associated with clear changes in the composition of the intratumoral T cell receptor repertoire, even when overall diversity appears stable. These results suggest that relying solely on global diversity metrics can obscure active clonal remodeling, underscoring the importance of monitoring individual T cell clonotypes to accurately capture intratumoral T cell dynamics over time.

GSE328306 SFTSV exploits PPM1K to inhibit apoptosis through the Bcl-2/BAX/Caspase-3 axis for efficient replication

Tue, 21 Apr 2026 00:00:00 -0400

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

In this study, transcriptomic profiling identified PPM1K as a prominently induced host factor in SFTSV-infected THP-1 cells. We further demonstrate that SFTSV infection promotes endoplasmic reticulum–mitochondria coupling, enabling the viral glycoprotein GC to interact with mitochondrial PPM1K and enhance its expression at both transcriptional and protein levels. Mechanistically, PPM1K dephosphorylates Bcl-2 at Ser248, decreases Bcl-2 ubiquitination, and stabilizes its anti-apoptotic activity, thereby suppressing the BAX–Caspase-3 signaling cascade. This anti-apoptotic remodeling markedly limits apoptosis in infected cells and facilitates efficient SFTSV replication. These findings uncover a previously unrecognized viral strategy in which SFTSV hijacks host PPM1K-dependent mitochondrial signaling to evade apoptosis and promote replication

GSE328302 Identification of two genes associated with recurrence in Paget’s disease and construction of a predictive model

Tue, 21 Apr 2026 00:00:00 -0400

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

In summary, RNA‑seq analysis revealed distinct functional profiles between MPD and EMPD, with recurrence in MPD associated with developmental and differentiation pathways, while EMPD recurrence was linked to immune and inflammatory processes. Using WGCNA, we identified KLF13 and TIA1 as hub genes, which were subsequently validated as independent prognostic biomarkers in internal and external datasets. A risk‑score model based on these genes effectively stratified patients by outcome. Further studies are needed to elucidate the detailed molecular mechanisms underlying their roles in PD progression and recurrence.

GSE328276 Host-pathogen dual targeting with repurposed drugs identifies a synergistic therapy for intracellular Staphylococcus aureus

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Blanca Lorente-Torres ; Helena Á. Ferrero ; Pablo Castañera ; Jesús Llano-Verdeja ; Sergio Fernández-Martínez ; Amanda Herrero-González ; Farzaneh Javadimarand ; Jesús F. Aparicio ; Andrew M. Edwards ; Volker Behrends ; Luis M. Mateos ; Álvaro Mourenza ; Michal Letek
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Background: Staphylococcus aureus causes persistent infections by surviving intracellularly, where it escapes immune defenses and antibiotics. Repurposing clinically approved drugs provides a rapid strategy to expand therapies against intracellular pathogens. Methods: A high-throughput screen of 5,599 approved compounds was performed in A549 cells infected with S. aureus USA300 LAC. Hits were validated across CA-MRSA, HA-MRSA, and MSSA strains and in non-tumorigenic bronchial epithelial cells. Mechanistic studies combined metabolomics, dual RNA sequencing, and DNA repair mutant panels. Efficacy was assessed in Galleria mellonella and a murine pneumonia model. Results: The nucleoside analog 5-fluoro-2′-deoxycytidine (5-FdC) and rifapentine formed a synergistic combination (5FR) effective across strains and host cell types. 5-FdC induced structural DNA damage beyond thymineless death, confirmed in DNA repair mutants, and triggered host DNA damage responses and metabolic rewiring. Dual RNA-seq revealed bacterial growth arrest alongside host stress pathway activation. The 5FR combination significantly reduced bacterial burdens in larvae and in murine lungs and spleen. Conclusions: This integrative pipeline, from screening to in vivo validation, identifies 5FR as a promising repurposed drug combination against intracellular S. aureus. Targeting both host and pathogen pathways may overcome monotherapy limitations, reduce resistance risk, and expand therapeutic options.

GSE328236 Transcriptomic profiling of Carfilzomib (CFZ) treatment in HSV-1 infected BV2 microglial cells

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Yaoxing Wu ; Weishan Shen
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

This study investigates the molecular mechanisms underlying the interaction between Carfilzomib (CFZ) and Herpes Simplex Virus type 1 (HSV-1) infection in microglial cells. Using the BV2 microglial cell line, we performed RNA sequencing to dissect the transcriptional responses under different conditions. Cells were either infected with HSV-1 (MOI=1) for 24 hours or left uninfected, and subsequently treated with 30 nM Carfilzomib (CFZ) or the vehicle control (DMSO) 6 hours post infection.

GSE328235 Single-cell sequencing of carfilzomib-associated HSV-1 encephalitis mouse model

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Yaoxing Wu ; Weishan Shen
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

A murine model of central nervous HSV-1 infection was established by corneal scarification with HSV-1 to investigate the dynamic cellular composition and transcriptional landscape following administration of carfilzomib(CFZ). Brain tissues were collected 5 days post-HSV-1 inoculation at the onset of encephalitis symptoms. Mice were intraperitoneally administered CFZ or saline every other day from inoculation until euthanasia.

GSE328230 ATAC-seq profiling reveals that KLF2 regulates chromatin accessibility programs in HCC

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Yining Li ; Yunjie Liu ; Hua Yu ; Xiaohua Yan
Series Type : Genome binding/occupancy profiling by high throughput sequencing
Organism : Homo sapiens

Krüppel-like factor 2 (KLF2) is a tumor-suppressive transcription factor implicated in the regulation of epithelial-mesenchymal plasticity in hepatocellular carcinoma (HCC). In this study, we performed ATAC-seq in HCCLM3 human HCC cells with or without KLF2 overexpression to characterize KLF2-associated changes in chromatin accessibility. Comparative analysis was used to identify differentially accessible chromatin regions and to investigate how KLF2 affects the transcriptional programs associated with Hippo/YAP signaling and EMT/pEMT-related cell plasticity.

GSE328225 Reprogramming CAR with cytokine signaling increases the efficacy of CAR-T cell therapy in solid tumour treatment and confers sustained immune memory [Tumor infiltrated CAR-T cells]

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Rongchen Sun ; Xue Yang ; Changshuai Che
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Chimeric antigen receptor (CAR) T-cell therapy has shown remarkable efficacy in hematologic malignancies but remains limited in solid tumors because of the immunosuppressive microenvironment, tumor heterogeneity, poor immune-cell infiltration, and progressive T-cell dysfunction. Because cytokine costimulation is critical for maintaining T-cell fitness, we developed a modular engineering strategy, distinct from previous approaches based on direct insertion of large cytokine receptor fragments, in which the intracellular CAR signaling domain was reconstructed to incorporate compact IL-2/IL-15 receptor–derived activation motifs, thereby enabling antigen-dependent coactivation while preserving the overall architecture of the parental CAR. Through systematic screening, we identified S71 as the optimal construct, with significantly greater antitumor activity than other mutants across multiple solid and hematologic tumor targets. Mechanistically, S71 rewired CAR signaling and reprogrammed tumor-induced metabolic responses through a self-sustaining mechanism, improving mitochondrial function and supporting durable T-cell activity. Functionally, S71 promoted enhanced persistence and robust immune memory responses against solid tumors. These findings demonstrate that modular integration of cytokine signaling motifs into CAR intracellular domains can improve CAR-T-cell fitness and antitumor efficacy, and they establish S71 as a promising strategy for overcoming barriers to CAR-T-cell therapy in solid tumors.

GSE328224 Reprogramming CAR with cytokine signaling increases the efficacy of CAR-T cell therapy in solid tumour treatment and confers sustained immune memory

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Rongchen Sun ; Xue Yang ; Changshuai Che
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

GSE327991 Effect of MSCs or tpMSCs on gene expression in hypoxia/LPS-induced dilated acute lung injury

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Yuantong Qi ; Jianxiang Zhang
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

To investigate the intrinsic mechanism of of MSCs or tpMSCs on gene expression in hypoxia/LPS-induced acute lung injury (ALI), we established hypoxia/LPS-induced ALI model mice and MSCs or tpMSCs treated mice, using healthy mice as the normal control. We then performed gene expression profiling analysis of the RNA-seq data obtained from the heart tissues of these three groups of mice.

GSE326685 Dynamic NFκB control during B-lymphopoiesis ensures proteostasis to enable phased proliferation and differentiation decisions

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Valentina Alonso ; Apeksha Singh ; Yu-sheng Lin ; Alexander Hoffmann
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Aging and inflammation reduce the bone marrow B cell output. While myeloid bias among multipotent progenitors is one cause, how the developmental cascade of B-committed progenitors is affected remains less well characterized. Here, we identify dynamic modulation of NFκB as a hallmark of healthy lymphopoiesis, which is diminished in aged, B-lymphopenic mice. Indeed, dysregulated NFκB dynamics result in severe B-lymphopenia. Model-aided analysis of in vivo progenitor populations and ex vivo experimental time courses reveal that accelerated differentiation of pro-B cells results in skipping critical proliferative phases. Single-cell transcriptomics confirmed premature cell-state transitions, characterized by inappropriate activation of NFκB target genes that cause wholesale increases in protein synthesis rates. This imbalanced proteostasis leaves little spare energetic capacity to support population expansion and impairs the functionality of the few B cells that do emerge. Our findings indicate that developmental NFκB dynamics pace and safeguard B-lymphopoiesis, thereby identifying additional mechanistic causes of age-associated humoral immune deficiency.

GSE326327 NanoString nCounter Mouse PanCancer Immune Profiling of CT26 tumors following chronic in vitro PMS2 inhibition and in vivo anti-PD-1 treatment

Tue, 21 Apr 2026 00:00:00 -0400

Contributor : Maria T Rodriguez Plata
Series Type : Expression profiling by array
Organism : Mus musculus

NanoString nCounter immune profiling revealed that PMS2 inhibitor NP1867-pretreated tumours mounted an enhanced immune response to anti-PD-1 therapy, characterized by increased infiltration of lymphocytes, including T cells and cytotoxic populations, together with enrichment of multiple immune-related pathways. These included adaptive immune responses, antigen processing and presentation, MHC signaling, and interferon pathways, indicating that NP1867 pretreatment primes tumors for improved immunological responsiveness to PD-1 blockade.

GSE325337 RANKL inhibits macrophage pro-inflammatory Toll-like receptor 2 and 4 signaling and impairs killing of intracellular bacteria

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Clara D Si ; Christopher T Peek ; Sana R Fatah ; Andrew J Beaudoin ; Anton R Zhelonkin ; Kara R Eichelberger ; Stacy L Hahn ; Robert O Watson ; Denis A Mogilenko ; James E Cassat
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Monocyte-macrophage lineage cells, crucial components of the innate immune system, can uniquely form bone-resorbing osteoclasts upon exposure to the cytokine receptor activator of NF-κB ligand (RANKL) in the bone microenvironment. Recent studies have also begun to uncover extensive extraskeletal roles of RANKL. However, how monocyte-macrophage lineage cells respond to RANKL outside of the bone, and the impact that this signaling pathway exerts on the host immune response, is not fully understood. In this study, we sought to define how RANKL exposure shapes the macrophage inflammatory response to pathogens by using the model intracellular bacterium Salmonella enterica serovar Typhimurium (STm), which co-opts macrophages to cause life-threatening infections. We found that exposing both mouse and human macrophages to sub-osteoclastogenic levels of RANKL increased intracellular STm burdens and decreased pro-inflammatory cytokine production. RNA sequencing revealed downregulation of pattern recognition receptor (PRR) signaling pathways in RANKL-treated macrophages during the early stages of infection. Therefore, we hypothesized that RANKL impairs PRR-dependent signaling pathways that are important for pro-inflammatory cytokine production. We discovered that RANKL-treated macrophages exhibit reduced NF-κB and IRF3 activation, specifically in response to Toll-like receptor (TLR) 2 and TLR4 stimulation. We determined that prior RANKL exposure decreases abundance of the TLR2 and TLR4 adaptor proteins TRAM and TIRAP. Together, these data suggest that RANKL exposure negatively impacts the macrophage TLR-mediated inflammatory response to bacteria.

GSE323389 Dual Activation of CD8+ and CD4+ T cells by a PD-1 targeted IL-15 Mutein in Viral Infection

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Jaroslav Zak ; Isaraphorn Pratumchai ; John R Teijaro ; Kristi L Marquardt
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Immune checkpoint inhibitors have transformed cancer therapy, yet many patients fail to achieve durable responses, in part due to insufficient T cell reinvigoration. Cytokines remain promising additions to immunotherapy to improve response rates; however, the low therapeutic index and associated side effects have hindered progress. In response to these challenges, immunocytokines, engineered fusion proteins that combine the specificity of antibodies with the immune-stimulatory properties of cytokines, have been employed to enable targeted delivery of cytokine signals to immune cells or the tumor microenvironment to minimize pathological consequences. Here, we describe SAR445877 (SAR’877), a novel PD-1-targeted immunocytokine that fuses a high-affinity anti-PD-1 antibody with a detuned IL-15/IL-15Rα sushi domain complex. SAR’877 simultaneously blocks PD-1/PD-L1 and PD-1/PD-L2 interactions and delivers IL-15 signals selectively to PD-1+ T cells. This design enhances the proliferation and activation of antigen-experienced CD8⁺ and CD4⁺ T cells, as well as NK cells, while limiting systemic inflammatory cytokine release. Mechanistically, SAR’877 preferentially activates STAT5 signaling in PD-1⁺ lymphocytes and restores effector function in exhausted T cells in vitro. A murine surrogate of SAR’877 accelerated viral clearance and reinvigorated exhausted T cells in the chronic LCMV Clone-13 infection model. In multiple syngeneic tumor models, the surrogate induced robust anti-tumor immunity by expanding cytotoxic CD8⁺ T cells and promoting Th1 polarization. Notably, SAR’877 outperformed combination therapy with anti-PD-1 and untargeted IL-15, underscoring the therapeutic potential of targeted IL-15 delivery to PD-1+ cells. These findings position SAR’877 as a promising next-generation checkpoint immunotherapy that augments efficacy while reducing cytokine-associated toxicities.

GSE320222 scRNA-seq of cerebral organoids derived from CBP mutant iPSCs

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Longxia Xu ; Hongwen Xuan ; Xiaobing Shi
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

CREB-binding protein (CBP/CREBBP) is a histone acetyltransferase essential for human development. Mutations in CBP are associated with Menke–Hennekam syndrome (MKHK), a neurodevelopmental disorder. To examine the impact of a disease-associated mutation, we performed single-cell RNA sequencing (scRNA-seq) on day 32 cerebral organoids derived from isogenic wild-type and CBP R1868 mutant human induced pluripotent stem cells (iPSCs). This scRNA-seq data captures cellular heterogeneity and gene expression programs during early neurodevelopment and reveals how the CBP R1868W mutation influences lineage specification and transcriptional states in human cerebral organoids.

GSE319859 RNA-seq profiling of cerebral organoids derived from CBP mutant iPSCs

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Longxia Xu ; Hongwen Xuan ; Xiaobing Shi
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

CREB-binding protein (CBP/CREBBP) is a histone acetyltransferase essential for human development. Mutations in CBP are associated with Menke–Hennekam syndrome (MKHK), a neurodevelopmental disorder. To examine the impact of a disease-associated mutation, we performed RNA sequencing on cerebral organoids derived from isogenic wild-type and CBP R1868 mutant human induced pluripotent stem cells (iPSCs) at Day6, Day12, Day18 and Day30 of differentiation. This time-course RNA-seq data captures gene expression programs during early neurodevelopment and reveals how the CBP R1868W mutation influences transcriptional states in human cerebral organoids.

GSE318780 Transcriptome analysis of breast tumour tissue and adjacent normal

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Eleanor J Tyler ; Eleni Maniati ; Oliver M Pearce
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Patients with cancer that respond to immunotherapy benefit from prolonged and possibly indefinite progression free survival. Response rates vary across cancer types, with solid carcinomas generally being the poorest responders at between 10-20 %. Understanding the differences between responders (the 10- 20%) and non-responders (the 80-90%) could identify ways to improve response rates. In this project we investigate transcriptome changes in breast cancer tissue which may help understanding the differences in treatment responses.

GSE318510 Epigenetic lockdown of type I interferon sensing and signalling in human pluripotent cells [CUT&Tag]

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : James H Holt ; Rocio Enriquez-Gasca ; Rachel P Wilson ; Elena G Bochukova ; Pierre V Maillard ; Helen M Rowe
Series Type : Genome binding/occupancy profiling by high throughput sequencing
Organism : Homo sapiens

The Human Silencing Hub (HUSH) complex safeguards genome integrity in human somatic cells by repressing transposable elements and regulating type I interferon (IFN-I) induction. In early development, the IFN-I pathway is inactive, yet its underlying regulation is poorly understood. Here, we use depletion of the HUSH complex in human induced pluripotent stem cells (iPSCs) as a tool to investigate epigenetic control of the IFN-I system in early development. We confirmed that human iPSCs display an attenuated IFN-I pathway, whereas iPSC-derived neural progenitor cells (NPCs) respond robustly to IFN-I pathway agonists. We found that, in iPSCs, depletion of MPP8, a core component of all HUSH complexes, was sufficient to induce both expression of young LINE-1 elements and genes linked to the IFN system including double-stranded RNA sensors and interferon-stimulated genes (ISGs). ISG upregulation had little effect on pluripotency markers and occurred without IFN signalling, suggesting that, in contrast to differentiated cells, these ISGs are direct transcriptional targets of the HUSH complex in early development. Chromatin profiling by CUT&Tag confirmed MPP8 enrichment at HUSH-regulated ISGs and revealed a bimodal binding profile of MPP8 to both ISGs and non-ISGs, the latter largely driven by young LINE-1 elements. We propose that shutdown of the IFN-I system in pluripotent stem cells is essential to prevent lethality from unwarranted self-nucleic acid sensing. This shutdown is achieved through a triple-layer of epigenetic lockdown acting on ligands, sensors, and effectors across the IFN-I pathway.

GSE318471 Epigenetic lockdown of type I interferon sensing and signalling in human pluripotent cells.

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : James H Holt ; Rocio Enriquez-Gasca ; Rachel P Wilson ; Elena G Bochukova ; Pierre V Maillard ; Helen M Rowe
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

GSE318223 Gallic acid chemoprevention of oral carcinogenesis

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Puja Upadhaya ; Felipe F Lamenza ; Ravi Ramalingam ; Kishan Nyati ; Steve Oghumu
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Naturally derived phytochemicals such as gallic acid (GA) exhibit multitargeted anticancer properties and favorable safety profiles, yet the molecular mechanisms underlying their chemopreventive effects in head and neck squamous cell carcinoma (HNSCC) remain incompletely defined. Using a 4 nitroquinoline 1 oxide (4NQO) induced oral carcinogenesis mouse model, we evaluated GA’s effects on tumor progression, and related molecular pathways. Phenotypic outcomes were assessed by histopathology, and proliferation markers. Transcriptomic changes were profiled by RNA sequencing, pathway enrichment and validation using RT qPCR. We report GA as a key modulator of transcriptional programs associated with oral carcinogenesis in a 4-nitroquinoline-1-oxide–induced mouse model. Comparative RNA sequencing of wild-type vehicle-treated (WtVeh) and GA-treated (WtGal) oral tissues revealed GA-dependent reprogramming of immune and stress-response pathways. Our data identifies unique molecular pathways associated with GA mediated oral cancer chemoprevention.

GSE313622 New insights into the interaction of the symbiotic bacterium Candidatus Erwinia dacicola with the adult olive fly Bactrocera oleae combining microscopy and proteomics analyses

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Georgia Pantidi ; Ioannis Livadaras ; Evangelia Skoufa ; Emmanuel Spanoudakis ; Sofia Kaforou ; Christos Andronis ; John Vontas ; Inga Siden-Kiamos
Series Type : Expression profiling by high throughput sequencing
Organism : Bactrocera oleae

The olive fruit fly Bactrocera oleae is the major pest of olive production. The fly is dependent upon the symbiotic bacterium Candidatus Erwinia dacicola for the survival of the larvae in unripe olives, and in the adult stage they enhance fecundity. A major site of symbiont colonization is the esophageal bulb, yet the molecular interactions within this tissue remain poorly understood. To investigate host gene expression in this symbiont-bearing organ, we performed a transcriptomic analysis of B. oleae esophageal bulbs. This dataset provides a foundational resource for elucidating the functional biology of this organ and offers insights into insect–microbe symbiosis.

GSE312714 Biomimetic graphitic carbon nitride nanoparticles enable multiscale biomodulation

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Anne Louise Askou ; Lin Lin
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Virtually all organic material on Earth has been produced converting solar energy through photosynthesis in chloroplasts, a sack-like, double membrane organelle in plants and algae, where transmembrane electron transfer occurs from lumen to stroma. Although animals hardly harness the power of photosynthesis, their bioelectrical signals extensively regulate complex electrophysiological behaviors, rendering it a superior target for biomedical innovation. Here, a crude structural mimicry of chloroplast has led us to discover that hollow sphere graphitic carbon nitride nanoparticles (hg-C3N4 NPs) endowed non-genetic, subcellular and intercellular photo-modulation of various excitable and non-excitable cells, accumulatively achieving modulation at tissue/organ function level. The homogeneous hg-C3N4 NPs showed responsiveness to light via both photoelectrochemical and photothermal mechanisms. The hg-C3N4 NPs can be spontaneously internalized with excellent cytocompatibility. Using a focusing laser, the hg-C3N4 NPs enable intracellular optical stimulation with subcellular resolution, inducing calcium transient release in multiple cells and propagation in primary cardiomyocytes and cardiac fibroblasts. At multicellular scale, optical pacing and synchronization of cardiomyocyte beating is readily achieved by LED. Further, we demonstrate that hg-C3N4 NPs can be safely injected into mouse eyes, restoring light sensitivity in blind mice. Finally, application of hg-C3N4 NPs to porcine retinal tissue ex vivo confirmed their modulation capability to reactivate RGCs activity under LED photostimulation. Taken together, these nanostructured biomimetic photocatalytic NPs offer high resolution, leadless optical probing, non-invasive delivery and great biocompatibility, serving as a versatile tool for addressing a range of complex biomedical challenges through subcellular, intercellular and tissue-level photo-modulation across a broad spectrum of scales.

GSE312675 Pressure Overload-Induced Ventricular Crosstalk Activates Regenerative Mechanisms in the Contralateral Ventricle in Neonatal Mice [RNA-Seq]

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Fabian Ebach ; Julia Nicke ; Tianyuan Hu ; Hemmen Sabir ; Andreas Müller ; Bernd K. Fleischmann ; Mona Malek Mohammadi
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Driven by clinical evidence of funcional recovery of the left ventricle (LV) in children with left ventricular dilated cardiomyopathy upon increased right ventricular (RV) pressure by pulmonary aretry banding (PAB) and considering the regenerative capacity of the neonatal mammalian heart, we have explored whether pressure overload in one ventricle could trigger regenerative mechanisms in the other ventricle. Using RNAseq, we identified 636 genes, that were upregulated following nPAB in both the LV and the RV compared to Sham controls. 1052 genes were upregulated in the RV alone, 191 in the LV alone. GO terms assicoated with genes that were upregulated in both ventricles include positive regulation of cell proliferation and angiogenesis. The here uploaded sequancing data supports echocardiographic and immunohistological evidence of an adaptive regulation of both the LV and the RV to an increased RV pressure.

GSE312674 Pressure Overload-Induced Ventricular Crosstalk Activates Regenerative Mechanisms in the Contralateral Ventricle in Neonatal Mice [scRNA-Seq]

Tue, 21 Apr 2026 00:00:00 -0400

Pulmonary artery banding (PAB) can restore left ventricular (LV) function in infants with end-stage LV dilated cardiomyopathy (LV-DCM), yet the underlying mechanisms remain unclear. Given the transient regenerative capacity of the neonatal heart, we investigated whether pressure overload in one ventricle activates adaptive and regenerative responses in the contralateral ventricle. We induced pressure overload in neonatal mice at postnatal day (P) 0-1 using pulmonary artery banding (nPAB) or transverse aortic constriction (nTAC). In both models, ventricular mass and wall thickness increased not only in the targeted ventricle but also in the contralateral ventricle. These changes were accompanied by cardiomyocyte hyperplasia, preserved systolic function, and enhanced angiogenesis without fibrosis. Bulk and single-nucleus RNA sequencing revealed coordinated activation of pro-proliferative and angiogenic gene programs in both ventricles, including expansion of a cycling cardiomyocyte subpopulation characterized by Ccnd2. In contrast, PAB at P7 resulted in maladaptive hypertrophy, fibrosis, loss of cardiomyocyte proliferation, and impaired biventricular function. These findings reveal an early-life window in which ventricular cross-talk enables a regenerative response to localized pressure overload, supporting the mechanistic rationale for clinical PAB in infants with LV-DCM.

GSE312304 CD8 T-cells, CD86+ macrophages, and TNF-α signaling pathways are correlated with fetlock osteoarthritis in racehorses

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Erica Secor ; Erik Chow ; Matthew Thomas ; Lynn Johnson ; Andrew Siefert ; Bettina Wagner ; Julie Engiles ; Heidi Reesink
Series Type : Expression profiling by high throughput sequencing
Organism : Equus caballus

Background: There is emerging evidence for the role of the immune system in osteoarthritis (OA) pathophysiology; however, little is known about how immune cells and the synovial transcriptome are altered in naturally occurring equine OA.

Objectives: To evaluate synovial fluid (SF) and synovial membrane (SM) immune cell populations and the SM transcriptome in racehorses with fetlock osteoarthritis.

Methods: Fetlock joints from racehorses euthanized on NY racetracks were considered for inclusion. SF and SM were analyzed by flow cytometry using T-cell (CD3, CD4, CD8) and macrophage (CD14, CD86, CD206) surface markers. OA severity was characterized by gross joint evaluation and SM histology. Bulk RNA-sequencing of SM was performed to identify differentially expressed genes. Flow cytometry data was analyzed with mixed linear modeling, including OA severity as a fixed effect and horse as a random effect. RNA-sequencing was evaluated with mixed linear and quadratic modeling using DREAMSeq method to capture differential gene expression over the range of OA severity.

Results: Twenty-four fetlocks from 12 horses met inclusion criteria. CD8+ T-cells (R2 = 0.25 for SM, 0.35 for SF) and CD86+ macrophages (R2 = 0.14 for SM) were positively correlated with OA severity, while CD4+ T-cells (R2 = 0.17 for SM, 0.31 for SF) were negatively correlated. Macrophages co-expressing CD86 and CD206 correlated with OA severity in SM (R2 = 0.31). Pathways including those associated with TNF-α signaling, connective tissue development, and cell and neuron projection organization/development were differentially regulated in SM with greater OA scores.

Main Limitations: Limited sample size, particularly of horses with severe OA.

Conclusions: CD8+ T-cells, CD86+ macrophages, and macrophages co-expressing CD206 and CD86 are enriched in horses with more advanced OA. Gene set analysis suggests the importance of TNF-α signaling and disinhibition of neuron and cell projection development in OA pathogenesis.

GSE303148 A critical role of necroptosis in the oil cyst formation associated with autologous fat transplantation

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Canxiang Lin ; Ruoxi Chen ; Hongwei Liu
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Autologous fat grafting is limited by unpredictable long-term outcomes, with oil cyst formation being a major complication whose molecular mechanisms remain elusive. We established a novel surgically-induced mouse model demonstrating that ischemia duration time as the primary driver of oil cyst pathogenesis. Through RNA-sequencing of viable grafts (n=5) versus oil cysts (n=5), we identified the activation of RIPK3-MLKL signaling axis, revealing necroptosis-related pathways as critical molecular divergences.

GSE302892 Transcriptomic Profiling of the Left Ventricle Using Single-Nucleus RNA Sequencing in Control and Post-MI Mice

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Pankaj S Dholaniya ; Helena Islam ; Syed Baseeruddin Alvi ; Muhamad Mergaye ; Mahmood Khan
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

This dataset features the single-nuclei RNA sequencing (snRNASeq) data from the left ventricle of mice hearts that were isolated post-myocardial infarction (MI) at different time points and were used for nuclei isolation, followed by RNA isolation and sequencing. The data provides insights into the gene expression changes that occur at the early (Week 1) and late (Week 4) phases of myocardial infarction in the mouse heart.

GSE302702 Single-nucleus RNA sequencing of human visceral adipose tissue biopsies from 11 Italian participants.

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Kyla Z Gelev ; Päivi Pajukanta ; Stefano Romeo
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

We performed single-nucleus RNA-sequencing on visceral adipose tissue biopsies from 11 Italian donors from the Molecular Architecture of FAtty Liver Disease in individuals with obesity undergoing bAriatric surgery (MAFALDA) cohort.

GSE302599 Single-nucleus RNA sequencing of human visceral adipose tissue biopsies from 63 Italian participants.

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Kyla Z Gelev ; Päivi Pajukanta ; Stefano Romeo
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

We performed single-nucleus RNA-sequencing on visceral adipose tissue (VAT) biopsies from 63 Italian donors from the Molecular Architecture of FAtty Liver Disease in individuals with obesity undergoing bAriatric surgery (MAFALDA) cohort.

GSE300718 Small RNA production in E13.5 placenta of intra-cytoplasmic sperm injection(ICSI)-F2 offspring

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Mito Kanatsu-Shinohara ; Yusuke Shiromoto ; Takashi Shinohara ; Narumi Ogoniki ; Kimiko Inoue ; Atsuo Ogura
Series Type : Non-coding RNA profiling by high throughput sequencing
Organism : Mus musculus

Various behavioural abnormalities were observed in the F2 offspring of ICSI (Kanatsu-Shinohara et al., 2023, J. Clin. Invest. 133(22):e170140). The data presented here aim to clarify the cause of these abnormalities, and gene expression in the neonatal brain was investigated using RNA sequencing (RNAseq). ICSI was performed using C57BL/6 epididymal sperm and oocytes. Males from the F1 generation were naturally mated with C57BL/6 females to produce the F2 generation. Small RNA production in E13.5 placenta of ICSI-F2 offspring was examined. Each group contains 5 biological replicates.

GSE300656 Expression data of neonatal brain from male intra-cytoplasmic sperm injection(ICSI)-F2 offspring

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Mito Kanatsu-Shinohara ; Takashi Shinohara ; Takuya Yamamoto ; Narumi Ogoniki ; Kimiko Inoue ; Atsuo Ogura
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Various behavioural abnormalities were observed in the F2 offspring of ICSI (Kanatsu-Shinohara et al., 2023, J. Clin. Invest. 133(22):e170140). The data presented here aim to clarify the cause of these abnormalities, and gene expression in the neonatal brain was investigated using RNA sequencing (RNAseq). ICSI was performed using C57BL/6 epididymal sperm and oocytes. Males from the F1 generation were naturally mated with C57BL/6 females to produce the F2 generation. Gene expression in the neonatal brains of male ICSI-F2 offspring was examined. Each group contains four biological replicates.

GSE300655 Expression data of E13.5 placenta from intra-cytoplasmic sperm injection(ICSI)-F2 offspring

Tue, 21 Apr 2026 00:00:00 -0400

Various behavioural abnormalities and congenital anomalies were observed in the F2 offspring of ICSI (Kanatsu-Shinohara et al., 2023, J. Clin.). Invest. 133(22): e170140). The data presented here aim to clarify the cause of these abnormalities. Gene expression in the ICSI-F2 placenta was investigated using RNA sequencing (RNA-seq). ICSI was performed using C57BL/6 epididymal sperm and oocytes. Male ICSI-F2 offspring was mated with wild-type C57BL/6 female, and placentae recovered from pregnant females at E13.5 were examined for gene expression. Each group contains five biological replicates.

GSE300654 Expression data of E19.5 placenta from intra-cytoplasmic sperm injection(ICSI)-F1/F2 offspring

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Mito Kanatsu-Shinohara ; Takashi Shinohara ; Takuya Yamamoto ; Narumi Ogoniki ; Kimiko Inoue ; Atsuo Ogura ; Keiji Mochida
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Various behavioural abnormalities and congenital anomalies were observed in the F2 offspring of ICSI (Kanatsu-Shinohara et al., 2023, J. Clin.). Invest. 133(22): e170140). The data presented here aim to clarify the cause of these abnormalities. Gene expression in the ICSI-F1/F2 placenta was investigated using RNA sequencing (RNA-seq). ICSI was performed using C57BL/6 epididymal sperm and oocytes. The ICSI-F2 generation was produced using the sperm of the ICSI-F1 generation via in vitro fertilisation. Placentae recovered by caesarean section at E19.5 were examined for gene expression. Each group contains four biological replicates.

GSE299978 Accelerated Reprogramming of hiPSCs into Functional Brain Endothelial Cells with Multiplexed CRISPR Activation

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Roy W Hwang ; Will J Costain ; Tyler Renner ; Ziying Liu
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

The blood-brain barrier (BBB) is comprised of brain endothelial cells, which are utilized in vitro to model the BBB under normal and disease conditions. Despite physiological shortcomings, in vitro BBB models derived from human induced pluripotent stem cells (hiPSC) are favored due to their species specificity and superior barrier qualities. Here, we demonstrate the generation of hiPSCs-derived brain endothelial cells (iBEC) using transcriptional reprogramming with a multiplex CRISPR/dCas9 activation (CRISPRa) strategy that selectively activates essential BEC genes. Transcriptional reprogramming simplified the differentiation of iPSCs into mature iBECs and accelerated differentiation from 13 to only five days. Furthermore, CRISPRa reprogrammed iBECs exhibit robust barrier formation with TEER values > 230 Ω x cm2 and correspondingly low transcellular permeability values (< 0.015 x10-3 cm/min). The iBECs expressed a panel of key BBB markers (Claudin-5, ZO-1, CDH5, PECAM1, Occludin, GLUT-1) and transporters involved in receptor-mediated transcytosis (TFR1, IGF1R, TMEM30A). Importantly, the CRISPRa iBECs exhibited a robust angiogenesis phenotype that was absent in the non-engineered iPSCs. This novel CRISPRa-directed differentiation strategy not only accelerates differentiation to the BEC phenotype but also demonstrates the utility of CRISPR gene regulation in modifying the phenotype of iPSC-derived cells.

GSE297989 HNF1B integrates signals in a feed-forward loop driving kidney disease progression [RNAseq_UUOd1]

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Pierre Isnard ; Munevver P Makinistoglu ; Frank Bienaime ; Fabiola Terzi ; Marco Pontoglio
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Chronic kidney disease (CKD) is a complex disorder with substantial unexplained heritability. While GWAS have identified common variants, rare variants and gene-environment interactions likely play a major role. HNF1B, a transcription factor essential for kidney development, is also a cause of monogenic CKD but its function in adult kidneys remains unclear. Here, we show that HNF1B loss in adult mouse kidneys induces rapid CKD with epithelial dedifferentiation, aberrant cell cycle re-entry, and replicative stress. Strikingly, suppression of the HNF1B transcriptional program is observed across multiple human and experimental CKD models, independent of cause. These findings position HNF1B as a central regulator of renal epithelial integrity and reveal a feed-forward mechanism in which HNF1B dysfunction contributes to and is reinforced by CKD progression. Our results provide insight into shared pathways underlying diverse forms of CKD and suggest new targets for therapeutic intervention.

GSE297988 HNF1B integrates signals in a feed-forward loop driving kidney disease progression [RNAseq_P60d2]

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Pierre Isnard ; Munevver P Makinistoglu ; Michel Leibovici ; Serge Garbay ; Fabiola Terzi ; Marco Pontoglio
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

GSE297987 HNF1B integrates signals in a feed-forward loop driving kidney disease progression [ChIPseq_Hnf1b]

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Pierre Isnard ; Munevver P Makinistoglu ; Michel Leibovici ; Serge Garbay ; Fabiola Terzi ; Marco Pontoglio
Series Type : Genome binding/occupancy profiling by high throughput sequencing
Organism : Mus musculus

GSE296364 Conservation and divergence of UVR8 photoreceptor-mediated UV-B signaling in Marchantia polymorpha

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Yuanke Liang ; Roman Podolec ; Roman Ulm
Series Type : Expression profiling by high throughput sequencing
Organism : Marchantia polymorpha

Ultraviolet-B radiation (UV-B) poses a major challenge to all forms of plant life. The liverwort Marchantia (Marchantia polymorpha) serves as a key model organism for studying signaling pathways and inferring their evolution throughout the green lineage. Marchantia expresses key components of UV-B signaling, including the photoreceptor UV RESISTANCE LOCUS 8 (MpUVR8), the WD40-repeat protein REPRESSOR OF UV-B PHOTOMORPHOGENESIS (MpRUP), the E3 ubiquitin ligase complex CONSTITUTIVELY PHOTOMORPHOGENIC 1 / SUPPRESSOR OF phyA-105 (MpCOP1/MpSPA), and the transcriptional regulator ELONGATED HYPOCOTYL 5 (MpHY5). Here, we show that whereas the core UVR8 photocycle is well conserved, regulatory roles of SPA and HY5 diverged during plant evolution. Unlike the case in Arabidopsis (Arabidopsis thaliana) and in contrast to the strong Mpcop1 mutant phenotype, Mpspa mutants developed only a very weak constitutive photomorphogenesis phenotype, indicating that COP1 function is much more independent of SPA in Marchantia than in Arabidopsis. Moreover, in contrast to Arabidopsis SPAs, Mpspa showed enhanced UV-B acclimation and UV stress tolerance, indicating that MpSPA is a negative regulator of MpUVR8 signaling. Similar to Arabidopsis HY5/HYH, MpHY5 functioned antagonistically to MpCOP1, but its role in UV-B-mediated gene expression changes was more limited. Our findings demonstrate that although core components of UV-B signaling existed in the last common ancestor of extant land plants, regulatory interactions have diversified in different lineages since their divergence more than 400 million years ago.

GSE296030 Conservation and divergence of UVR8 photoreceptor-mediated UV-B signaling in Marchantia polymorpha

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Yuanke Liang ; Roman Podolec ; Roman Ulm
Series Type : Expression profiling by high throughput sequencing
Organism : Marchantia polymorpha

GSE295939 Conservation and divergence of UVR8 photoreceptor-mediated UV-B signaling in Marchantia polymorpha

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Yuanke Liang ; Roman Podolec ; Roman Ulm
Series Type : Expression profiling by high throughput sequencing
Organism : Marchantia polymorpha

GSE295329 RNA Folding Energy Regulates Discontinuous Transcription in Coronaviruses

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Stephen J Ross ; Chengjin Ye ; Simon Moxon ; Elke Mühlberger ; Luis Martinez-Sobrino ; Daniel Cifuentes
Series Type : Expression profiling by high throughput sequencing
Organism : Chlorocebus aethiops ; Mus musculus

Coronaviruses use discontinuous transcription to generate subgenomic RNAs (sgRNAs) that encode structural and accessory proteins. However, the factors regulating sgRNA abundance remain unclear. Here, we combined strand-specific RNA sequencing, RNA:RNA interaction mapping, thermodynamic modeling, and targeted mutagenesis to define the regulation of (-) sgRNA synthesis in SARS-CoV-2 infection. We demonstrate that the relative (-) sgRNA abundance across viral genes is stable throughout infection and strongly correlates with corresponding (+) sgmRNA levels. Through meta-analysis of published SPLASH data, we found that the frequency of long-range interactions between the 5′ genomic transcription regulatory sequence (TRS)-Leader and downstream TRS-Body sequences correlates with sgRNA abundance. Notably, the thermodynamic stability (ΔG) of these duplexes quantitatively predicts (-) sgRNA transcript levels. Mutations in non-coding regulatory regions that altered the ΔG resulted in corresponding changes in (-) sgRNA expression, establishing a causal role for TRS duplex stability in transcriptional regulation. Analysis of naturally occurring mutations near regulatory sites further suggests that modulation of duplex stability may also serve as an evolutionary mechanism to fine-tune viral gene expression. Together, our findings identify TRS-Leader:TRS-Body thermodynamics as a key determinant of discontinuous transcription and reveal how RNA structure encodes gene expression levels in the coronavirus genome.

GSE295237 Excitatory neurons and astrocytes-specific dysregulation and aberrant interactions are vulnerable to FCDI as suggested by single-cell spatial transcriptomics [Spatial transcriptomic]

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Yaqian Zhang ; Qihang Zou ; Yingying Liu ; Liemin Zhou
Series Type : Other
Organism : Homo sapiens

Focal cortical dysplasia (FCD) is a common neurodevelopmental disorder characterized by malformations of cortical development and is a leading cause of drug-resistant epilepsy. In this study, we employed single-nucleus RNA sequencing (snRNA-seq) and spatial transcriptomics sequencing (ST-seq) to investigate the molecular pathological features of FCD type I (FCDI) brain tissue from both cell type-specific and spatial heterogeneity perspectives. This integrated analysis provides novel theoretical insights into the pathogenesis of FCDI associated epilepsy.

GSE295236 Excitatory neurons and astrocytes-specific dysregulation and aberrant interactions are vulnerable to FCDI as suggested by single-cell spatial transcriptomics [snRNA-seq]

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Yaqian Zhang ; Qihang Zou ; Yingying Liu ; Liemin Zhou
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

GSE295220 FABP4 Mediated Fatty Acid Transport Promotes Proliferation and Survival of Platinum-Resistant Ovarian Cancer Cells

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Ana Maria Isac ; Andres Valdivia ; Ujin Kim ; Yinu Wang ; Jian-Jun Wei ; Guangyuan Zhao ; Vanessa Hernandez ; Chinamyee V Prabhu Dessai ; Sandra Orsulic ; Ji-Xin Cheng ; Daniela Matei
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Background: Ovarian cancer (OC) depends on fat as fuel for metastasis and growth. We previously demonstrated that cisplatin resistant (Pt-R) OC cells uptake higher amounts of fatty acids (FAs) compared to sensitive (Pt-S) cells– a process which facilitates cancer cell survival under cisplatin-induced oxidative stress. Results: Here we report that Pt-R OC cells are dependent on unsaturated FAs compared to Pt-S cells and upregulate key lipid transporters to allow increased uptake of FAs. Cell viability assays showed Pt-R cells were less viable under serum depletion, with oleic acid (OA, unsaturated) promoting proliferation of OC cells. OA alone rescued the inhibition of cell proliferation under conditions of serum depletion exerting more significant effects in Pt-R vs Pt-S cells. OA also reduced apoptosis, as shown by Annexin V assays, and decreased Caspase-3 and -8 cleavage. RNA-sequencing analysis linked OA-rescued cell proliferation to upregulation of cell cycle-related pathways, including G2/M checkpoints, driven by E2F1. OA increased S- and G2/M phase cell populations (6.95% to 11.6%; p<0.05), while E2F1 inhibition reduced OA-induced cell proliferation. Pt-R cells also expressed higher levels of FA transporter proteins FABP4 and CD36. Inhibiting FABPs reduced the IC50 to Pt and blocked OC growth in vivo. FABP4 was overexpressed in metastatic and recurrent vs. primary ovarian tumors. Implication: Pt-R OC cells are dependent on unsaturated FAs compared to Pt-S cells and upregulate key transporters to increase FAs uptake. OA supports proliferation of Pt-R cells by promoting cell cycle progression from G1 to S- and G2/M phases. Inhibiting FA transport reduces OC progression in vivo.

GSE295204 Transcriptomic profiling of iPSC-derived microglia(iMGL) reveals FGL2-mediated Aβ uptake impairment and argatroban rescue associated with rs73375428 genotype.

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Jichang Yu ; Jinsoo Seo
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

To elucidate how the rs73375428 major allele impairs Aβ uptake and how argatroban rescues this impairment independently of thrombin inhibition, we performed RNA sequencing and bioinformatic analyses in iPSC-derived microglia(iMGL). These datasets provide insight into transcriptomic changes associated with FGL2 modulation and Alzheimer’s disease risk.

GSE294579 The effect of menin-inhibition on the human AML cell line MV4-11

Tue, 21 Apr 2026 00:00:00 -0400

Series Type : Expression profiling by array ; Genome binding/occupancy profiling by high throughput sequencing
Organism : Homo sapiens

This SuperSeries is composed of the SubSeries listed below.

GSE294576 The effect of menin-inhibition on the human AML cell line MV4-11 [ATAC-seq]

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Geoffroy Andrieux ; Eyleen Corrales ; Viktor Fetsch ; Schwobel Lennard ; Robert Zeiser ; Melanie Boerries
Series Type : Genome binding/occupancy profiling by high throughput sequencing
Organism : Homo sapiens

Allogeneic hematopoietic stem cell transplantation remains the most efficacious treatment for many hematological malignancies. However, its therapeutic potential is affected by the most prominent side effect graft versus host disease. Despite advances in the treatment of graft versus host disease in recent years, morbidity and mortality remains high, which requires the development of new treatment approaches. In vitro, we have observed an upregulation of MHC / HLA molecules in several AML cell lines after treatment with the menin-inhibitor MI-463. We hypothesize that menin-inhibition increases the graft-versus-leukemia effect via targeting and sensitizing MLL-mutant AML cells, thus enhancing HLA-dependent killing.

GSE294457 TCA cycle rewiring underpins histone acetylation sourcing and cell-fate transitions during exit from naive pluripotency

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Eleni Kafkia ; David Pladevall-Morera ; Jan Jakub Zylicz
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Metabolism has emerged as a crucial regulator of development and stem cell epigenome. This coupling is particularly evident during the in vitro exit from naïve pluripotency. However, our understanding of the dynamic metabolic rewiring at this developmental stage remains rudimentary. In this study, we reconstruct intracellular metabolite routings in pre- and post-implantation mouse embryos and their dynamic stem cell models. Our findings reveal that, instead of a simple TCA cycle shutdown, there is spatio-temporally programmed TCA cycle rewiring at implantation. Focusing on the pluripotency spectrum, we identify pyruvate as a key metabolic nexus. Indeed, pyruvate carboxylase and malic enzyme activity is essential for maintaining a balanced metabolic and transcriptional state as well as timely exit from naïve pluripotency. Additionally, we discover that formative and primed pluripotent cells exhibit increased glutamine uptake, reduced oxidative TCA activity, and reciprocal reductive glutamine metabolism. This metabolic rewiring supports increased histone acetylation turnover, primarily using glutamine as a carbon source, supplemented by pyruvate cycling. Thus, we uncover diverse nutrient strategies that are functionally coupled to epigenome programming and dynamic pluripotency cell state transitions at the time of implantation.

GSE294258 Intracellular iron homeostasis-regulated epigenetic reprogramming contributes to -7/del(7q) leukemia

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Yiman Peng ; Jianan Zheng ; Xintong Deng ; Zhongwang Wang
Series Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencing
Organism : Mus musculus

Chromosome copy number variations (CNVs) are among the most critical yet poorly understood genetic drivers of human malignancies. -7/del(7q) is one of the most common CNVs in acute myeloid leukemia (AML) and is associated with poor prognosis. It has been proposed that there might be multiple tumor suppressor genes (TSGs) in these CNVs. Previously, we identified KMT2C, a histone methyltransferase, as a tumor suppressor gene in chromosome 7q. In this study, we performed a differentiation CRISPR screening of hematopoietic stem and progenitor cells (HSPCs) and discovered that ABCB8, encoding a mitochondrial iron transporter, is essential for HSPC differentiation. ABCB8 deficiency accelerated leukemogenesis in vivo and disrupted iron homeostasis, reducing cytoplasmic iron availability and impairing iron-dependent enzymes, including the histone demethylase KDM6A. Consequently, ABCB8 loss elevated H3K27me3 levels, repressing differentiation genes in an iron- and KDM6A-dependent manner. Notably, ABCB8 and KMT2C, neighboring genes on 7q, cooperatively regulated H3K27me3 to suppress leukemogenesis. Our findings reveal ABCB8 as a novel TSG in -7/del(7q) AML and uncover an unprecedented epigenetic collaboration between neighboring TSGs, driven by iron-mediated chromatin remodeling.

GSE291782 Single-Cell Transcriptomics Highlights Macrophage-Driven Regulation of EndMT and Repair in Injured Muscle

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Filipa Timóteo-Ferreira ; Riccardo Gamberale ; Cristiana Barone ; Mauro Bergamaschi ; Anna Sofia Tascini ; Raffaella Meneveri ; Emanuele Azzoni ; Silvia Brunelli
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

This study investigates the interactions between innate immune cells and vascular-associated cells within the regenerating muscle niche. Specifically, the transcriptomes of Cdh5-CreERT2:R26R-tdTomato mice were analysed following the partial ablation of infiltrating macrophages (MPs) to understand their influence on endothelial cell (EC) behaviour after injury. This work provides a comprehensive transcriptomic signature of the regenerative muscle niche and highlights key molecular interactions between MPs and ECs.

GSE289299 Syrah: a pipeline to maximize spatial transcriptomics data output

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Carolyn E Brewster ; Frederick G Mann Jr ; Blair Benham-Pyle ; Alejandro Sánchez Alvarado
Series Type : Other
Organism : Schmidtea mediterranea

Spatial analysis of gene expression patterns has been a key technique for revealing the functions of genes. Traditionally, these analyses were constrained to examining only a few candidate genes per sample. However, the advent of spatial transcriptomic techniques like Slide-seqV2 has transformed this field, enabling unbiased and massively parallel exploration of gene expression patterns within their tissue contexts through RNA sequencing. Despite its potential, Slide-seq datasets often suffer from low read counts, loss of data points, and poor quality. We have identified that a significant source of these errors stems from the chemical synthesis of mRNA capture oligonucleotides used in Slide-seqV2. To address this issue, we have developed "Syrah," an analysis pipeline designed to correct these errors. Syrah can dramatically enhance Slide-seqV2 datasets by recovering nearly 30% more reads. Unlike other dataset improvement methods that rely on complex mathematical imputation or single-cell RNA-seq references, Syrah operates independently, requiring no additional datasets or intricate calculations. This innovative technique promises to salvage previously unusable Slide-seq datasets by restoring valuable reads that were inadvertently discarded during analysis.

GSE286215 Temporal mapping of B cell diversification mechanisms in vivo

Tue, 21 Apr 2026 00:00:00 -0400

Contributor : Oliver P Skinner
Series Type : Expression profiling by high throughput sequencing ; Other
Organism : Mus musculus

Naive B cells amplify and diversify their responses when activated by cognate antigen, via clonal expansion, immunoglobulin isotype switching, phenotypic variation, and somatic hypermutation (SHM). Since diversity in the antigenic targets, functional classes, and production kinetics of parasite-specific antibodies influences immunity to malaria, we test here whether individual B cell clones diversify over time in vivo during Plasmodium infection and treatment. During the first week of infection, amid widespread bystander activation, isotype switching initiates soon after Myc up-regulation, and overlaps partially with clonal expansion, resulting in isotype variegation amongst clones. During the second week of infection, expanded clones that seed germinal centres (GC) bifurcate into extra-follicular plasmablasts, exhibit isotype variegation, and initiate SHM, revealing substantial intra-clonal diversification. Over the following month, GC clones exhibit SHM at a constant rate. Anti-malarial intervention does not impede SHM, but instead exerts quantitative limits on GC size, plasma cell emergence, circulating antibody levels, and protection against re-infection. Finally, contemporaneous B cell development relocates from bone marrow to spleen during infection and treatment. Thus, multiple temporally overlapping mechanisms combine in vivo to amplify, diversify, and safeguard humoral immune responses.

GSE285345 Mitochondrial metabolism and signaling direct dendritic cell function in antitumor immunity [ATAC-seq1]

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Hao Shi ; Zhiyuan You ; Hongbo Chi
Series Type : Genome binding/occupancy profiling by high throughput sequencing
Organism : Mus musculus

ATAC-seq profiling of WT and OPA1-deficient cDC1s

GSE284151 Multisensory integration at the dawn of land plant evolution

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Bruno Catarino ; Fernando Rodríguez-Marín ; Cristina Úrbez ; Christina Arvanitidou ; Eva Álvarez ; Federico Valverde ; José M Franco-Zorrilla ; Francisco Romero-Campero ; Miguel A Blázquez
Series Type : Expression profiling by high throughput sequencing
Organism : Arabidopsis thaliana ; Marchantia polymorpha ; Mesotaenium endlicherianum ; Ostreococcus tauri

Land plant colonization was a pivotal event in the evolution of photosynthetic eukaryotes. The transition from aquatic to terrestrial environments required complex multisensory systems that enabled plants to perceive and integrate a broader range of environmental cues, such as light intensity and temperature. However, it remains unclear whether this ability was a pre-adaptation or an innovation during early plant terrestrialization. Here, we show that the aquatic streptophyte ancestor of land plants could integrate light and temperature through a complex regulatory network. A conserved regulatory nexus, comprising phytochromes and transcription factors, was active in the last common ancestor of land plants, allowing the first terrestrial colonizers to adapt and flourish on the harsh terrestrial surface of our planet. Thus, we propose that the multisensory integration that enables extant plants to achieve perceptual disambiguation and fine-tune growth in various ecological niches was a pre-adaptation encoded in the genomes of ancestral land plants.

GSE283360 Gene expression alteration in mouse articular chondrocytes by 25-hydroxycholesterol, 25-hydroxycholesterol-3-sulfate and GW3965 treatment

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Huanbo Wang ; Chao Zheng ; Liu Yang ; Bowei Ni
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Previous studies have demonstrated that 25-hydroxycholesterol (25HC), which is involved in the initiation and progression of osteoarthritis (OA), can be sulfated by SULT2B1 to produce 25-hydroxycholesterol-3-sulfate (25HC3S). Given this background, this study aims to investigate whether 25HC3S and 25HC have different functional effects on articular chondrocytes. Additionally, since 25HC has been proven to be an endogenous ligand of liver X receptor (LXR), this study also compares the effects elicited by the LXR agonist GW3965 on articular chondrocytes to provide insights into whether 25HC and its sulfated derivative, 25HC3S, exert distinct influences on the LXR signaling pathway.

GSE282556 Single cell variant to enhancer to gene map for coronary artery disease [ChIP-seq]

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Chang Jie Mick Lee ; Anene-Nzelu Chukwuemeka ; Roger Foo ; Amrute Junedh ; Stitziel Nathan
Series Type : Genome binding/occupancy profiling by high throughput sequencing
Organism : Homo sapiens

Although genome wide association studies (GWAS) in large populations have identified hundreds of variants associated with common diseases such as coronary artery disease (CAD), most variants lie within non-coding regions of the genome, rendering it difficult to determine the downstream causal gene and cell type. Here, we performed paired single nucleus gene expression and chromatin accessibility profiling from 44 human coronary arteries. To link disease variants to molecular traits, we developed a meta-map of 88 samples and discovered 11,182 single-cell chromatin accessibility quantitative trait loci (caQTLs). Heritability enrichment analysis and disease variant mapping demonstrated that smooth muscle cells (SMCs) harbor the greatest genetic risk for CAD. To capture the continuum of SMC cell states in disease we used single cell caQTL modeling for the first time in tissue to uncover QTLs which are cell state aware and expand our insight into gene regulation in heterogenous cell populations. We identified a variant in the COL4A1/COL4A2 CAD GWAS locus which becomes a caQTL as SMCs de-differentiate through a transcription factor binding site change for EGR1/2. To unbiasedly prioritize functional candidate genes, we built a genome-wide single cell variant to enhancer to gene (scV2E2G) map in human CAD to link disease variants to causal genes in cell types. Using this approach, we found several hundred genes predicted to be linked to disease variants in different cell types. We validated these predictions using enhancer targeted perturb sequencing (TAP-seq). Next, we performed genome-wide HiC in 16 human coronary arteries to build tissue specific gene regulatory networks and map disease variants to integrated chromatin hubs and distal target genes not previously implicated. Using this approach, we show that rs4887091 within the ADAMTS7 GWAS locus modulates function of a super chromatin interactome through a change in a CTCF binding site. Finally, by integrating human genetics with single cell multi-omics we show that CAD genetic risk is enriched in de-differentiated fibromyocytes. Collectively we provide a disease agnostic framework to translate human genetic findings to identify pathologic cell states and genes driving disease, producing a comprehensive scV2E2G map with genetic and tissue level conviction for future mechanistic and therapeutic studies.

GSE264529 Gelsenicine disrupted the intestinal barrier of Caenorhabditis elegans

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Zekai Wu ; Jian Zhang ; Yajiao Wu ; Mengting Chen
Series Type : Expression profiling by high throughput sequencing
Organism : Caenorhabditis elegans

The treatment of gelsenicine resulted in the increase of nematode intestinal permeability. The toxicological mechanisms underlying this effect involved the disruption of intestinal barrier integrity, an imbalance between oxidative and antioxidant processes mediated by the SKN-1/DAF-16 pathway, and abnormal unfolded protein reaction.

GSE262046 YAP rejuvenates cardiomyocytes by changing mitochondrial substrate utilization

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Lin Liu ; Xiao Li ; Yi Zhao ; James F Martin
Series Type : Expression profiling by high throughput sequencing
Organism : Mus musculus

Postnatal cardiomyocyte (CM) maturation, marked by a metabolic transition from glycolysis to fatty acid oxidation, impedes adult CM proliferation and heart regeneration. Our research reveals that Hippo-YAP signaling facilitates CM cell cycle re-entry by reducing lipid utilization in CMs, thereby preserving mitochondrial homeostasis, and promoting CM rejuvenation. On the other hand, overloaded fat by a maternal high-fat diet significantly enhances fatty acid oxidation and maturation in neonatal CMs, counteracting YAP-mediated rejuvenation effects. Through metabolomic and transcriptomic analyses, we discovered that YAP-induced mitochondrial substrate utilization change predominantly depends on reducing Cpt1b activity. Additionally, we identified Mef2 as a crucial activator for CM maturation, which is inhibited upon YAP overexpression, leading to decreased Cpt1b levels in CMs. Our results highlight the heterogeneity and adaptability of neonatal CM energy metabolism and establish YAP as a key regulator of CM substrate utilization. Furthermore, we elucidate a mechanistic framework by which YAP reverses metabolic maturation in cardiomyocytes, thereby facilitating heart regeneration. This insight advances our understanding of metabolic remodeling in heart regeneration and the therapeutic potential of YAP.

GSE244759 An ERF-CEP5 Induced Root Hair Formation module: A Drought Adaptation Mechanism Unveiled by Flavobacterium

Tue, 21 Apr 2026 00:00:00 -0400

Series Type : Expression profiling by high throughput sequencing
Organism : Arabidopsis thaliana

This SuperSeries is composed of the SubSeries listed below.

GSE244750 Arabidopsis transcriptomic response to Flavobacterium sp. 98 inoculation

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Salma Balazadeh ; Arezoo Rahimi ; Guillermo Edigo ; Victor Carion Bravo
Series Type : Expression profiling by high throughput sequencing
Organism : Arabidopsis thaliana

Drought is one of the most detrimental environmental factors that adversely affect crop production, thus jeopardizing food supplies for a growing world population. Over the past years, it has become evident that microorganisms associated with plants can enhance drought tolerance. However, the specific genetic and molecular mechanisms underpinning bacterial induction of drought tolerance in plants are still largely unknown. In our work, we have shown that a root endophytic Flavobacterium sp. 98 confers significant drought tolerance to Arabidopsis thaliana without compromising growth and yield. Here, we compared the transcriptome of Arabidopsis seedlings inoculated with Flavobacterium or mock (time series) to identify transcription reprograming induced by Flavo in plants.

GSE244749 Identification of ERF115 and ERF114 downstream genes

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Salma Balazadeh ; Arezoo Rahimi ; Guillermo Edigo ; Victor Carion Bravo
Series Type : Expression profiling by high throughput sequencing
Organism : Arabidopsis thaliana

Drought is one of the most detrimental environmental factors that adversely affect crop production, thus jeopardizing food supplies for a growing world population. Over the past years, it has become evident that microorganisms associated with plants can enhance drought tolerance. However, the specific genetic and molecular mechanisms underpinning bacterial induction of drought tolerance in plants are still largely unknown.In our work, we have shown that a root endophytic Flavobacterium confers significant drought tolerance to Arabidopsis thaliana. We showed that the bacterium enhances drought tolerance by maintaining (and inducing) root hair formation and elongation under drought. By combining molecular, genetics, and omics technologies we identified an essential role of ethylene and two ethylene-induced transcription factors belonging to the ERF family (ERF115 and ERF114) through which flavobacterium exerts its effect on plant root hair formation and drought tolerance. Here we performed transcriptome analysis using RNA-seq to identify genes downstream of the two ERF transcription factors.

GSE242349 Expression data from MDA-MB-231 and MCF10 cells

Tue, 21 Apr 2026 00:00:00 -0400

Contributor : Monica M Rostom
Series Type : Expression profiling by array
Organism : Homo sapiens

MDA-MB-231 cells are treated with Maraviroc and DZH_2 and MCF10 are treated by DZH_2 for evaluation of cytotoxic effect on normal breast cells
We used microarrays to compare the differential gene expression after treatment with Maraviroc and DZH_2 and investigate the possible pathway of DZH_2.

GSE233849 The effect of menin-inhibition on the human AML cell line MV4-11 [gene expression]

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Andrieux Geoffroy ; Viktor Fetsch ; Lennard Schwobel ; Zeiser Robert ; Boerries Melanie
Series Type : Expression profiling by array
Organism : Homo sapiens

GSE230562 Anti-epileptic drugs are endocrine disruptors for the human fetal testis ex vivo.

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Laurianne Lesné ; Indusha Kugathas ; Séverine Mazaud-Guittot ; Frédéric Chalmel
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Identifying and characterizing the effects of valproic acid (VPA) on the differentiation and function of the different testicular cell types, and at understanding the mechanisms underlying these effects.

GSE230252 The imbalance of Th17/Treg cells induced by prenatal chronic stress exposure is associated with activation of the PI3K/Akt/NF-κB signaling pathway in offspring

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Ye Li ; Guixiang Yao
Series Type : Expression profiling by high throughput sequencing
Organism : Rattus norvegicus

Maternal immune dysregulation, caused by gestational psychological stress, infection, and other perturbations, results in altered offspring immune development and increases risk for immune related disorders. However, the number of studies reporting the effects of prenatal stress on immune system of offspring is very limited. In this study, we examined whether prenatal stress stimuli, based on the CUMS model, may activate the PI3K/Akt/NF-κB signaling pathway and cause an imbalance of Treg/Th17 in the offspring's spleen. Through the establishment of CUMS model, we discovered that prenatal stress increased the plasma levels of corticosterone, IL-1β and IL-6 in the rats that were exposed to it, as well as the serum levels of IL-6, TNF-α and TGF-β in the offspring. We also discovered a correlation between the levels of cytokines in the female rats and the offspring. Additionally, the outcomes of the transcriptome sequencing and PCR experiment demonstrated that the differentially expressed mRNAs in offspring exposed to prenatal stress may cause an imbalance of Th17/Treg via activating the Gng3-related PI3K/Akt/NF-B pathway.

GSE174160 SFPQ rescues F508del-CFTR expression and function in cystic fibrosis bronchial epithelial cells

Tue, 21 Apr 2026 00:00:00 -0400

Contributors : Roopa Biswas ; Myriam Gorospe ; Supriyo De
Series Type : Expression profiling by high throughput sequencing
Organism : Homo sapiens

Here, we investigated the role of SFPQ in the regulation of expression and function of F508del-CFTR in CF lung epithelial cells. We find that the expression of SFPQ is reduced in F508del-CFTR CF epithelial cells compared to WT-CFTR control cells. Interestingly, the overexpression of SFPQ in CF cells increases the expression as well as rescues the function of F508delCFTR. Further, comprehensive transcriptome analyses indicate that SFPQ plays a key role in activating the mutant F508del-CFTR by modulating several cellular signaling pathways. This is the first report on the role of SFPQ in the regulation of expression and function of F508del-CFTR in CF lung disease.