<?xml version="1.0" encoding="UTF-8"?>
<rss xmlns:atom="http://www.w3.org/2005/Atom" version="2.0">
  <channel>
    <title>New GEO Series</title>
    <link>http://www.ncbi.nlm.nih.gov/geo/</link>
    <atom:link href="http://www.ncbi.nlm.nih.gov/geo/feed/series/" rel="self" type="application/rss+xml"/>
    <description>GEO series published today</description>
    <pubDate>Mon, 20 Apr 2026 03:13:27 -0400</pubDate>
    <item>
      <title>GSE328250 scRNA-seq of cardiac neural crest cells following left atrial ligation</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE328250</link>
      <guid isPermaLink="false">GSE328250</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Stephanie E Lindsey ; Robert  Porter ; Aining  Fan&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Gallus gallus&lt;p&gt;We have employed a single cell sequencing approach using 10x Genomics scRNAseq to study the affect of altered hemodynamic patterning on cardac neural crest cells (CNCCs). CNCCs play an important role in tunica media formation of the great vessels, cardiac septation,  and contribute to cardiomyocytes of he ventricle.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Gallus gallus</category>
    </item>
    <item>
      <title>GSE328169 CRISP enables comparisons of image-based spatial transcriptomic segmentation quality across ten organs</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE328169</link>
      <guid isPermaLink="false">GSE328169</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Rose  James Richard ; Vanover  Daryll ; Santangelo  Philip&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Other&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Mus musculus&lt;p&gt;This dataset comprises 10x Xenium image-based spatial transcriptomics data from a mouse tissue microarray (TMA) containing ten organs (brain, female reproductive tract, heart, kidney, large intestine, liver, lung, small intestine, spleen, and stomach) collected from C57BL/6J mice treated with lipid nanoparticle-delivered β-Galactosidase mRNA or vehicle control and profiled with a 5,006-gene panel.</description>
      <category>Other</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE328112 RNA-seq profiling of non-muscle invasive bladder cancer (NMIBC) tumors</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE328112</link>
      <guid isPermaLink="false">GSE328112</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Robert T Lawrence ; Joseph D Dekker&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Homo sapiens&lt;p&gt;Bulk RNA-seq was performed on fresh-frozen non-muscle invasive bladder cancer (NMIBC) tumor biopsies obtained from commercial biobanks (BioIVT and Proteogenex). These data were generated to characterize the transcriptomic landscape of NMIBC tumors and support preclinical studies of integrin beta-6 (ITGB6)-targeted therapies. RNA was extracted from 25 untreated surgical specimens and sequenced using paired-end Illumina sequencing by Azenta Life Sciences.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE327677 Using iCLIP-seq to analyze the distribution of XRCC5/6 on HBV RNA</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE327677</link>
      <guid isPermaLink="false">GSE327677</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Jiangpeng  Feng ; Wuxiang  Guan&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Other&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Homo sapiens&lt;p&gt;In this study, we found that XRCC5/6, as pseudourindine reader proteins, can bind Ψ on HBV RNA and regulate HBV expresion. To directly analyze the binding sites of XRCC5/6 on HBV RNA, iCLIP-seq was performed in HepG2.2.15 cells using antibodies against XRCC5 and XRCC6, PUS1. The results revealed that XRCC5/6, PUS1, specifically bind 3'UTR of HBV RNA, with significant enrichment around the Ψ sites.</description>
      <category>Other</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE327675 Using Chip-seq to analyze the distribution of XRCC5/6 on HBV DNA</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE327675</link>
      <guid isPermaLink="false">GSE327675</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Jiangpeng  Feng ; Wuxiang  Guan&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Genome binding/occupancy profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Homo sapiens&lt;p&gt;In this study, we found that XRCC5/6, as DNA-binding proteins, can bind to HBV DNA and regulate HBV transcription. To directly analyze the binding regions of XRCC5/6 on HBV DNA, ChIP-seq was performed in HepG2.2.15 cells using antibodies against XRCC5 and XRCC6. The results revealed that XRCC5/6 were abundantly distributed across the HBV genomic DNA, with significant enrichment around the HBV promoters.</description>
      <category>Genome binding/occupancy profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE327651 An SPFH Protein Couples Membrane Stress to Differentiation in Bacillus subtilis</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE327651</link>
      <guid isPermaLink="false">GSE327651</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Sarah S Baur ; Urška  Repnik ; Tobias  Busche ; Louisa  Rau ; Alisa  Mondry ; Marc  Bramkamp&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Bacillus subtilis subsp. subtilis str. 168&lt;p&gt;Bacillus subtilis adapts to fluctuating environmental stress, such as membrane perturbation or alkaline conditions, using membrane-associated regulatory complexes. Here, we rename the previously termed pspA-ydjGHI operon to pspA-samGHI (for starvation and motility) to reflect its functional roles in membrane envelope stress signalling. The SamG–SamH membrane proteins recruit SamI, a cytosolic SPFH protein, which stabilizes focal membrane localization and recruitment of PspA, an ESCRT-III homolog. Under normal conditions, this system transiently assembles at the membrane, stabilizing it and allowing proper motility, secretion, and biofilm formation. Loss of SamI (ΔsamI/ΔydjI) leads to unbalanced SamG–SamH activity leading to a constitutive stress signalling, and global transcriptional changes reminiscent of starvation situations. This, in turn, blocks secretion of the matrix protein BslA, preventing biofilm formation, and reducing motility. Deletion of samH in combination with ΔsamI restores biofilm formation, while ΔpspA mutants form biofilms normally, indicating that PspA is dispensable for the developmental phenotype. Our findings reveal that beside membrane integrity SamGHI coordinates transcriptional homeostasis and multicellular development through formation of a membrane integral stress sensor complex.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Bacillus subtilis subsp. subtilis str. 168</category>
    </item>
    <item>
      <title>GSE327509 Tectochrysin alleviates Ang II-induced pathological cardiac hypertrophy by binding to STING and inhibiting STING/NFκB-mediated inflammation</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE327509</link>
      <guid isPermaLink="false">GSE327509</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Yanghao  Chen ; Zhiyu  Ling&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Mus musculus&lt;p&gt;Angiotensin II (Ang II)-induced cardiac inflammation plays a pivotal role in the pathogenesis of pathological cardiac hypertrophy and hypertension-related heart failure. Tectochrysin (Tec) is a flavonoid natural compound exhibiting significant anti-inflammatory activity. However, the role of Tec in hypertensive heart failure and its molecular targets remain unclear. The therapeutic efficacy of Tec was assessed in the Ang II-induced mouse model using echocardiography, histopathological staining, and serological tests. Its anti-hypertrophic effect was further examined in vitro by phalloidin staining. Investigate the mechanism of action of Tec through transcriptome sequencing. The interaction of Tec with STING was detected by DARTS, CETSA, and SPR assays. Western blotting assay detected the effect of Tec on Ang II-induced activation of the STING/NFκB pathway. The functional dependency of Tec on STING was demonstrated using the STING inhibitor H151. In vivo experiments confirmed that Tec alleviates Ang II-induced myocardial inflammation, pathological hypertrophy, myocardial fibrosis, and cardiac dysfunction. Further in vitro studies revealed the efficacy of Tec in inhibiting cardiomyocyte hypertrophy. Mechanistically, Tec significantly suppressed Ang II-induced activation of the STING/NFκB signalling pathway by targeting STING. Crucially, administration of the STING inhibitor H151 alleviates pathological myocardial hypertrophy, however its use diminishes the therapeutic effect of Tec. Our findings confirmed STING as a critical therapeutic target in pathological ventricular remodeling, with Tec exerting its anti-hypertrophic effects through STING inhibition.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE327442 Cellular Signatures of Melanocortin Pathway Genes Across the Locus Coeruleus [snRNA-seq]</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE327442</link>
      <guid isPermaLink="false">GSE327442</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Alisha  Basak ; Fahrünisa Meryem Betül  Erol ; Maria Caterina  De Rosa ; Zhangji  Dong ; Victor  Ogbolu ; Hannah J Glover ; Rick  Rausch ; Gunnar  Hargus ; Jordi  Creus-Muncunill ; Heather  Buchanan ; Yu  Bai ; Qi  Su ; Betty  Chang ; Christina  Adler ; Delaney  Flaherty ; Benjamin  Ciener ; Harrison  Xiao ; Hasini  Reddy ; Pascaline  Aime-Wilson ; Christiane  Reitz ; Mark W Sleeman ; Judith Y Altarejos ; Rudolph L Leibel ; Liang Oscar  Qiang ; Andrew F Teich ; Claudia A Doege&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Homo sapiens&lt;p&gt;Obesity and Alzheimer’s disease (AD) are epidemiologically associated. The locus coeruleus (LC) – the brain’s primary and most significant source of norepinephrine – is one of the earliest sites of neurodegeneration in AD. The LC participates in feeding behavior through connections with the hypothalamus. The cellular composition of the LC has been characterized at single-cell resolution. However, the constituent cellular signatures of genes related to energy homeostasis – such as the melanocortin pathway genes – in the LC are unclear. We performed single-nucleus RNA sequencing and spatial transcriptomics (Visium) in the human LC, and HiPlex RNAscope in the LC of mice. The melanocortin pathway gene MRAP2 was expressed in the majority of DBH neurons across the LC. Mrap2 was also co-expressed with AD-associated genes such as App, Psen1, Psen2, and Sorl1. More than 20% of Dbh neurons in the LC were positive for Mrap2, App, Psen1, and Psen2. Mrap2 is expressed in the central nervous system and modulates the trafficking and signaling of all five G-protein coupled receptors (GPCRs) of the melanocortin receptor family: Mc1r, Mc2r, Mc3r, Mc4r, and Mc5r. In mice, among the melanocortin receptors, Mc5r showed the highest co-expression with Mrap2, accounting for 17.9% of Mrap2-positive cells, followed by Mc2r with 10.9% of Mrap2-positive cells. Mc1r, Mc3r, and Mc4r showed very limited co-expression with Mrap2. Our study reveals that many Mrap2-positive cells do not express any melanocortin receptor genes, warranting future studies into metabolically relevant GPCRs downstream of MRAP2 in the LC. In summary, our study characterizes melanocortin molecular substrates in the human and mouse LC and highlights MRAP2 as a potential link between pathways of energy homeostasis and neurodegeneration.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE327441 Cellular Signatures of Melanocortin Pathway Genes Across the Locus Coeruleus [Spatial Transcriptomics]</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE327441</link>
      <guid isPermaLink="false">GSE327441</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Alisha  Basak ; Fahrünisa Meryem Betül  Erol ; Maria Caterina  De Rosa ; Zhangji  Dong ; Victor  Ogbolu ; Hannah J Glover ; Rick  Rausch ; Gunnar  Hargus ; Jordi  Creus-Muncunill ; Heather  Buchanan ; Yu  Bai ; Qi  Su ; Betty  Chang ; Christina  Adler ; Delaney  Flaherty ; Benjamin  Ciener ; Harrison  Xiao ; Hasini  Reddy ; Pascaline  Aime-Wilson ; Christiane  Reitz ; Mark W Sleeman ; Judith Y Altarejos ; Rudolph L Leibel ; Liang Oscar  Qiang ; Andrew F Teich ; Claudia A Doege&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Other&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Homo sapiens&lt;p&gt;Obesity and Alzheimer’s disease (AD) are epidemiologically associated. The locus coeruleus (LC) – the brain’s primary and most significant source of norepinephrine – is one of the earliest sites of neurodegeneration in AD. The LC participates in feeding behavior through connections with the hypothalamus. The cellular composition of the LC has been characterized at single-cell resolution. However, the constituent cellular signatures of genes related to energy homeostasis – such as the melanocortin pathway genes – in the LC are unclear. We performed single-nucleus RNA sequencing and spatial transcriptomics (Visium) in the human LC, and HiPlex RNAscope in the LC of mice. The melanocortin pathway gene MRAP2 was expressed in the majority of DBH neurons across the LC. Mrap2 was also co-expressed with AD-associated genes such as App, Psen1, Psen2, and Sorl1. More than 20% of Dbh neurons in the LC were positive for Mrap2, App, Psen1, and Psen2. Mrap2 is expressed in the central nervous system and modulates the trafficking and signaling of all five G-protein coupled receptors (GPCRs) of the melanocortin receptor family: Mc1r, Mc2r, Mc3r, Mc4r, and Mc5r. In mice, among the melanocortin receptors, Mc5r showed the highest co-expression with Mrap2, accounting for 17.9% of Mrap2-positive cells, followed by Mc2r with 10.9% of Mrap2-positive cells. Mc1r, Mc3r, and Mc4r showed very limited co-expression with Mrap2. Our study reveals that many Mrap2-positive cells do not express any melanocortin receptor genes, warranting future studies into metabolically relevant GPCRs downstream of MRAP2 in the LC. In summary, our study characterizes melanocortin molecular substrates in the human and mouse LC and highlights MRAP2 as a potential link between pathways of energy homeostasis and neurodegeneration.</description>
      <category>Other</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE325517 Methylation of the Cg12712415 Locus Suppresses TAK1 Expression to Mediate Immune Paralysis in Severe Pneumonia</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE325517</link>
      <guid isPermaLink="false">GSE325517</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributor&lt;/i&gt; : Shi  Zhang&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Homo sapiens&lt;p&gt;Severe pneumonia lethality often arises not from excessive inflammation, but from subsequent immune system "paralysis" (immunoparalysis), a clinical challenge lacking specific biomarkers and effective therapies. Our study addressed this by identifying key epigenetic checkpoints driving immunoparalysis. Herein, we identify that DNA methylation at the Cg12712415 locus acts as an epigenetic switch to distinguish and predict secondary immunoparalysis in severe pneumonia patients. Mechanistically, DNMT3A specifically catalyzes this methylation, silencing transcription of the critical kinase TAK1 by blocking RNA polymerase II binding. TAK1 loss impairs monocyte/macrophage functions, disrupts intercellular crosstalk, induces CD8⁺ T cell exhaustion and regulatory T cell expansion, and causes systemic immunosuppression. Importantly, macrophage-derived exosome-mediated TAK1 delivery reversed immunoparalysis and improved survival in animal models. Our findings establish the "DNMT3A–Cg12712415–TAK1" axis as a novel regulatory pathway, provide a new immunoparalysis biomarker, and lay the foundation for an epigenetic-based targeted therapy.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Genome binding/occupancy profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE325391 Unique transcriptional profiles of adult human immature neurons in healthy aging, Alzheimer’s disease, and cognitive resilience</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE325391</link>
      <guid isPermaLink="false">GSE325391</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Giorgia  Tosoni ; Dilara  Ayyildiz ; Sarah  Snoeck ; Elena P.  Moreno-Jiménez ; Amber  Penning ; Estibaliz  Santiago-Mujika ; Olmo  Ruiz Ormaechea ; Hyunah  Lee ; Suresh  Poovathingal ; Kristofer  Davie ; Julien  Bryois ; Will  Macnair ; Jasper  Anink ; Luuk E.  De Vries ; Sahand  Farmand ; Erik  Nutma ; Dick F.  Swaab ; Eleonora  Aronica ; Jinte  Middeldorp ; Sandrine  Thuret ; Laurent  Roybon ; Onur  Basak ; Carlos P.  Fitzsimons ; Paul J.  Lucassen ; Evgenia  Salta&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Homo sapiens&lt;p&gt;The existence and putative functional significance of immature neurons in the adult human brain, particularly in the context of neurodegenerative disorders, remains an open question. While rodent studies have highlighted active roles for adult-born immature neurons in the hippocampus under both healthy conditions and in Alzheimer’s disease (AD), evidence from the human brain is limited and lacks detailed molecular characterization. To address this gap, we performed single-nucleus RNA sequencing in aged healthy, AD and dementia-resilient human hippocampus to probe immature neuronal signatures and gene expression alterations associated with AD pathology and resilience. Employing a novel experimental and computational pipeline, we identified persistent populations of immature neurons across all donor groups, with transcriptional profiles reflecting ‘juvenile’ cellular functions, which are compromised in AD. Our findings suggest that the presence of these immature neuronal populations per se may actively contribute to maintaining homeostasis within the aged human hippocampus, and cognitive resilience in AD.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE322787 A skin-hypothalamus axis couples heat stress and metabolic dysfunction</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE322787</link>
      <guid isPermaLink="false">GSE322787</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Hai-Yan  Zhou ; Xu  Feng ; Xiang-Hang  Luo&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Mus musculus&lt;p&gt;With the ongoing rise in global temperatures, heat stress is increasingly implicated in chronic metabolic disorders; however, whether a transient high-temperature experience leads to enduring metabolic vulnerability and persistent hypothalamic adaptations remains unclear. To address this question, we established a controlled heat stress (HS) mouse model. Eight-week-old male mice with comparable body weights were assigned to HS or paired-fed (PF) conditions. HS mice were exposed to 37 °C for 6 h during the dark phase for 1 week with ad libitum access to food. PF mice were maintained at room temperature and pair-fed to match the food intake consumed by HS mice during the 6-h exposure window, followed by ad libitum feeding for the remaining 18 h to ensure comparable total daily intake. After HS, mice were returned to room temperature for a 2-week quiescent stage (QS), during which blood glucose and serum corticosterone normalized, indicating recovery from acute stress. Hypothalamic cells were collected from PF, HS, and QS groups for single-cell RNA sequencing to characterize heat stress–associated changes in hypothalamic cellular composition and transcriptional states. We observed a sustained increase in astrocyte abundance after HS that persisted into QS, and identified an expanded astrocyte subpopulation marked by high Lrrc7 expression, providing a foundation for further investigation of persistent hypothalamic responses to heat exposure in the context of metabolic regulation.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE318514 Organ injury in systemic autoimmunity is mediated by stem-like CD8 T cells arising from tissue-draining lymph nodes</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE318514</link>
      <guid isPermaLink="false">GSE318514</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Jafar  Al Souz ; Yulong  Wei ; Can  Cui ; Rihao  Qu ; Jin-Young  Choi ; Fang  Wang ; Steven  Moioffer ; Julia  Barrett ; Irene  Chernova ; Manvitha  Nadella ; Emilly R Siniscalco ; Gilbert  Moeckel ; Nikhil S Joshi ; Ping-Min  Chen ; Arnon  Arazi ; Ya-Chi  Ho ; Joseph  Craft&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Genome binding/occupancy profiling by high throughput sequencing ; Expression profiling by high throughput sequencing ; Other&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Mus musculus&lt;p&gt;Chronic antigen exposure in cancer and infection generates hypofunctional, stem-like CD8 T cells that replenish tissue effector cells for tumor or pathogen control. CD8 T cells infiltrate kidneys in systemic lupus erythematosus, but their origin, differentiation, and function remain incompletely understood. We identified in lupus-prone mice TCF1⁺ stem-like CD8 T cells in renal-draining lymph nodes that underwent TCR-dependent, antigen-driven expansion with differentiation into cytotoxic kidney-infiltrating cells that promoted tissue injury contingent on CD4 T cell help and IL-21/IL-15 signaling. CD8 T cell differentiation was marked by persistent AP-1 activity and cytotoxic function despite immune checkpoint upregulation. We found a parallel program of CD8 T cell differentiation in kidneys of patients with lupus nephritis, reflecting shared pathogenesis. This T cell differentiation program is analogous to that in chronic infections and cancer, indicating conservation across states of chronic antigen stimulation; however, CD8 T cells in systemic autoimmunity retain effector function despite terminal differentiation.</description>
      <category>Genome binding/occupancy profiling by high throughput sequencing</category>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Other</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE311311 UBA1-CDK16: A Female-Specific Chimeric RNA Emerging Through Evolution and Involved in Immune Regulation</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE311311</link>
      <guid isPermaLink="false">GSE311311</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Xinrui  Shi ; Loryn  Facemire ; Sandeep  Singh ; Shailesh  Kumar ; Robert  Cornelison ; Chen  Liang ; Fujun  Qin ; Aiqun  Liu ; Shitong  Lin ; Yue  Tang ; Justin  Elfman ; Thomas  Manley ; Martyna  Glowczyk ; Anam  Tajammal ; Shafaque  Zahra ; Timothy  Bullock ; Doris M  Haverstick ; Peng  Wu ; Hui  Li&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Homo sapiens&lt;p&gt;Chimeric RNAs resulting from intergenic splicing represent a novel mechanism for transcriptome expansion. To explore the role of this new layer of the transcriptome in sex-specific immunity, we analyzed RNA-seq data from 425 blood samples and identified the first female-specific chimeric RNA, UBA1-CDK16, which was further validated in over 1,200 blood samples. This chimeric RNA forms via cis-splicing between two adjacent X-linked parental genes, UBA1 and CDK16, despite both being expressed in both sexes. We demonstrated that a female-specific chromatin loop at the UBA1-CDK16 junction sites facilitates the intergenic splicing. Evolutionary analysis revealed that UBA1-CDK16 became female-specific in humans through at least two independent paths. Functional studies suggested UBA1-CDK16 is enriched in the myeloid lineage and may regulate myeloid cell development and inflammatory responses. Notably, its abnormal expression in female COVID-19 patients correlates with altered neutrophil counts, highlighting its potential role in disease pathogenesis.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE311226 Baseline and Follow-up Methylation Profiling of Whole Blood DNA in Normoglycemia, Prediabetes, and Type 2 Diabetes</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE311226</link>
      <guid isPermaLink="false">GSE311226</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Gopika  Satheesh ; Abdul  Jaleel&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Methylation profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Homo sapiens&lt;p&gt;This longitudinal study analyzed whole-blood DNA methylation profiles in adults classified as normoglycemic, prediabetic, or type 2 diabetes mellitus (T2DM). Oxford Nanopore PromethION long-read sequencing (PCR-free ligation preparation) was used to generate genome-wide CpG methylation data at baseline and at six-year follow-up. The dataset includes raw nanopore reads (available in SRA) and processed methylation outputs, including CpG-wise differential methylation, methylation summaries, promoter/CpG island annotation, HOMER functional annotation, and gene–pathway mapping</description>
      <category>Methylation profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE295199 KCNN4 mediated potassium ion efflux maintains mitochondrial functions leading to platelet biogenesis</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE295199</link>
      <guid isPermaLink="false">GSE295199</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Qihao  Chen ; Takuya  Yamamoto ; Sou  Nakamura ; Koji  Eto&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Homo sapiens&lt;p&gt;Background: While potassium ion (K+) is known to be vital to platelet functions, we have limited knowledge about K+ channels involved in thrombopoiesis from imMKCLs, the iPSC-derived megakaryocyte progenitor cell lines that we have established for ex vivo manufacturing of platelet products for clinical use. Objective: We aimed to elucidate how K+ channels contribute to platelet biogenesis and focused on the role of Ca2+-activated K+ channel KCNN4 (also known as KCa3.1). Methods: Using imMKCLs and human cord blood hematopoietic stem cell-derived megakaryocytes (CB-megakaryocytes), we examined the dynamic changes of intracellular cations during platelet biogenesis. Along with RNA-seq profiling of K+ channels, we investigated the role of KCNN4 by using inhibitors or by direct gene knockdown in proplatelet formation or platelet production. We further examined its relationship with tubulin reorganization, mitochondrial functions, and reactive oxygen species (ROS) levels. Results: Continuous reduction of intracellular K+ levels ([K+]i) was observed during the 6-day of maturing imMKCLs. KCNN4 was expressed at the initiation of platelet generation in megakaryocytes and KCNN4 inhibition resulted in impaired proplatelet formation and reduced platelet productivity in imMKCLs and CB-megakaryocytes, accompanied by decreased [K+]i, diminished mitochondrial membrane potential and an elevated level of ROS. Conclusions: Our findings suggest that the decline of [K+]i via KCNN4 is a key mechanism linking tubulin regulation, ROS, and mitochondrial functions to proplatelet formation and intact thrombopoiesis. This study sheds new light on thrombopoiesis mechanism that contributes to improved ex vivo platelet manufacturing.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE294511 Gene expression profiling of tumor organoids of colorectal liver metastases.</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE294511</link>
      <guid isPermaLink="false">GSE294511</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Anita  Sveen ; Kushtrim  Kryeziu ; Ragnhild A Lothe&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by array&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Homo sapiens&lt;p&gt;We have performed gene expression profiling of patient-derived tumor organoids (PDOs) and tissue samples of resected liver metastases from patients with metastatic colorectal cancer.</description>
      <category>Expression profiling by array</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE294444 16s rDNA amplicon sequencing from Drosophila associated with age-dependent sleep fragmentation</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE294444</link>
      <guid isPermaLink="false">GSE294444</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Yukinori  Hirano ; Priyanshu  Bhagava&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Other&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Drosophila melanogaster&lt;p&gt;In Drosophila, we tried to determine the microbiota associated with age-dependent sleep fragmentation. To this end, the aged male flies showing sleep fragmentation was sampled to compare with those without showing sleep fragmentation. Using an optimized data analysis workflow, we obtained about 0.1 million reads of 16s rDNA from single flies. Data indicated different microbiome between two groups.</description>
      <category>Other</category>
      <category>Drosophila melanogaster</category>
    </item>
    <item>
      <title>GSE294309 RNA-seq from Drosophila heads and bodies associated with age-dependent sleep fragmentation</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE294309</link>
      <guid isPermaLink="false">GSE294309</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Yukinori  Hirano ; Priyanshu  Bhagava&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Drosophila melanogaster&lt;p&gt;In Drosophila, In Drosophila, we tried to determine the genes associated with age-dependent sleep fragmentation. To this end, the aged male flies showing sleep fragmentation was sampled to compare with those without showing sleep fragmentation. Using an optimized data analysis workflow, we mapped about 0.2-0.6 million reads to Drosophila reference genome, dm6. The genes showing significant difference were found in most between naive group and shocked group showing medium avoidance from a confined space. Our study demonstrated differentially expressed genes in aged flies showing sleep fragmentation.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Drosophila melanogaster</category>
    </item>
    <item>
      <title>GSE294159 RNA-seq from Drosophila heads differentiating place preference</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE294159</link>
      <guid isPermaLink="false">GSE294159</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Yukinori  Hirano ; Abdalla G Alia&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Drosophila melanogaster&lt;p&gt;In Drosophila, we tried to determine the stress-induced gene expression change associated with the behavioral mode examined by a place preference test. We conducted RNA-seq analysis from total RNA obtained from individual Drosophila heads, either in naive state or after electric shock. Using an optimized data analysis workflow, we mapped about 6-12 million reads to Drosophila reference genome, dm6. The genes showing significant difference were found in most between naive group and shocked group showing medium avoidance from a confined space.  Our study demonstrated that Toll-signaling related genes are enriched after electric shock.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Drosophila melanogaster</category>
    </item>
    <item>
      <title>GSE279841 Transcripts identified by microarray analysis that were deregulated in E15.5 Pax2-cre/+;Trp63(dN-flox/dN-flox) (ΔNp63-cKO) ureters</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE279841</link>
      <guid isPermaLink="false">GSE279841</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Andreas  Kispert ; Fairouz  Qasrawi&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by array&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Mus musculus&lt;p&gt;Evaluation of the transcriptional changes in E15.5 ureters upon loss of ΔNp63 in the ureteric epithelium.</description>
      <category>Expression profiling by array</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE279840 Transcripts identified by microarray analysis that were deregulated in E18.5 Pax2-cre/+;Trp63(dN-flox/dN-flox) (ΔNp63-cKO) ureters</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE279840</link>
      <guid isPermaLink="false">GSE279840</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Andreas  Kispert ; Fairouz  Qasrawi&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by array&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Mus musculus&lt;p&gt;Evaluation of the transcriptional changes in E18.5 ureters upon loss of ΔNp63 in the ureteric epithelium.</description>
      <category>Expression profiling by array</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE278562 Hypoxic injury triggers maladaptive repair in human kidney organoids</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE278562</link>
      <guid isPermaLink="false">GSE278562</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Ana B.  Nunez-Nescolarde ; M  Piran ; Laura  Perlaza-Jimenez ; David J.  Nikolic-Paterson ; Alexander N.  Combes&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Homo sapiens&lt;p&gt;Acute kidney injury (AKI) is a common clinical disorder linked to high rates of illness and death. Ischemia is a leading cause of AKI, which can result in chronic kidney disease (CKD) through a maladaptive repair process characterised by failed epithelial regeneration, inflammation, and metabolic dysregulation. No targeted therapies exist to prevent AKI from progressing to CKD, and insight into ischemic AKI and maladaptive repair in humans remains limited. In this study, we report that human kidney organoids recapitulate select molecular and metabolic signatures of AKI and maladaptive repair in response to hypoxic injury. Transcriptional, proteomic, and metabolomic profiling revealed signatures of tubular injury, cell death, cell cycle arrest and altered metabolism in kidney organoids cultured in hypoxic conditions. After a recovery period in normoxic conditions, hypoxic injured organoids had increased signatures associated with maladaptive repair like the TNF signalling pathways and S100A8/9. Single cell RNA sequencing localised AKI and maladaptive repair markers such as GDF15, MMP7, ICAM1, TGFB1, SPP1, C3 and CCN1 to injured proximal and distal tubules. Metabolic phenotypes linked to CKD were also evident including dysregulated glycolysis and gluconeogenesis, amino acid, bicarbonate and lipid metabolism, and elevated ceramide levels. In addition, by developing a kidney organoid-macrophage co-culture model, we showed a significant activation of macrophages in response to hypoxia, marked by a shift towards an inflammatory state. In summary, our multi-omic analysis provides compelling evidence for the use of kidney organoids as a model of human ischemic AKI and maladaptive repair, highlighting new and conserved biomarkers and mechanisms, and opportunities for drug screening.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE275308 Single cell RNA sequencing (scRNA-seq) of embryonic zebrafish and human aortic endothelial cells following flow modulation</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE275308</link>
      <guid isPermaLink="false">GSE275308</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Aryan  Kaveh ; Antonio G Salazar-Martin ; Wei  Dai ; Aaron P Kithcart ; Emily  Pan ; Ashmita  KC ; Tyler R Reinoso ; Franki  Vetrano-Olsen ; Kusumika  Saha ; Manu  Beerens ; Peter  Libby ; Elazer R Edelman ; Calum A MacRae&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Danio rerio ; Homo sapiens&lt;p&gt;The earliest vascular manifestations during atherosclerosis development are incompletely understood. We utilize low density lipoprotein receptor knockout (ldlr-/-) zebrafish and human aortic endothelial cells (HAECs) to discern developmental and flow-dependent features underlying atherosclerosis. ScRNA-seq was used to analyze the transcripitional heterogeneity of endothelial cells from embryonic ldlr-/- zebrafish and HAECs following flow modulation.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Danio rerio</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE268881 Evolutionary diversity of cell-type-specific expression and stress response in Brassicaceae roots</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE268881</link>
      <guid isPermaLink="false">GSE268881</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Guanann  Wang ; Kook H Ryu ; Andrea  Dinneny ; Jiyoung  Lee ; Dong-Ha  Oh ; Prashanth  Ramachandran ; Marina  Oliva ; Ryan  Lister ; José R Dinneny ; John  Schiefelbein ; Maheshi  Dassanayake&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Arabidopsis thaliana ; Camelina sativa ; Eutrema salsugineum ; Schrenkiella parvula ; Sisymbrium irio&lt;p&gt;Environmental stresses trigger distinct responses between stress-sensitive and stress-adapted plants. To explore these stress adaptations at the cellular level, we built root single-cell transcriptome atlases for five biodiverse Brassicaceae species, including two stress-sensitive models (Arabidopsis thaliana and Sisymbrium irio), two extremophytes (Eutrema salsugineum and Schrenkiella parvula), and a polyploid oil crop (Camelina sativa), under control, salt, and ABA treatments. Although these species share similar root anatomy, most Arabidopsis cell type markers were not conserved across species. Cortex cell populations with distinct transcriptomes were spatially segregated among species. Lineage-specific gains in stress responses were more common than losses among cell-type responses across species. The homeologs in the allohexaploid C. sativa showed stress response divergence that was often decoupled from the divergence in their coding sequences and control expression levels. Our dataset provides a foundational root atlas across multiple Brassicaceae species enhanced for user accessibility with a cross species searchable browser and provides an analytical framework for comparative single-cell transcriptomics that can be readily transferred to any multi-species system.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Arabidopsis thaliana</category>
      <category>Camelina sativa</category>
      <category>Eutrema salsugineum</category>
      <category>Schrenkiella parvula</category>
      <category>Sisymbrium irio</category>
    </item>
    <item>
      <title>GSE266881 Hypoxia-Induced Neural-BBB Coupling via Extracellular Vesicles Delivering CircOGDH</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE266881</link>
      <guid isPermaLink="false">GSE266881</guid>
      <pubDate>Mon, 20 Apr 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Wei  Chen ; Dan  Lu ; Anding  Xu ; Hongcheng  Mai&lt;br&gt;&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Homo sapiens&lt;p&gt;Many nervous system diseases involve changes in neurovascular coupling, the connection between neurons and the blood-brain barrier(BBB). CircOGDH is a circular RNA linked to hypoxic neurons. In this study, we investigated how neuron-derived CircOGDH affects BBB-associated endothelial cells under hypoxic conditions. We reduced neuronal CircOGDH expression in MCAO/R(middle cerebral artery occlusion/reperfusion) mice using a neuron-specific AAV, which led to compromised BBB structure and maintenance in ischemic stroke mice. We found that giving CircOGDH-rich sEVs(small extracellular vesicles) to brain tumors helped blood vessels stay integrity in a glioblastoma model. In addition, we revealed that hypoxic neurons transfer CircOGDH from sEVs to ECs in vitro co-culture system, leading to increased COL4A4 expression and improved ECs functionality. Additionally, analyzing CircOGDH levels in AIS patients' plasma(with and without hemorrhagic transformation) showed a strong link between CircOGDH expression and BBB damage. These findings indicate that neurons under hypoxic stress release sEVs containing CircOGDH into the microenvironment, which interact with ECs and regulate COL4A4 expression, strengthening vascular integrity.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
  </channel>
</rss>

