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    <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>Sat, 06 Jun 2026 04:47:22 -0400</pubDate>
    <item>
      <title>GSE334050 Effects of an autophagy-related protein degrader on murine 4T1 breast cancer model</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE334050</link>
      <guid isPermaLink="false">GSE334050</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributor&lt;/i&gt; : Cheng  Xu&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;We developed an targeted protein degrader that could degrade VPS34, a key factor for autophagy initiation, to inhibit autophagy pathway in tumor. We did bulk RNA-seq to investigate how such protein degrader modulated the gene expression regarding autophagy pathway and immune response.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE333984 OsELP3/ELP4, rice Elongator factor complex subunits, epigenetically regulates rice blast resistance</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE333984</link>
      <guid isPermaLink="false">GSE333984</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Yanfei  Wu ; Zhenshneg  Qiao ; Yuquan  Fu ; Zixiang  Li ; Zhichao  Wang ; Xuezhu  Du ; Feng  Sheng&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; : Oryza sativa&lt;p&gt;Rice blast, caused by Magnaporthe oryzae (M.oryzae), is one of the three most devastating rice diseases, significantly reducing both yield and grain quality. The Elongator complex, first characterized in Arabidopsis thaliana, regulates growth, development, and innate immunity by tightly associating with hyperphosphorylated RNA polymerase II. However, its immunological role in rice remains unexplored. Here, we demonstrate that Elongator plays an essential role in rice blast resistance. The OsELP3 subunit mutant exhibited susceptibility to M.oryzae, while its overexpression increased resistance. OsELP3 interacts with its homologous subunit OsELP4 in the nucleus, and that OsELP4 also positively regulates rice blast resistance. RNA-seq and histone acetylation analyses demonstrated that OsELP3/ELP4 enhances transcriptional activation of key rice blast resistance genes by modulating histone acetylation levels in both the jasmonic acid (JA) signaling pathway (OsAOS1, OsLOX6, OsPROPEP3) and lignin biosynthesis pathway (OsMYB30, OsMYB55, OsMYB110), thereby strengthening plant defense mechanisms against M. oryzae. These findings reveal that OsELP3/ELP4 regulates histone acetylation-mediated defense responses against M.oryzae, providing both theoretical foundations and genetic resources for developing blast-resistant rice cultivars.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Oryza sativa</category>
    </item>
    <item>
      <title>GSE333980 Knockouts of sulfur metabolism genes induce chronic inflammation and immune dysregulation in Drosophila melanogaster</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE333980</link>
      <guid isPermaLink="false">GSE333980</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : O.G  Zatsepina ; V.A  Shilova ; M.B.  Evgen’ev ; A.P  Rezvykh ; D.G  Garbuz&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 this study, we examined a unique collection of Drosophila melanogaster strains with knockouts of three key genes involved in H₂S synthesis and metabolism, with the aim of elucidating the role of this adaptive system in immunity. Genetic disruptions in sulfur metabolism—specifically, combined deletions of the cbs, cse, and tst1 genes—lead to reduced H₂S levels and hyperhomocysteinemia in flies. These metabolic changes induce oxidative stress and trigger chronic inflammatory responses. Transcriptomic analysis and q-PCR revealed significant activation of major immune pathways, including IMD, Toll, and Jac-Stat. A septic injection of Bacillus subtilis induces increased expression of antimicrobial peptides (AMPs) and pattern recognition receptors in knockout flies. Notably, double- and triple-knockout strains exhibit prolonged immune activation. The triple knockout exhibits the worst survival rate following septic injury induced by Bacillus subtilis. These results highlight the critical role of H₂S in modulating innate immunity and suggest that sulfur metabolism is an important regulator of inflammatory homeostasis in Drosophila.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Drosophila melanogaster</category>
    </item>
    <item>
      <title>GSE333910 Transcriptomic profiling of C2C12 myotubes treated with D-galactose and red ginseng-derived interventions</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE333910</link>
      <guid isPermaLink="false">GSE333910</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Byeong-Don  Min ; Aeyung  Kim ; Seokwon  Kim ; No soo  Kim ; Sang-Min  Park&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;This study investigated transcriptomic alterations in differentiated C2C12 myotubes following treatment with D-galactose and red ginseng-derived interventions. Fully differentiated C2C12 myotubes were treated with Korean Red Ginseng water extract (RGW), saponin fraction (SFr), non-saponin fraction (NSFr), or ginsenoside Rb2 either alone or in combination with D-galactose. Bulk RNA sequencing was performed to characterize the transcriptional effects of each intervention under basal conditions and to evaluate their modulatory effects on D-galactose-induced cellular aging-associated transcriptomic changes.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE333495 SETDB1 regulates gene expression in mouse brown adipose tissue and primary brown adipocytes</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE333495</link>
      <guid isPermaLink="false">GSE333495</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributor&lt;/i&gt; : Qiang  Chen&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;SETDB1 is a histone methyltransferase that catalyzes H3K9me3 and plays critical roles in transcriptional repression. To investigate its function in brown adipose tissue (BAT), we performed RNA-seq across three complementary models: (1) BAT tissue from BAT-specific Setdb1 knockout mice (Setdb1 AKO) vs control mice under thermoneutral conditions; (2) primary brown adipocytes from Setdb1 flox/flox; Rosa26Cre-ERT2 mice treated with 4-hydroxytamoxifen (4-OHT) vs vehicle (ETOH); and (3) primary brown adipocytes transfected with siRNA targeting Setdb1 (siSetdb1) vs non-targeting control siRNA (siNC).</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE326308 Bulk RNA sequencing of murine mesenchymal stromal cells (MSCs) under cardiac stress induced by transverse aortic constriction.</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE326308</link>
      <guid isPermaLink="false">GSE326308</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Manabe  Ichiro ; Nakayama  Yukiteru ; Goto  Kohsaku&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;We performed bulk RNA-seq to investigate how cardiac stress influences the transcriptional profiles of murine MSCs. MSCs were isolated from bone marrow of control (sham-operated) and mice subjected to transverse aortic constriction (TAC) for four weeks. Comparative analysis of transcriptomes was conducted to identify stress-induced alterations in MSC states.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE326121 Single-cell RNA sequencing (scRNA-seq) of murine mesenchymal stromal cells (MSCs) under cardiac stress induced by transverse aortic constriction.</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE326121</link>
      <guid isPermaLink="false">GSE326121</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Manabe  Ichiro ; Nakayama  Yukiteru ; Goto  Kohsaku&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;We performed scRNA-seq using the 10x Genomics platform to investigate how cardiac stress influences the transcriptional profiles of female murine MSCs. MSCs were isolated from bone marrow of control (sham-operated) and mice subjected to transverse aortic constriction (TAC) for four weeks. Comparative analysis of single-cell transcriptomes was conducted to identify stress-induced alterations in MSC states.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE326120 Single-cell RNA sequencing (scRNA-seq) of murine hematopoietic stem and progenitor cells (HSPCs) and mesenchymal stromal cells (MSCs) under cardiac stress induced by transverse aortic constriction.</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE326120</link>
      <guid isPermaLink="false">GSE326120</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Manabe  Ichiro ; Nakayama  Yukiteru ; Goto  Kohsaku&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;We performed scRNA-seq using the 10x Genomics platform to investigate how cardiac stress influences the transcriptional profiles of murine HSPCs and MSCs. HSPCs and MSCs were isolated from bone marrow of control (sham-operated) and mice subjected to transverse aortic constriction (TAC) for four weeks. Comparative analysis of single-cell transcriptomes was conducted to identify stress-induced alterations in hematopoietic differentiation and MSC states. Integrated analysis of HSPCs and MSCs enabled the characterization of cell–cell communication networks and niche remodeling associated with cardiac stress.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE313448 Nynrin Sustains Leukemia Stem Cell Viability via TXNIP Destabilization to Maintain Redox Homeostasis and Confer Venetoclax Resistance [KG-1a RNA-Seq]</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE313448</link>
      <guid isPermaLink="false">GSE313448</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributor&lt;/i&gt; : Jianming  Wang&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 myeloid leukemia (AML) is driven by chemotherapy-resistant leukemia stem cells (LSCs), which rely on precise regulation of reactive oxygen species (ROS) for survival. We identify NYNRIN as a novel post-transcriptional regulator of LSC redox homeostasis. NYNRIN is selectively overexpressed in ROS-low LSCs and correlates with poor clinical outcomes in AML patients. Genetic targeting of Nynrin in murine models impairs LSC self-renewal, reduces leukemic burden, and prolongs survival, while sparing normal hematopoietic stem and progenitor cells. Mechanistically, NYNRIN binds to TXNIP mRNA, promoting its degradation and maintaining redox balance. Loss of NYNRIN leads to TXNIP stabilization, oxidative stress, mitochondrial dysfunction, and LSC apoptosis, which can be rescued by TXNIP knockdown or ROS scavenging. Notably, Nynrin ablation synergizes with venetoclax to overcome resistance, enhancing LSC cytotoxicity in vitro and in vivo. These findings highlight the NYNRIN-TXNIP-ROS axis as crucial for LSC maintenance and suggest NYNRIN inhibition as a potential therapeutic strategy for relapsed AML.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE311388 Nynrin Sustains Leukemia Stem Cell Viability via TXNIP Destabilization to Maintain Redox Homeostasis and Confer Venetoclax Resistance</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE311388</link>
      <guid isPermaLink="false">GSE311388</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributor&lt;/i&gt; : Jianming  Wang&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;Acute myeloid leukemia (AML) is driven by chemotherapy-resistant leukemia stem cells (LSCs), which rely on precise regulation of reactive oxygen species (ROS) for survival. We identify NYNRIN as a novel post-transcriptional regulator of LSC redox homeostasis. NYNRIN is selectively overexpressed in ROS-low LSCs and correlates with poor clinical outcomes in AML patients. Genetic targeting of Nynrin in murine models impairs LSC self-renewal, reduces leukemic burden, and prolongs survival, while sparing normal hematopoietic stem and progenitor cells. Mechanistically, NYNRIN binds to TXNIP mRNA, promoting its degradation and maintaining redox balance. Loss of NYNRIN leads to TXNIP stabilization, oxidative stress, mitochondrial dysfunction, and LSC apoptosis, which can be rescued by TXNIP knockdown or ROS scavenging. Notably, Nynrin ablation synergizes with venetoclax to overcome resistance, enhancing LSC cytotoxicity in vitro and in vivo. These findings highlight the NYNRIN-TXNIP-ROS axis as crucial for LSC maintenance and suggest NYNRIN inhibition as a potential therapeutic strategy for relapsed AML.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE311133 Transcriptome analysis of human coronary artery smooth muscle cells under pro-differentiation and pro-dedifferentiation treatments</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE311133</link>
      <guid isPermaLink="false">GSE311133</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Fengfeng  Li ; Bixuan  Yue ; Luoxing  Xia ; Yunxiang  Long ; Chenjie  Zhao ; Zhi  Zeng&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;This study explores the transcriptomic landscape of human coronary artery smooth muscle cells (HCASMCs) in response to stimuli that promote differentiation (Repsox) or dedifferentiation (PDGF-BB, IL-1b). Our RNA sequencing analysis identifies DNA damage-inducible transcript 4 (DDIT4) as a key regulator of vascular smooth muscle cell (VSMC) phenotypic switching, showing its significant upregulation in synthetic phenotypes and downregulation in contractile phenotypes. This dataset provides a resource for understanding the transcriptional programs governing VSMC plasticity in the context of vascular remodeling and atherosclerotic disease.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE311116 DDIT4 overexpression reshapes the histone modification landscape in human coronary artery smooth muscle cells: an H3K9ac and H3K27ac CUT&amp;Tag study</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE311116</link>
      <guid isPermaLink="false">GSE311116</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Fengfeng  Li ; Bixuan  Yue ; Luoxing  Xia ; Yunxiang  Long ; Chenjie  Zhao ; Miaoyun  Qiu ; Zhi  Zeng&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;This study investigates the epigenetic mechanisms by which DDIT4 promotes vascular smooth muscle cell (VSMC) dedifferentiation. We performed CUT&amp;Tag sequencing for the active histone marks H3K9ac and H3K27ac in HCASMCs following DDIT4 overexpression. Our findings reveal that DDIT4, by inhibiting the pyruvate dehydrogenase complex, reduces acetyl-CoA levels and globally decreases histone acetylation. Specifically, we observe loss of H3K9ac and H3K27ac at the promoters of key contractile genes, providing an epigenetic explanation for the DDIT4-mediated suppression of the contractile phenotype and acceleration of atherosclerosis.</description>
      <category>Genome binding/occupancy profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE310361 Gain- and loss-of-function RNA-seq analysis reveals DDIT4-driven transcriptional programs in human coronary artery smooth muscle cells</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE310361</link>
      <guid isPermaLink="false">GSE310361</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Fengfeng  Li ; Bixuan  Yue ; Luoxing  Xia ; Yunxiang  Long ; Chenjie  Zhao ; Zhi  Zeng&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;This dataset profiles the transcriptomic changes resulting from DDIT4 manipulation in human coronary artery smooth muscle cells (HCASMCs). We performed RNA sequencing on HCASMCs following adenovirus-mediated DDIT4 overexpression or shRNA-mediated DDIT4 knockdown. Our analysis reveals that DDIT4 is both necessary and sufficient to drive a transcriptional program characteristic of VSMC dedifferentiation, establishing its critical role in phenotypic switching. These findings provide mechanistic insight into how this stress-responsive gene promotes proliferative arterial disease.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE306644 In vivo safety assessment of METTL3 inhibitors STM2457 in neuroblastoma therapy</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE306644</link>
      <guid isPermaLink="false">GSE306644</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Tian  Lin ; Xinghe  Chen ; He  Huang ; Jianxing  Zhang ; Yali  Xu ; Junshan  Lin&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;Neuroblastoma (NB) is one of the most common malignant tumors in children, characterized by high heterogeneity and poor prognosis, posing notable therapeutic challenges. The present study investigated the therapeutic potential and safety profile of two N6-adenosine-methyltransferase 70 kDa subunit (METTL3) inhibitors, UZH1a and STM2457, in NB. A toxicity test of zebrafish showed that the maximum tolerated concentration of UZH1a and STM2457 was 20 μg/ml, and there were some toxic reactions including delayed yolk sac absorption but without notable mortality. Furthermore, through a series of in vitro and in vivo experiments, both UZH1a and STM2457 markedly inhibited SK-N-SH cells viability, migration and invasion, while potently promoting apoptosis, and effectively inhibiting the growth and migration of zebrafish xenograft tumors. Mechanistically, molecular analysis revealed that UZH1a and STM2457 downregulated the gene expression levels of pro-tumorigenic factors (basic helix-loop-helix family member e41, SREBF chaperone, IL-6, and IL-1β) and upregulated the expression of antitumor cytokine (TNF-α). Transcriptomic sequencing results further indicated that the neuroactive ligand-receptor interaction is a key pathway through which STM2457 affected NB development. In conclusion, UZH1a and STM2457 exhibited potent anti-NB activity both in vitro and in vivo by inhibiting viability, migration, invasion, and promoting apoptosis. These findings provide a notable theoretical basis for potential use of METTL3 inhibitors as therapeutic agents against NB.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE302415 Adaptive downregulated liver Recucalcin enhances tolerance defense to intestinal infection by mediating interorgan immunometabolic communication</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE302415</link>
      <guid isPermaLink="false">GSE302415</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Kaiyan  Yang ; Yi  Yang ; Lei  Pan&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;The gut-liver communication is vital for coordinating a systemic response to intestinal infection, as the liver plays a crucial role in regulating immune tolerance through metabolic reprogramming. However, the mechanisms underlying gut-liver communication during intestinal infection, and the key factors linking these processes, remain poorly investigated. In this study, we identified that Regucalcin expression in the remote liver/fat body (Drosophila analogous) is downregulated in response to intestinal infection. And this adaptive downregulated liver Recucalcin could enhance tolerance defense by limiting intestinal infection-induced lipid wasting. Mechanistically, we uncovered that the loss of Regucalcin facilitated calcium-dependent Dilp6 secretion and suppressed excessive lipid catabolism through the insulin-PI3K-Akt signaling pathway during intestinal infection. Therefore, our work reveals Regucalcin as a novel mediator that orchestrates the cross-talk between the intestine and the liver/fatbody, thereby modulating metabolic tolerance to intestinal infection.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Drosophila melanogaster</category>
    </item>
    <item>
      <title>GSE300539 Generation of Tetraploid Organs in Mice [heart scRNA-seq]</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE300539</link>
      <guid isPermaLink="false">GSE300539</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Shu  Wei ; Guowei  Zou ; Yanyan  Zhang ; Shuaipeng  Li ; Mei  Hu ; Juan  Du ; Jiawen  Liu ; Lin  Ran ; Chikai  Zhou ; Jiangwei  Lin&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;Tetraploidy is rare in mammals but common in plants and fish, a phenomenon that offers evolutionary benefits. In mammals, tetraploid cells naturally occur in the liver, heart, and pancreas. Although previous studies have shown that tetraploid embryonic stem cells (4N-ESCs) can contribute to the liver and heart, the extent of their potential for regenerating entire organs remains underexplored. Here, we injected 4N-ESCs into blastocysts which lacked specific organs due to Hhex, Nkx2.5, and Pdx1 deficiencies, successfully generating functional tetraploid livers, hearts, and pancreata, which are smaller than their diploid counterparts. FACS analyses showed significant contributions of 4N-ESCs, with up to 84.3% of liver cells, 79.5% of heart cells, and 43.6%of pancreatic cells being tdTomato-positive. Our results indicate that 4N-ESCs preferentially contribute to the formation of tetraploid livers and hearts, and contribute to the pancreata. These findings highlight the potential of 4N-ESCs for human organ regeneration and suggest a new strategy for addressing organ shortages in clinical settings.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE300538 Generation of Tetraploid Organs in Mice [liver scRNA-seq]</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE300538</link>
      <guid isPermaLink="false">GSE300538</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Shu  Wei ; Guowei  Zou ; Yanyan  Zhang ; Shuaipeng  Li ; Mei  Hu ; Juan  Du ; Jiawen  Liu ; Lin  Ran ; Chikai  Zhou ; Jiangwei  Lin&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;Tetraploidy is rare in mammals but common in plants and fish, a phenomenon that offers evolutionary benefits. In mammals, tetraploid cells naturally occur in the liver, heart, and pancreas. Although previous studies have shown that tetraploid embryonic stem cells (4N-ESCs) can contribute to the liver and heart, the extent of their potential for regenerating entire organs remains underexplored. Here, we injected 4N-ESCs into blastocysts which lacked specific organs due to Hhex, Nkx2.5, and Pdx1 deficiencies, successfully generating functional tetraploid livers, hearts, and pancreata, which are smaller than their diploid counterparts. FACS analyses showed significant contributions of 4N-ESCs, with up to 84.3% of liver cells, 79.5% of heart cells, and 43.6%of pancreatic cells being tdTomato-positive. Our results indicate that 4N-ESCs preferentially contribute to the formation of tetraploid livers and hearts, and contribute to the pancreata. These findings highlight the potential of 4N-ESCs for human organ regeneration and suggest a new strategy for addressing organ shortages in clinical settings.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE300535 Generation of Tetraploid Organs in Mice [E18.5]</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE300535</link>
      <guid isPermaLink="false">GSE300535</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Shu  Wei ; Guowei  Zou ; Yanyan  Zhang ; Shuaipeng  Li ; Mei  Hu ; Juan  Du ; Jiawen  Liu ; Lin  Ran ; Chikai  Zhou ; Jiangwei  Lin&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;Tetraploidy is rare in mammals but common in plants and fish, a phenomenon that offers evolutionary benefits. In mammals, tetraploid cells naturally occur in the liver, heart, and pancreas. Although previous studies have shown that tetraploid embryonic stem cells (4N-ESCs) can contribute to the liver and heart, the extent of their potential for regenerating entire organs remains underexplored. Here, we injected 4N-ESCs into blastocysts which lacked specific organs due to Hhex, Nkx2.5, and Pdx1 deficiencies, successfully generating functional tetraploid livers, hearts, and pancreata, which are smaller than their diploid counterparts. FACS analyses showed significant contributions of 4N-ESCs, with up to 84.3% of liver cells, 79.5% of heart cells, and 43.6%of pancreatic cells being tdTomato-positive. Our results indicate that 4N-ESCs preferentially contribute to the formation of tetraploid livers and hearts, and contribute to the pancreata. These findings highlight the potential of 4N-ESCs for human organ regeneration and suggest a new strategy for addressing organ shortages in clinical settings.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE299451 Cardiomyocyte-Specific Smad7 protects the pressure-overloaded heart, inhibiting the TbR1/Smad2/3 cascade [Smad7 knockout]</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE299451</link>
      <guid isPermaLink="false">GSE299451</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Claudio  Humeres ; Izabela  Tuleta ; Arti V Shinde ; Anis  Hanna ; Aadya  Deepak ; Nikolaos G Frangogiannis&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;Cardiomyocytes are the major effectors of cardiac remodeling under pressure overload, undergoing hypertrophy and contractile dysfunction in response to sustained mechanical stress. These maladaptive changes are orchestrated by transforming growth factor beta (TGF-β), a key mediator of hypertrophic and profibrotic signaling. Smad7, an inhibitory Smad, negatively regulates TGF-β signaling, but its cardiomyocyte-specific role in pathological remodeling is unclear. We hypothesized that Smad7 acts as an endogenous inhibitor of cardiomyocyte dysfunction during pressure overload. To investigate this, we generated cardiomyocyte-specific Smad7 knockout (CMS7KO) mice and subjected them to transverse aortic constriction (TAC). Echocardiography, RNA-sequencing, histological, and molecular analyses were performed. Smad7 expression was upregulated in cardiomyocytes of TAC mouse hearts and in patients with non-ischemic cardiomyopathy. While baseline cardiac function was preserved in CMS7KO mice, TAC induced an increase in systolic and diastolic dysfunction, ventricular dilation, and hypertrophy compared to controls. Histological analysis revealed increased cardiomyocyte size and macrophage infiltration, without significant fibrosis. Transcriptomic profiling showed downregulation of contractile and sarcomeric genes. Cardiomyocyte-specific Smad7 loss enhanced TGF-β/Smad3 and ERBB2 signaling in vivo. In H9c2 cardiomyocyte-like cells, Smad7 knockdown increased TbR1 and Smad3 phosphorylation, confirming a direct inhibitory effect. These findings identify cardiomyocyte Smad7 as a critical regulator of pathological remodeling and a potential therapeutic target in heart failure.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE299359 Cardiomyocyte-Specific Smad7 protects the pressure-overloaded heart, inhibiting the TbR1/Smad2/3 cascade</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE299359</link>
      <guid isPermaLink="false">GSE299359</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Claudio  Humeres ; Izabela  Tuleta ; Arti V Shinde ; Anis  Hanna ; Aadya  Deepak ; Nikolaos G Frangogiannis&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;Cardiomyocytes are the major effectors of cardiac remodeling under pressure overload, undergoing hypertrophy and contractile dysfunction in response to sustained mechanical stress. These maladaptive changes are orchestrated by transforming growth factor beta (TGF-β), a key mediator of hypertrophic and profibrotic signaling. Smad7, an inhibitory Smad, negatively regulates TGF-β signaling, but its cardiomyocyte-specific role in pathological remodeling is unclear. We hypothesized that Smad7 acts as an endogenous inhibitor of cardiomyocyte dysfunction during pressure overload. To investigate this, we generated cardiomyocyte-specific Smad7 knockout (CMS7KO) mice and subjected them to transverse aortic constriction (TAC). Echocardiography, RNA-sequencing, histological, and molecular analyses were performed. Smad7 expression was upregulated in cardiomyocytes of TAC mouse hearts and in patients with non-ischemic cardiomyopathy. While baseline cardiac function was preserved in CMS7KO mice, TAC induced an increase in systolic and diastolic dysfunction, ventricular dilation, and hypertrophy compared to controls. Histological analysis revealed increased cardiomyocyte size and macrophage infiltration, without significant fibrosis. Transcriptomic profiling showed downregulation of contractile and sarcomeric genes. Cardiomyocyte-specific Smad7 loss enhanced TGF-β/Smad3 and ERBB2 signaling in vivo. In H9c2 cardiomyocyte-like cells, Smad7 knockdown increased TbR1 and Smad3 phosphorylation, confirming a direct inhibitory effect. These findings identify cardiomyocyte Smad7 as a critical regulator of pathological remodeling and a potential therapeutic target in heart failure.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE299267 Single cell gene expression profiling of triple negative breast cancer organoids</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE299267</link>
      <guid isPermaLink="false">GSE299267</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Michael P East ; Jose F Olivares-Quintero ; Gary L Johnson&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;Triple negative breast cancer (TNBC) is a heterogenous disease driven by aberrant activation of receptor tyrosine kinases and the proliferative MEK-ERK signaling pathway. Heterogeneity in kinase expression levels across two TNBC organoid lines was used in combination with the Atlas of substrate specificities for the human Ser/Thr kinome to predict phenotypic differences between the two organoid lines. Single nucleus RNAseq validated these predictions showing high enrichment of immune and inflammatory signatures within a subpopulation of tumor cells.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE299240 Ectothermic vertebrates evolved gut-associated germinal center-like structures</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE299240</link>
      <guid isPermaLink="false">GSE299240</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Weiguang  Kong ; Peng  Yang&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; : Cyprinus carpio&lt;p&gt;Germinal centers (GCs), specialized microanatomical structures that emerged in endothermic vertebrates, serve as critical hubs for immune surveillance and lymphocyte activation. The constant exposure to foodborne pathogens drives the evolutionary selection for potent gut mucosal immune defenses in vertebrate species. Despite retaining ancestral ectothermic traits including underdeveloped lymph nodes, teleost fish have evolved specialized gut-associated lymphoid tissue capable of generating robust antigen-specific immune responses. How and where ectothermic vertebrates initiate adaptive immunity in the gut remains enigmatic. Through single-cell RNA sequencing (scRNA-seq), we comprehensively mapped the dynamic immune landscape of common carp (Cyprinus carpio) in the gut and head kidney (HK) following Spring Viremia of Carp Virus (SVCV) challenge. Strikingly, lymphocytes within gut exhibited pronounced upregulation of memory-related genes upon secondary viral exposure, oncomitant with robust expression of canonical GC markers in B cells. Furthermore, using FISH, we observed SVCV co-localization with CXCR5⁺ B cells within the lamina propria basement of the gut and perivascular niches of the HK, encircled by a peripheral ring of AICDA⁺/MKI67⁺/CXCR4⁺ B cells. Notably, within these same microanatomical niches, we detected distinct aggregates composed of highly proliferative IgM⁺ B cells undergoing significant apoptosis and antigen (Ag)-specific B cells. Collectively, our findings reveal that teleosts have evolved GC-like structures in the gut, offering novel insights into the evolutionary origins of GCs.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Cyprinus carpio</category>
    </item>
    <item>
      <title>GSE299019 Innate immunocompetent iNSpheroids: A hiPSC-derived 3D model to study the central nervous system captures an early CNS response to rAAV</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE299019</link>
      <guid isPermaLink="false">GSE299019</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Catarina M Gomes ; Gabriela  Silva ; Mafalda  Aleixo ; Daniel  Simão ; Stephan  Holtkamp ; Diana D Lobo ; Pradeep  Harish ; Lekh  Dahal ; Rui J Nobre ; Luís P Almeida ; Mark  Trautwein ; Paula M Alves ; Catarina  Brito&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;Gene therapies using adeno-associated viruses (AAVs) for central nervous system (CNS) disorders face challenges due to host immune responses not represented in classical preclinical models. Here, we present a human-induced pluripotent stem cell (hiPSC)-derived innate immunocompetent 3D CNS model that recapitulates neuroinflammatory hallmarks, serving as a platform for preclinical gene therapy development. Utilizing various scales of stirred-tank bioreactor systems, we produced iNSpheroids composed of neurons, astrocytes, and oligodendrocytes, alongside microglial cells (iMGL) to mimic the neuro-immune axis. These systems enabled large-scale production of iNSpheroids and subsequent miniaturization for co-culture experiments and screening of inflammatory stimuli, while maintaining a highly controlled environment. The iMGL-iNSpheroids demonstrated active neuron-microglia crosstalk and exhibited distinct inflammatory responses to a series of neuroinflammatory factors. iMGL-iNSpheroids mounted a mild and transient response to rAAV9, mediated by the activation of inflammatory pathways (e.g., TNF-via NF-κB activation) in glial cell populations.. This model offers a valuable tool to dissect neuroinflammatory mechanisms, accelerating gene therapy development.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Homo sapiens</category>
    </item>
    <item>
      <title>GSE285325 Single-cell RNA-seq analysis identifies the atlas of lymph fluid and reveal a sepsis-related T cell subset</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE285325</link>
      <guid isPermaLink="false">GSE285325</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Hui  Wang ; Jianguang  Wang&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; : Rattus norvegicus&lt;p&gt;The lymphoid cycle as the sentinel of immune response, its cell subtypes and immune properties and functions during sepsis are still unclear. This study described a comprehensive picture of immune cells in rat lymph fluid by single-cell RNA sequencing and identified a unique subset of CD4+ T cells (CD4_Icos) in the early state of sepsis, confirming its crucial role in Treg cell production. Transferring with CD4+Icos+ T cells significantly alleviated CLP-induced organ injury, while Icosfl/flCd4-CreERT2 mice showed reduced number of Treg and increased inflammation and mortality risk. Further screening and validation experiments identified Npas2 as an Icos-specific transcription factor that regulates Icos expression and promotes the differentiation of CD4+Icos+ T cells. Clinical results disclosed the negative correlation between the expression of ICOS in CD4+ T cells and SOFA score in septic patients, which affected the prognosis of septic patients. These findings indicated the protective role of CD4+ T cells in sepsis.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Rattus norvegicus</category>
    </item>
    <item>
      <title>GSE272962 Co-transcriptional RNA processing boosts zygotic genes and restrains noncoding transcription</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE272962</link>
      <guid isPermaLink="false">GSE272962</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Jingzhao  Xu ; Xiaohua  Shen&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;Transcription decodes protein-coding genes and interprets regulatory information embedded in the genome by generating RNA. In eukaryotes, gene transcription is coupled with RNA processing via the carboxyl terminal domain (CTD) of RNA polymerase (Pol) II to enhance mRNA production. Here we propose that co-transcriptional RNA processing is essential for zygotic gene activation (ZGA), which shifts from noncoding to protein-centered gene expression post-fertilization. Truncating the Pol II CTD in mouse embryonic stem cells disrupts this coupling, halting global mRNA synthesis and causing widespread intergenic transcription. This triggers transcriptional and epigenetic reprogramming and nuclear reorganization towards totipotency, resembling early two-cell embryos before ZGA. Mechanistically, the CTD suppresses noncoding transcription by restraining polymerase activity on chromatin, but facilitates promoter-proximal pausing, transcription directionality, velocity, and elongation efficacy at genes through coupled RNA processing. The evolution of longer CTD lengths enhances gene activity, likely accommodating the increasingly abundant noncoding genome sequences in mammals.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE269503 Application of Transcriptomics Dose-Response Modeling to Risk-Based Prioritization of Contaminants Detected in Tributaries of the North American Great Lakes [P. promelas]</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE269503</link>
      <guid isPermaLink="false">GSE269503</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Jenna E Cavallin ; Kendra  Bush ; Steven R Corsi ; Laura A De Cicco ; Kevin  Flynn ; Monique  Hazemi ; Erin E Maloney ; Peter G Schumann ; Alex  Kasparek ; Daniel L Villeneuve&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; : Pimephales promelas&lt;p&gt;As part of the Great Lakes Restoration Initiative, a series of chemical monitoring and surveillance efforts have detected approximately 550 chemicals in Great Lakes tributaries. Among these, there were 140 chemicals for which no empirical toxicity data were available to support prioritization. The aim of the present study was to generate transcriptomic points of departure (tPODs) for 10 of these compounds and demonstrate how they could be applied in a screening-level prioritization. Organisms representing three different trophic levels of the aquatic food-web (Pimephales promelas – secondary consumer, Daphnia magna-primary consumer, and R. subcapitata-primary producer). were exposed for 24 h to a ½-log dilution series of nominal exposure concentrations typically ranging from 66.7 to 0.021 µM of each chemical. In addition to observations of apical effects such as survival and morphology, whole body transcriptomic responses to each chemical were evaluated with targeted analysis using TempO-seq for P. promelas and D. magna and non-targeted full RNA-seq for R. subcapitata. Benchmark concentrations (BMCs) were calculated for each gene showing a concentration-dependent expression pattern. The tPOD for each chemical-species combination was defined as the 10th percentile of the BMCs. The tPODs ranged from 0.18 to 10.8 µM for P. promelas and 0.32 to 29 µM for D. magna, with the most potent of the chemicals tested being fipronil carboxamide. For R. subcapitata, the tPODs ranged from 0.04 to 1.77 µM, with gabapentin as the most potent chemical tested. Empirically derived tPODs from these data poor chemicals, as well as tPODs from previously tested data rich chemicals, were compared with concentrations detected in the Great Lakes basin. This work demonstrates the potential utility of emerging ecological high-throughput transcriptomics assays to support timely screening and prioritization of data poor environmental contaminants.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Pimephales promelas</category>
    </item>
    <item>
      <title>GSE269233 The roles of Nudt15 in leukemic and hematopoietic stem cells</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE269233</link>
      <guid isPermaLink="false">GSE269233</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributor&lt;/i&gt; : Zhonghui  Zhang&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;NUDT15 encodes nucleotide triphosphate diphosphatase that is responsible for metabolizing purine analog drugs, and its genetic mutation results in severe side effects from thiopurine therapy. However, the functions of Nudt15 in leukemic stem cells (LSCs) and hematopoietic stem cells (HSCs) remain unknown. Here we reveal the Nudt15-regulating self-renewal of both mouse LSCs and HSCs. Our data show that Nudt15 negatively regulates murine leukemogenesis and its deficiency prolongs the survival of murine AML recipients by impairing LSC self-renewal, while Nudt15 ablation markedly enhances mouse HSC regenerative potential and self-renewal. Mechanistically, Nudt15 modulates inflammatory signaling in mouse LSCs and HSCs, leading to divergent self-renewal outcomes. Nudt15 depletion inhibits mouse LSC self-renewal by downregulating Ifi30, resulting in elevating intracellular ROS levels. Gata2, a key regulator, is required for Nudt15-mediating inflammatory signaling in mouse HSCs. Collectively, our results present new crucial roles of Nudt15 in maintaining the functions of mouse LSC and HSC through inflammatory signaling and have a new insight into clinical implications.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE236613 Anti-osteoporosis mechanism of resistance exercise in ovariectomized rats based on transcriptome analysis: a pilot study</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE236613</link>
      <guid isPermaLink="false">GSE236613</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Series Type&lt;/i&gt; : Expression profiling by high throughput sequencing&lt;br&gt;&lt;i&gt;Organism&lt;/i&gt; : Rattus norvegicus&lt;p&gt;Postmenopausal osteoporosis is the main cause of fractures in women. Resistance exercise has a positive effect on bone mineral density in postmenopausal osteoporosis patients, but its mechanism is unclear. The purpose of this study was to explore the mechanism of resistance exercise in improving ovariectomized osteoporotic rats based on the transcriptome sequencing technique. Eighteen female Sprague-Dawley rats were randomly divided into the sham-operated group, the non-exercise group, and the resistance exercise group. The rat model of postmenopausal osteoporosis was established by bilateral ovariectomy. Ten weeks after the operation, the resistance exercise group received 2 weeks of adaptive training, and 12 weeks of resistance exercise began in the 13th week. The rats were trained 5 days per week, in 4 sets of 3 repetitions per day. After the intervention, all rats were sacrificed, and the body weight, bone mineral density, trabecular bone microarchitecture, and bone biomechanics were examined. At the same time, RNA-seq and enrichment analysis of gene ontology and Kyoto Encyclopedia of Genes and Genomes were performed on the left tibias, followed by Elisa and RT-qPCR verification. It had been found that resistance exercise can effectively counteract the weight gain of ovariectomized osteoporotic rats, and has a good effect on bone mineral density and trabecular bone microarchitecture. Enrichment analysis showed that regulation of gene expression and osteoclast differentiation is the most closely related biological process and signaling pathway shared by RE/Ovx and NE/Ovx groups. Our results revealed that resistance exercise can play a role in inhibiting osteoclast activation and preventing the enhancement of osteoclast bone resorption function in ovariectomized osteoporotic rats by inhibiting Fos/Fosb-regulated TRAP activation and relieving Calcr inhibition, which has important application value in preventing bone loss caused by estrogen deficiency.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Rattus norvegicus</category>
    </item>
    <item>
      <title>GSE235016 RNA-seq revealed the anti-pyroptotic effect of suramin by suppressing NLRP3/caspase-1/GSDMD pathway in LPS-induced MH-S alveolar macrophages</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE235016</link>
      <guid isPermaLink="false">GSE235016</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Yuhui  Zhu ; Haidong  Zhou&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;Background:&lt;br&gt;Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), acting as one common sepsis-associated organ injury, induces uncontrolled and self-amplifies pulmonary inflammation. Given the lack of clinically effective approaches, the mortality rate of it still remains high. Suramin(SUR) was found to ameliorate sepsis associated ALI in our previous work. However, the underlying mechanism of its protective effects has not been clarified. Pyroptosis, categorized as an inflammatory form of programmed cell death, could aggravate lung inflammatory responses via inducing alveolar macrophages (AM) pyroptosis.&lt;br&gt;Methods:&lt;br&gt;MH-S AM cell line was stimulated with or without lipopolysaccharide (LPS) or suramin, and the differential expression genes (DEGs) were excavated using RNA sequencing (RNA-Seq). To identify the regulatory roles of these genes, pyroptosis-related genes (PRGs), GO/KEGG and GSEA analysis were conducted. We also performed WB, qRT-PCR and ELISA to validate the RNA-seq results and further expound the protective effect of suramin.&lt;br&gt;Results:&lt;br&gt;624 DEGs were identified between CON and lipopolysaccharide (LPS) groups, and enrichment analysis of these genes revealed significantly enriched pathways that related to immune system and signal transduction. Meanwhile, 500 DEGs were identified in LPS/SUR+LPS group. In addition to the pathways mentioned above, IL-17 pathway and C-type lectin receptor signaling pathway were also enriched. All 6 pathways were connected with pyroptosis. Concurrently, the “DESeq2” R package was used to identify differentially expressed PRGs. Nod1, Nod2, interleukin (IL)-1, IL-6, tumor necrosis factor (TNF), NLRP3 were upregulated under LPS stimulation. Then, in SUR+LPS group, Nod2, IL-6, IL-1, NLRP3 were downregulated. The validation results of WB, qRT-PCR, and ELISA showed: the protein and mRNA expression levels of NLRP3, caspase-1, GSDMD and the concentrations of IL-1, IL-18 were decreased when treated with suramin and LPS.&lt;br&gt;Conclusion:&lt;br&gt;Suramin could inhibit NLRP3/caspase-1/GSDMD canonical pyroptosis pathway in LPS-induced MH-S alveolar macrophages.</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
    <item>
      <title>GSE234458 Smart-seq2 analyses of ESCs-derived CD144 population transplanting-derived Lin-Sca-1+c-Kit- cells</title>
      <link>http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE234458</link>
      <guid isPermaLink="false">GSE234458</guid>
      <pubDate>Sat, 06 Jun 2026 00:00:00 -0400</pubDate>
      <description>&lt;i&gt;Contributors&lt;/i&gt; : Wei  Shan ; Pengxu  Qian ; Xiangjun  Zeng&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;Smart-seq2 was further performed to investigate transcriptome characteristics of the in vivo Lin-Sca-1+c-Kit- lymphoid progenitors (ESC-derived Lin-Sca-1+c-Kit-) obtained from the primary recipients and wild-type LSK HSPCs from the bone marrow of C57BL/6 mice (wt-LSK).</description>
      <category>Expression profiling by high throughput sequencing</category>
      <category>Mus musculus</category>
    </item>
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