GEO 数据集

主题由标题与摘要自动归类；样本量为数据集标注之和，SuperSeries 可能与其 SubSeries 重复计算。

• MORC2A is required for DNA methylation and H3K9me3 at retrotransposons in the male germline [smallRNA-seq]
  GSE335167Mus musculus6 个样本2026-10-31

  Transposable elements pose a particular threat to the germline, where their activation can compromise fertility and generate heritable mutations. In male germ cells, transposon silencing depends on repressive epigenetic states, including CpG methylation and H3K9me3. Here, we identify MORC2A as an essential regulator of transposon repression in the mouse male germline. Conditional deletion of Morc2a in primordial germ cells caused complete male infertility, testicular atrophy, germ cell loss and meiotic arrest. MORC2A-deficient testes displayed derepression of evolutionarily young retrotransposons, accompanied by DNA damage and apoptosis. Genome-wide profiling revealed loss of CpG methylation and H3K9me3 at these elements. Small RNA sequencing showed that piRNA biogenesis and ping-pong amplification remain largely intact. Together, these datasets identify MORC2A as a male germline chromatin regulator required for epigenetic silencing of young transposable elements.
• MORC2A is required for DNA methylation and H3K9me3 at retrotransposons in the male germline [RNA-seq]
  GSE335166Mus musculus10 个样本2026-10-31

  Transposable elements pose a particular threat to the germline, where their activation can compromise fertility and generate heritable mutations. In male germ cells, transposon silencing depends on repressive epigenetic states, including CpG methylation and H3K9me3. Here, we identify MORC2A as an essential regulator of transposon repression in the mouse male germline. Conditional deletion of Morc2a in primordial germ cells caused complete male infertility, testicular atrophy, germ cell loss and meiotic arrest. MORC2A-deficient testes displayed derepression of evolutionarily young retrotransposons, accompanied by DNA damage and apoptosis. Genome-wide profiling revealed loss of CpG methylation and H3K9me3 at these elements. Small RNA sequencing showed that piRNA biogenesis and ping-pong amplification remain largely intact. Together, these datasets identify MORC2A as a male germline chromatin regulator required for epigenetic silencing of young transposable elements.
• MORC2A is required for DNA methylation and H3K9me3 at retrotransposons in the male germline [EM-seq]
  GSE335165Mus musculus6 个样本2026-10-31

  Transposable elements pose a particular threat to the germline, where their activation can compromise fertility and generate heritable mutations. In male germ cells, transposon silencing depends on repressive epigenetic states, including CpG methylation and H3K9me3. Here, we identify MORC2A as an essential regulator of transposon repression in the mouse male germline. Conditional deletion of Morc2a in primordial germ cells caused complete male infertility, testicular atrophy, germ cell loss and meiotic arrest. MORC2A-deficient testes displayed derepression of evolutionarily young retrotransposons, accompanied by DNA damage and apoptosis. Genome-wide profiling revealed loss of CpG methylation and H3K9me3 at these elements. Small RNA sequencing showed that piRNA biogenesis and ping-pong amplification remain largely intact. Together, these datasets identify MORC2A as a male germline chromatin regulator required for epigenetic silencing of young transposable elements.
• MORC2A is required for DNA methylation and H3K9me3 at retrotransposons in the male germline [CUT&RUN]
  GSE335164Mus musculus7 个样本2026-10-31

  Transposable elements pose a particular threat to the germline, where their activation can compromise fertility and generate heritable mutations. In male germ cells, transposon silencing depends on repressive epigenetic states, including CpG methylation and H3K9me3. Here, we identify MORC2A as an essential regulator of transposon repression in the mouse male germline. Conditional deletion of Morc2a in primordial germ cells caused complete male infertility, testicular atrophy, germ cell loss and meiotic arrest. MORC2A-deficient testes displayed derepression of evolutionarily young retrotransposons, accompanied by DNA damage and apoptosis. Genome-wide profiling revealed loss of CpG methylation and H3K9me3 at these elements. Small RNA sequencing showed that piRNA biogenesis and ping-pong amplification remain largely intact. Together, these datasets identify MORC2A as a male germline chromatin regulator required for epigenetic silencing of young transposable elements.
• TREX1 limits anti-tumor immunity by degrading short cytosolic DNA molecules
  GSE334899Mus musculus4 个样本2026-10-31

  TREX1 has recently emerged as a promising therapeutic target in cancer owing to its role in degrading cytosolic DNA and suppressing type I interferon signaling. However, the nature of the immunostimulatory DNA species degraded by TREX1 remains elusive. Here, we show that TREX1 deficiency in murine lung and melanoma tumor cells leads to a substantial, MRE11-dependent increase in short cytosolic DNA fragments that originate preferentially from transcriptionally active regions of the genome, without a corresponding increase in micronuclei. These fragments robustly activate interferon-stimulated genes and drive differentiation of pro-inflammatory macrophages. In syngeneic mice, tumors derived from Trex1-knockout cells exhibit delayed growth, increased sensitivity to anti-PD-1 immune checkpoint blockade, and extended survival. These effects depend on an intact immune system and foster durable anti-tumor memory. Together, our results reveal that short, transcription-derived cytosolic DNA fragments are key TREX1 substrates mediating immune activation in cancer, establishing TREX1 inhibition as a compelling strategy to enhance tumor immunogenicity.
• Transcriptomic characterization of macrophage subtype and behavior in early stage myocardial infarction
  GSE333790Mus musculus9 个样本2026-10-31

  Elucidate the spatiotemporal behavior of specific macrophage subtypes during AMI and identify novel genes with prospective therapeutic potential.
• EZH2 inactivation drives MAPK-dependent vulnerability to MEK inhibition in RAS-mutant CMML
  GSE333450Mus musculus7 个样本2026-10-31

  Chronic myelomonocytic leukemia (CMML) is a heterogeneous hematologic malignancy with limited therapeutic options. Although RAS and RAS-modifying mutations (RASmut) are common and associated with poor prognosis, targeting RAS signaling has shown limited clinical success. Here, we define co-occurrence of RASmut and EZH2 inactivation (EZH2inact) as a distinct molecular subgroup of CMML characterized by aggressive disease biology. Mechanistically, RASmutEZH2inact drives selective MAPK/ERK hyperactivation in mature myeloid cells and hematopoietic stem and progenitor compartments. Transcriptomic analysis of a large independent myeloid neoplasm cohort (Beat-AML) further supports this finding, demonstrating selective activation of gene signatures of MAPK/ERK activation in RASmutEZH2inact cases. Functionally, this signaling activation promotes proliferation and myelomonocytic differentiation in human and murine models. Therapeutically, this MAPK/ERK upregulation confers increased sensitivity to MEK inhibition (MEKi). In a murine RasmutEzh2inact-driven CMML model, MEKi suppresses MAPK/ERK activity and reduces leukemic burden by impairing proliferation and myelomonocytic differentiation without inducing cell death. In primary human CMML samples ex vivo, MEKi shows stronger anti-proliferative effects in RASmutEZH2inact specimens compared with RASmut samples. Drug-sensitivity data from the Beat-AML cohort further supported this. Ultimately, these findings were confirmed in a patient-derived xenograft model, where MEKi reduced the leukemic burden by selectively inhibiting the proliferation of transplanted human RASmutEZH2inact leukemic cells. In summary, our data define RASmutEZH2inact CMML as a clinically relevant subgroup with selective MAPK/ERK hyperactivation and increased sensitivity to MEKi. They provide a mechanistic explanation for the limited efficacy of MEK inhibitors in unselected CMML and support molecularly guided use of MEK-targeted therapy in this patient population.
• Sarm1 Gates the Transition from Protective to Repair Schwann Cell States Following Nerve Injury [snRNA-Seq]
  GSE332913Mus musculus11 个样本2026-10-31

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

  单细胞
• Sarm1 Gates the Transition from Protective to Repair Schwann Cell States Following Nerve Injury [RNA-seq]
  GSE332854Mus musculus12 个样本2026-10-31

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

  单细胞
• Single cell transcriptomic sequencing in common mouse models of atherosclerosis
  GSE332811Mus musculus8 个样本2026-10-31

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

  单细胞
• Stereo-seq of aortic atherosclerotic lesions in common mouse models
  GSE331239Mus musculus3 个样本2026-10-31

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

  空间转录组
• Microglia modulate concussion biomarkers and recovery in male mice
  GSE330926Mus musculus55 个样本2026-10-31

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

  单细胞
• Exposure to perfluorooctanoic acid perturbs serotonin signaling in maternal pancreatic islets and induces gestational diabetes in mice
  GSE330582Mus musculus8 个样本2026-10-31

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

  扰动筛选
• GPR124 upregulation protects AML blasts from lipotoxicity
  GSE329506Mus musculus12 个样本2026-10-31

  GPR124 (ADGRA2), a member of the Adhesion G Protein-Coupled Receptor family, has an established role in the embryonic development of the central nervous system vasculature. However, its function in the context of acute myeloid leukemia (AML) remains unexplored. Transcriptome studies revealed upregulation of GPR124 in AML CD34+ blasts compared to healthy counterparts. Lentiviral overexpression of an GPR124-EGFP fusion protein indicated both plasma membrane and intracellular localization. Immunoprecipitation followed by LC-MS/MS showed strong enrichment of intracellular proteins associated with vesicles and vesicle transport, focal adhesion, actin cytoskeleton, and lipid droplets (LDs). In murine bone marrow mesenchymal stromal cells stimulated towards adipocytic differentiation, CRISPR-Cas9 mediated knockout of Gpr124 (Gpr124KO) reduced LD size, while total neutral lipid accumulation showed an increasing trend. In AML cells, lipidomic studies revealed increased baseline triacylglycerol (TG) levels in GPR124KO cells, suggesting altered LD metabolism. Since TGs are key components of LDs and its accumulation is a known response to lipid peroxidation, we next assessed ferroptosis sensitivity. Indeed, GPR124KO cells were significantly more sensitive to ferroptosis induction by GPX4 inhibition, accompanied by increased reactive oxygen species (ROS) and accumulation of lipid peroxidation. Additionally, GPR124KO cells were more sensitive to DGAT1 inhibition, a key enzyme in LD formation, and combination with the ferroptosis inducer RSL3 was synergistic in GPR124KO cells. Together, our findings indicate that GPR124 is essential for maintaining stable lipid homeostasis in AML and identify GPR124 and LD metabolism as potential therapeutic targets for inducing ferroptosis-mediated cell death.
• Small RNA sequencing of fibrotic intestinal tissues from TNBS-induced mice
  GSE326149Mus musculus10 个样本2026-10-31

  To investigate miRNA expression changes associated with intestinal fibrosis, we performed small RNA sequencing on colon tissues from TNBS-induced fibrotic mice and control mice. This dataset was generated to identify fibrosis-associated miRNAs and provide a basis for subsequent functional and mechanistic studies of intestinal fibrosis.
• mRNA expression profiling of intestinal fibrosis in TNBS-induced mice
  GSE326147Mus musculus10 个样本2026-10-31

  To characterize transcriptomic alterations associated with intestinal fibrosis, we performed mRNA sequencing on colon tissues from TNBS-induced fibrotic mice and control mice. This dataset was generated to identify differentially expressed genes and signaling pathways involved in intestinal fibrosis.
• Comparative study of the osseointegration capacity of porous tantalum, titanium, and HA/PA66
  GSE325408Mus musculus9 个样本2026-10-31

  Obtaining long-term and stable osseointegration of biomaterials in vivo remains a significant challenge. In recent years, pure titanium, HA/PA66, and porous tantalum have been widely used in the field of orthopedic implants. However, there is no comparative study of these three materials in the field of osseointegration. In this study, the physical properties, biosafety, osteogenic differentiation, and osseointegration of these three materials were comparatively investigated through material characterization, in vitro experiments, and in vivo experiments. In vitro experiments showed that porous tantalum has the roughest surface and better hydrophilicity, which is more conducive to osteoblast adhesion, proliferation, and differentiation. In vivo experiments confirmed that porous tantalum has the best osseointegration effect after implantation in vivo, with more surrounding new bone tissue and higher bonding strength. The results of this study are of great significance in guiding the improvement of biomaterials and promoting the selection of materials for practical clinical applications.
• RNA-seq of Mus musculus 2-cell embryos (WT vs Tcl1 KO) with CDCA treatment
  GSE323388Mus musculus14 个样本2026-10-31

  This study includes paired-end bulk RNA-seq data generated from Mus musculus embryos at the 2-cell stage. Samples comprise wild-type (WT) and Tcl1 knockout (KO) embryos, with and without CDCA treatment, with biological replicates. Raw sequencing data are available in SRA and linked here via SRA Run accessions.
• Complement C3-Mediated Hippocampal CA2 Synaptic Impairments Underlie Social Deficits by Srpx2 Deficiency in Maternal Immune Activation
  GSE315602Mus musculus6 个样本2026-10-31

  Social behavior deficits are hallmark features of neurodevelopmental disorders. The hippocampal CA2 region and complement system are critical for social function and neurodevelopment. Here, we show SRPX2 interacts with complement protein C1Q and regulates complement-coagulation pathways, specifically downregulating C3 in astrocytes. Srpx2 deficiency induces transient C3 upregulation and selective excitatory synapse loss in hippocampal CA2 during adolescence. Moreover, Srpx2 deficiency and prenatal maternal immune activation interact to disrupt social behavior, accompanied by enhanced C3 expression and excitatory synapse loss in CA2. Our findings identify SRPX2 as a key regulator of complement-mediated synaptic function in CA2, providing insights into the molecular mechanisms underlying neurodevelopmental disorder-related social deficits.
• Cooperative interaction of Foxp3 and STAT5 confers regulatory T cell fitness by tuning IL-2 induced gene expression
  GSE311192Mus musculus27 个样本2026-10-31

  This SuperSeries is composed of the SubSeries listed below.

  SuperSeries
• Cooperative interaction of Foxp3 and STAT5 confers regulatory T cell fitness by tuning IL-2 induced gene expression [Cut & Run]
  GSE311187Mus musculus15 个样本2026-10-31

  Transcription factor Foxp3, with its singular role in differentiation and function of regulatory T (Treg) cells in physiologic and inflammatory settings, is thought to act by modulating transcriptional responses to activatory extracellular cues including pro-inflammatory cytokines. However, the underlying mechanisms remain largely unknown. After Foxp3 is induced during Treg differentiation upon STAT5 activation downstream of interleukin-2 receptor (IL-2R), sustained STAT5 signaling facilitates fitness and suppressive capacity of mature Treg cells. We found that Foxp3 and phospho-STAT5 (pSTAT5) form a stable transcriptional complex. Upon IL-2 sensing, Foxp3 is recruited in a pSTAT5-dependent manner to GAS-motif-enriched cis-regulatory elements that are developmentally primed by STAT5 in Treg precursors prior to Foxp3 expression. Using chemogenetically and pharmacologically induced protein degradation, we demonstrate that Foxp3 modulates STAT5 signaling in activated Treg cells to selectively modulate their transcriptional response to IL-2, most prominently involving a Myc-dependent gene module. Our studies suggest that direct Foxp3-STAT5 cooperativity fine-tunes STAT5 signaling downstream of IL-2 receptor activation to support functionality of differentiated Treg cells.
• Cooperative interaction of Foxp3 and STAT5 confers regulatory T cell fitness by tuning IL-2 induced gene expression [RNA-Seq]
  GSE311182Mus musculus12 个样本2026-10-31

  Transcription factor Foxp3, with its singular role in differentiation and function of regulatory T (Treg) cells in physiologic and inflammatory settings, is thought to act by modulating transcriptional responses to activatory extracellular cues including pro-inflammatory cytokines. However, the underlying mechanisms remain largely unknown. After Foxp3 is induced during Treg differentiation upon STAT5 activation downstream of interleukin-2 receptor (IL-2R), sustained STAT5 signaling facilitates fitness and suppressive capacity of mature Treg cells. We found that Foxp3 and phospho-STAT5 (pSTAT5) form a stable transcriptional complex. Upon IL-2 sensing, Foxp3 is recruited in a pSTAT5-dependent manner to GAS-motif-enriched cis-regulatory elements that are developmentally primed by STAT5 in Treg precursors prior to Foxp3 expression. Using chemogenetically and pharmacologically induced protein degradation, we demonstrate that Foxp3 modulates STAT5 signaling in activated Treg cells to selectively modulate their transcriptional response to IL-2, most prominently involving a Myc-dependent gene module. Our studies suggest that direct Foxp3-STAT5 cooperativity fine-tunes STAT5 signaling downstream of IL-2 receptor activation to support functionality of differentiated Treg cells.
• Social Stress Differentially Affects the Behavior and the Transcriptome of the adBNST between Male and Female Mice.
  GSE287634Mus musculus20 个样本2026-10-31

  Stress can be broken down into systemic and processive stressors with processive stressors requiring higher limbic processing. These are also often called social stressors as they require an understanding of social dynamics as opposed to physical based stressors. This differing of processing necessitates we study both phenomena. Additionally, sex is an important aspect of stress research as men and women show differing responses to stress and mood disorder development. To study this, we used a chronic social instability stress (CSIS) paradigm to stress male and female mice. This paradigm is approximately 7-weeks long and involves changing the cage mates of a mouse every 3 days so stable social dynamics cannot form. Afterwards, one cohort was used for avoidance behavior testing using the open field test, the elevated plus maze, the light/dark box emergence test, and the novelty suppressed feeding test. A second cohort was used for bulk RNA-Sequencing of the anterodorsal bed nucleus of the stria terminalis which is a limbic structure known to be related to chronic stress signaling. In the behavior assays, CSIS caused the females to be less avoidant, while the males became more avoidant. Additionally, we found that a low estrogen state in the females caused them to be less avoidant than in a high estrogen state. In the transcriptome, we found major differences between the males and females with the males expressing more genes related to transcription whereas the females expressed more genes related to synaptic transmission. We also found that the transcriptome in the males is more sensitive to the stress than the females. In summary, we have found how social stress is differentially regulated between males and females and how this may be related to the development of stress-related behavioral changes.
• Nephrin-associated phospho-protein network necessary for filtration at the slit-diaphragm and podocyte adhesion.
  GSE284774Mus musculus25 个样本2026-10-31

  Minimal Change Disease (MCD) is characterized by nephrotic syndrome. In a subgroup of patients, pathogenic antibodies against the slit-diaphragm (SD) protein Nephrin encoded by the gene NPSH1 were identified in blood and biopsy samples. Nephrin is essential for the SD as specific NPHS1 variants result in congenital nephrotic syndrome. Intact Nephrin is a structural component of the SD, but also transmits signals to the actin cytoskeleton of podocyte foot processes (FP) thereby presumably stabilizing podocyte FP morphology. Thus, analyzing the Nephrin signalosome is attractive to identify potential targets for therapeutic intervention in MCD. We employed a model of MCD with antibody-mediated clustering of Nephrin leading to tyrosine phosphorylation-dependent signal transduction in podocyte culture. Phospho-proteome analysis after antibody-mediated Nephrin clustering revealed approx. 180 differentially phosphorylated peptides. Gene set analysis showed that among others the biological process ‘cell matrix adhesion’ was enriched. We verified that two thirds of the identified proteins were necessary for filtration in vivo employing a knockdown approach with consecutive analysis by an in-vivo filtration assay in Drosophila melanogaster nephrocytes. One of the phosphorylated proteins following Nephrin activation in the phospho-proteome analysis was the activating factor of the small GTPase Rap1 – Rapgef1. The significance of this Nephrin effector Rapgef1 for SD and focal adhesion integrity was exemplary studied generating a Rapgef1 knockout (Rapgef1KO) in the metanephric mesenchyme of mice. We confirmed that an early Rapgef1 knockout in podocytes - like transgenic Nephrin mice deficient in tyrosine-dependent signaling – resulted in nephrotic syndrome and an MCD/focal segmental glomerulosclerosis (FSGS) phenotype. RNA sequencing of Rapgef1 knockout mice glomeruli revealed significant regulation of genes involved in cell signaling, cell adhesion, and extracellular matrix organization. Changes in glomerular basement membrane (GBM), focal adhesion (FA) composition, and significant podocyte loss were confirmed by immunofluorescence analysis in Rapgef1 knockout mice glomeruli. Altogether, we identified a Nephrin-associated phospho-protein network necessary for filtration at the slit-diaphragm and podocyte adhesion.
• Chronic Inflammatory Responses in Diabetic Lung and its’ Implications for Tuberculosis Infection.
  GSE280089Mus musculus8 个样本2026-10-31

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

  单细胞
• Krüppel-like factor 5 remodels lipid metabolism in exercised skeletal muscle
  GSE279425Mus musculus16 个样本2026-10-31

  Regular physical activity induces a variety of health benefits, preventing and counteracting diseases caused by a sedentary lifestyle. However, the molecular underpinnings of skeletal muscle plasticity in exercise remain poorly understood. We identified a role of the Krüppel-Like Factor 5 (Klf5) in this process, in particular in the regulation of lipid homeostasis. Surprisingly, gain- and loss-of-function studies in muscle in vivo revealed seemingly opposite functions of Klf5 in the response to an acute exercise bout and chronic training, modulating lipid oxidation and synthesis, respectively. Thus, even though only transiently induced, the function of Klf5 is complex and integral for a normal long-term training response. These findings highlight the importance of this mediator of external stress response to adaptive remodeling of skeletal muscle tissue.
• TAF1-dependent transcriptional dysregulation underlies multiple sclerosis
  GSE255578Mus musculus12 个样本2026-10-31

  In the search for new targets for therapeutic intervention, MS-associated common variants provide clues about etiology-relevant molecular mechanisms, but the individual effect of each variant is minimal. A current priority to better understand the molecular basis of MS and to identify targets for designing progression-modifying therapies, is therefore to detect in the CNS of MS patients specific biochemical alterations -likely related to environmental factors and/or GWAS-identified molecular mechanisms- that per se would suffice to cause MS progression.
• Deciphering the interaction between Twist1 and PPARγ during adipocyte differentiation
  GSE246718Mus musculus12 个样本2026-10-31

  Obesity, a worldwide epidemic in recent years, is mainly due to the uncontrolled development of adipose tissues, which includes adipocyte hypertrophy and hyperplasia. Adipocyte differentiation is a process involving multiple transcription factor cascades, and the exact mechanism has not yet been defined. As a bHLH transcription factor, Twist1 exerts its activity by forming homo- or heterodimers with other factors. In this study, we showed Twist1 restricts adipogenesis through PPARγ. Expression of various differentiation markers (including PPARγ and adiponectin) and triglyceride-containing lipid droplets were decreased with overexpression of Twist1. Pathway enrichment analysis of RNA-seq data showed that differentially expressed genes (DEGs) caused by Twist1 overexpression were significantly related to lipolysis and PPARγ signaling. This implicates that Twist1 plays important regulatory roles in these processes. ChIP and dual luciferase assays showed that Twist1 could bind either PPARγ or adiponectin promoter to repress their respective transcription or directly to PPARγ protein to regulate its transcriptional activity. Furthermore, Twist1 directly interacted RXRα, which usually forms heterodimer with PPARγ to regulate adipogenesis. Taken together, our results suggest that Twist1 is an inhibitory modulator of adipogenesis and its function is likely through direct interaction with PPARγ protein or its gene promoter.
• mouse B16-F10 melanoma cells vs. Runx3 expressing B16-F10 cells
  GSE161992Mus musculus1 个样本2026-10-31

  Transcriptional profiling of the mock control mouse B16-F10 melanoma cells compares with that of the B16-F10 cells retrovirally expressing Runx3. Runx3 reduced the lung metastasis potential of the B16-F10 melanoma cells. This transcriptional profiling was used to uncover the differentially expressed genes that were regulated by Runx3.
• mouse B16-F0 melanoma cells vs. B16-F10 melanoma cells
  GSE161991Mus musculus1 个样本2026-10-31

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