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。

• Cooperative interaction of Foxp3 and STAT5 confers regulatory T cell fitness by tuning IL-2-induced gene expression [Myc_RNA]
  GSE352602Mus musculus6 个样本2026-10-31

  The transcription factor Foxp3, with its singular role in the differentiation and function of regulatory T (Treg) cells, is thought to modulate their responses to activatory extracellular cues. However, the underlying mechanisms remain largely unknown. Beyond its requirement for Foxp3 induction during Treg differentiation, STAT5 activation downstream of interleukin-2 (IL-2) signaling is essential for the fitness, activation, and suppressive capacity of mature Treg cells. Here, we demonstrate that IL-2-induced phospho-STAT5 directly binds Foxp3, endowing Foxp3 with a new binding specificity and enabling its recruitment to a distinct set of GAS motif-enriched cis-regulatory elements. Using acute chemogenetic and pharmacological protein degradation strategies, we show that Foxp3 selectively modulates STAT5-dependent transcriptional responses of activated Treg cells to IL-2, including a Myc-dependent gene module. These results suggest that Foxp3-STAT5 complexes “customize” transcriptional responses of activated Treg cells to IL-2 stimulation to support their fitness and functionality.
• Local chromatin, 3D genome folding and transposon cargo shape Sleeping Beauty transposition [pADam]
  GSE352286Mus musculus8 个样本2026-10-31

  The cut-and-paste DNA transposon Sleeping Beauty (SB) is widely used for genome engineering, mutagenesis and gene delivery. When mobilized from a genomic donor position (“launch site”), SB preferentially reintegrates locally (< 2 Mb), but factors governing its transposition from genomic sites remain incompletely understood. Here we analysed local transposition experiments in mouse embryonic stem cells to determine the influence of chromatin context and transposon cargo on SB transposition. Transposons in launch sites with transcriptionally active, accessible chromatin showed lower transposition efficiency. Large cargo and cargo with higher transcriptional activity also result in reduced transposition efficiency. After excision, local reintegration patterns closely resembled 3D contact frequencies of the launch site. This indicates that chromosome folding is a major determinant of the transposition pattern. Surprisingly, we did not detect any effect of the destination chromatin composition on reintegration efficiency. Cargo sequence modified the reintegration patterns: promoter-containing cargo increased both very proximal (<10kb) and interchromosomal transpositions, while CTCF binding sites in the cargo increased reintegration on the launch chromosome. Together, these results define key determinants of SB transposition in chromosomes and inform the design of SB-based genome engineering strategies.
• Liver Kinase B1 depletion disrupts the pantothenic acid: coenzyme A pathway in astrocytes
  GSE351587Mus musculus8 个样本2026-10-31

  Previous studies showed conditional knockout of Liver Kinase B1 (LKB1) from astrocytes exacerbated disease severity and glial cell activation in a mouse model of Multiple Sclerosis (MS). A major function of LKB1 is to maintain energy supplies under conditions of metabolic stress, suggesting that loss of LKB1 could alter astrocytic metabolic processes. Following siRNA mediated knockdown (KD) of LKB1 from primary mouse astrocytes, untargeted metabolomic screening identified significant increases in Pantothenic Acid (PA) and related metabolites; and pathway analysis showed the PA:Coenzyme A (PA:CoA) pathway was significantly modified. This pathway was also identified by bulk RNA sequencing. In LKB1 KD cells, relative mRNA levels of enzymes in the PA:CoA pathway were reduced, and PA Kinase 2 (Pank2, which converts PA to phosphoPA) expression was reduced. Deficiencies in Pank2 are known to cause iron accumulation, which we confirmed occurs in LKB1 KD astrocytes. The KD cells also showed increased sensitivity to induction of ferroptosis. Measurement of serum PA levels showed a positive correlation with age at diagnosis in relapsing remitting MS patients harboring a variant in the gene encoding LKB1. Together, these results indicate that metabolic disturbance leads to dysregulation of the PA:CoA pathway in astrocytes and suggest that plasma PA levels could provide a novel biomarker for MS disease.
• Single-cell analysis reveals sex-specific ERβ regulation of neurovascular protection in the AppNL-G-F mouse model of Alzheimer’s disease
  GSE350656Mus musculus4 个样本2026-10-31

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

  单细胞
• Gene Expression in the Glioblastoma Cell Line (GL261) Transcriptome Following Treatment with Magnetic Nanoparticles (MNPQ)
  GSE349688Mus musculus9 个样本2026-10-31

  GL261 cells are a widely used glioma tumor model system; following in situ transplantation, they stably form glioblastoma and are extensively utilized as a preclinical evaluation model for brain gliomas. Magnetic nanomedicines (MNPQ), with their advantages of magnetically responsive targeted enrichment and locally controlled release, have demonstrated effective antitumor potential against gliomas; however, how they reshape the gene expression profile of tumor cells at the transcriptomic level remains unclear. Our study has one primary objective: to identify differentially expressed genes and their enriched signaling pathways in the GL261 cell transcriptome before and after MNPQ treatment, thereby elucidating the molecular mechanisms underlying its antitumor effects.
• Gene expression in pericental and periportal hepatocytes
  GSE349461Mus musculus4 个样本2026-10-31

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

  空间转录组
• Id2 orchestrates IL-33-driven metabolic reprogramming in pathogenic Th2 cells (RNA-seq)
  GSE344612Mus musculus8 个样本2026-10-31

  The transcription factor Id2 licenses the transition of stem‑like Th2 cells to pathogenic ST2⁺ Tpath2 cells by orchestrating IL‑33‑ST2 signaling to drive glycolytic reprogramming. Id2 transcriptionally represses Pten by sequestering E proteins at its promoter, amplifying PI3K‑AKT signaling and glycolytic flux, which supports histone acetylation at Il1rl1 and Il5. Id2‑deficient Th2 cells fail to establish this epigenetic state; pyruvate supplementation rescues the defect. Pharmacological Id2 inhibition attenuates Tpath2 responses and airway inflammation in vivo, and cross‑species analysis confirms conserved PTEN dynamics in human asthma. Thus, the IL‑33–Id2–PI3K‑AKT axis represents a metabolic–epigenetic checkpoint and therapeutic target for allergic airway disease.
• Local effect of Ixodes scapularia TNFBP gene silence on transcriptome of bitten skin of mouse
  GSE344220Mus musculus9 个样本2026-10-31

  To explore their potential role in tick-host interactions, RNA-seq was performed on the skin of mice bitten by TNFBP1 and TNFBP2 silenced ticks. The transcriptome was altered after feeding on gene silenced ticks compared with control ticks, and defined pathways including legionellosis, HIF-1TNF, IL-17 signaling pathway, phagosome were significantly enriched in the downregulated genes.
• Specification of bone marrow sinusoids requires TIE2-mediated positive feedback involving COUP-TFII and VEGFR3 [Nr2f2_ecko P5bm]
  GSE342123Mus musculus6 个样本2026-10-31

  The bone marrow (BM) vascular network drives bone development and supports hematopoiesis, yet the mechanisms governing its specialized sinusoidal architecture remain poorly characterized. Here, we show that the angiopoietin receptor TIE2 is highly expressed by BM sinusoidal endothelial cells (BM_SECs), and its endothelial deletion triggers sinusoidal capillarization, characterized by reduced vessel diameter and aberrant mural cell coverage. Mechanistically, TIE2 insufficiency drives a downregulation of VEGFR3 in BM_SECs, while leaving hepatic sinusoidal VEGFR3 unaffected. Notably, BM sinusoidal VEGFR3 downregulation occurred within 48 hours of induced endothelial Tek deletion. RNA-sequencing revealed that TIE2 insufficiency downregulated pathways related to sinusoidal development, alongside an aberrant upregulation of arterial and angiogenic genes. We validated this phenotype using inducible Tek deletion specifically within VEGFR3+ SECs, or in mutant mice with the insufficiency of TIE2 ligand ANGPT1. Furthermore, endothelial deletion of the transcription factor Nr2f2 (COUP-TFII) recapitulated these defects, yielding reductions in BM sinusoidal TIE2 and VEGFR3 expression. Finally, induced endothelial deletion of Flt4 produced a similar phenotype of defective BM sinusoidal formation. Together, our findings demonstrate that ANGPT1/TIE2 and COUP-TFII form a reciprocal regulatory loop essential for coordinating BM sinusoidal specification by sustaining VEGFR3 expression.
• Specification of bone marrow sinusoids requires TIE2-mediated positive feedback involving COUP-TFII and VEGFR3 [Tek_ecko P3bm]
  GSE342122Mus musculus8 个样本2026-10-31

  The bone marrow (BM) vascular network drives bone development and supports hematopoiesis, yet the mechanisms governing its specialized sinusoidal architecture remain poorly characterized. Here, we show that the angiopoietin receptor TIE2 is highly expressed by BM sinusoidal endothelial cells (BM_SECs), and its endothelial deletion triggers sinusoidal capillarization, characterized by reduced vessel diameter and aberrant mural cell coverage. Mechanistically, TIE2 insufficiency drives a downregulation of VEGFR3 in BM_SECs, while leaving hepatic sinusoidal VEGFR3 unaffected. Notably, BM sinusoidal VEGFR3 downregulation occurred within 48 hours of induced endothelial Tek deletion. RNA-sequencing revealed that TIE2 insufficiency downregulated pathways related to sinusoidal development, alongside an aberrant upregulation of arterial and angiogenic genes. We validated this phenotype using inducible Tek deletion specifically within VEGFR3+ SECs, or in mutant mice with the insufficiency of TIE2 ligand ANGPT1. Furthermore, endothelial deletion of the transcription factor Nr2f2 (COUP-TFII) recapitulated these defects, yielding reductions in BM sinusoidal TIE2 and VEGFR3 expression. Finally, induced endothelial deletion of Flt4 produced a similar phenotype of defective BM sinusoidal formation. Together, our findings demonstrate that ANGPT1/TIE2 and COUP-TFII form a reciprocal regulatory loop essential for coordinating BM sinusoidal specification by sustaining VEGFR3 expression.
• Specification of bone marrow sinusoids requires TIE2-mediated positive feedback involving COUP-TFII and VEGFR3 [Tek_ecko P11bm]
  GSE342121Mus musculus6 个样本2026-10-31

  The bone marrow (BM) vascular network drives bone development and supports hematopoiesis, yet the mechanisms governing its specialized sinusoidal architecture remain poorly characterized. Here, we show that the angiopoietin receptor TIE2 is highly expressed by BM sinusoidal endothelial cells (BM_SECs), and its endothelial deletion triggers sinusoidal capillarization, characterized by reduced vessel diameter and aberrant mural cell coverage. Mechanistically, TIE2 insufficiency drives a downregulation of VEGFR3 in BM_SECs, while leaving hepatic sinusoidal VEGFR3 unaffected. Notably, BM sinusoidal VEGFR3 downregulation occurred within 48 hours of induced endothelial Tek deletion. RNA-sequencing revealed that TIE2 insufficiency downregulated pathways related to sinusoidal development, alongside an aberrant upregulation of arterial and angiogenic genes. We validated this phenotype using inducible Tek deletion specifically within VEGFR3+ SECs, or in mutant mice with the insufficiency of TIE2 ligand ANGPT1. Furthermore, endothelial deletion of the transcription factor Nr2f2 (COUP-TFII) recapitulated these defects, yielding reductions in BM sinusoidal TIE2 and VEGFR3 expression. Finally, induced endothelial deletion of Flt4 produced a similar phenotype of defective BM sinusoidal formation. Together, our findings demonstrate that ANGPT1/TIE2 and COUP-TFII form a reciprocal regulatory loop essential for coordinating BM sinusoidal specification by sustaining VEGFR3 expression.
• 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 [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.
• 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
• 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
• 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.
• 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.
• 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
• 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.
• Alcohol-induced suppression of miR-1948-3p promotes an adaptive HIF-1α response to limit hepatic steatosis
  GSE352328Mus musculus8 个样本2026-10-30

  To investigate the role of HIF-1α in alcohol-associated liver disease, we performed transcriptomic profiling on liver tissues from chronic alcohol-fed mice (AF) and mice with hepatocyte-specific Hif-1α knockdown (AF+Hif-1α KD). RNA-seq analysis revealed that Hif-1α deficiency markedly altered the hepatic transcriptional landscape and identified the disruption of the PPAR signaling pathway. Overall, this dataset provides insights into the molecular mechanisms by which HIF-1α limits hepatic steatosis during alcohol exposure.
• Heterogeneity and interaction of microglia and macrophages after retinal detachment
  GSE351957Mus musculus5 个样本2026-10-30

  This study aims to systematically investigate the evolutionary processes of microglia and macrophages during the onset and progression of retinal detachment (RD).
• Single-cell RNA sequencing of pooled orthotopic pancreatic tumors derived from PKM2-WT and PKM2-K89R cells
  GSE351631Mus musculus2 个样本2026-10-30

  We performed single-cell RNA sequencing of orthotopic pancreatic tumors established in NCG mice using pancreatic cancer cells expressing wild-type PKM2 (PKM2-WT) or the lactylation-deficient PKM2 K89R mutant (PKM2-K89R). For each group, tumor tissues from five mice were pooled before single-cell library preparation, resulting in one library per group. The dataset was used to characterize the tumor microenvironment and compare cell-type composition and cellular transcriptional states between the PKM2-WT and PKM2-K89R groups, with particular focus on fibroblast and cancer-associated fibroblast (CAF) subpopulations.

  单细胞
• Inactivation of Irs1 in pericentral hepatocytes promotes lipid oxidation
  GSE349448Mus musculus4 个样本2026-10-30

  Hepatic metabolic zonation enables periportal (PP) and pericentral (PC) hepatocytes to perform distinct functions in glucose and lipid metabolism. Insulin signaling is also spatially organized across the liver lobule, but the transcriptional role of insulin signaling in PC hepatocytes remains incompletely understood. To define the gene-expression programs regulated by insulin signaling in PC hepatocytes, we generated mice with inducible PC-specific deletion of insulin receptor substrate 1 (Irs1) using Cyp1a2CreER (Irs1-Cyp1a2 mice). RNA sequencing was performed to compare liver gene-expression profiles between Irs1-Cyp1a2 mice and littermate controls. This dataset provides a transcriptomic resource for identifying pathways regulated by PC IRS1 signaling and for understanding how spatial insulin signaling contributes to hepatic glucose and lipid metabolism.

  空间转录组
• Early Pitx2 modulation of Fgf10 directs asymmetric lung morphology
  GSE347452Mus musculus8 个样本2026-10-30

  Both the molecular cascade establishing Left-Right asymmetric anatomy, including the transcription factor Pitx2, and the signaling pathways controlling branching morphogenesis of the lung (a Left-Right asymmetric process) have been intensively studied. However, the two have never been linked. We identify Fgf10 as a Pitx2-sensitive signal in the mesenchyme of the developing mouse lung. Pitx2 suppresses Fgf10 expression, making the right lung, which lacks Pitx2 expression, grow faster than the left during the budding stage. Modulating Fgf10 dosage in the left mesenchyme is sufficient to shift levels of epithelial proliferation and thereby alter lung budding asymmetry. Pitx2 activity during the earliest lung bud stages is sufficient to establish differences in the primary airway branches, leading to subsequent asymmetric branching patterns that eventually manifest as the left-right differences in lung morphology. Thus, Pitx2 converts left-right mesenchymal identity into organ asymmetry by quantitatively tuning Fgf10-dependent epithelial growth during early lung organogenesis.