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。

• Sleep-dependent DNA methylation remodeling in basolateral amygdala fear engrams [PIP-Seq]
  GSE348705Mus musculus16 个样本2026-10-31

  How memory consolidates via DNA methylation mechanisms during sleep in the basolateral amygdala (BLA), a critical brain region for fear memory, remains unknown. We performed whole-genome bisulfite sequencing (WGBS) on fear conditioning (FC)-activated cells from the BLAs of adult male mice experiencing either sleep or sleep deprivation following FC learning, evaluated at Day 7 and Day 28 timepoints. Additionally, Day 7 samples include paired single-nucleus RNA sequencing (snRNA-seq) using PIPseq technology. This dataset enables the integration of multi-omics (methylome and transcriptome) to understand learning-induced epigenomic programming in the BLA.

  单细胞多组学
• Habitual betel nut chewing promotes oral squamous cell carcinoma tumorigenesis by inhibiting global methylation in normal oral mucosa
  GSE280233Homo sapiens33 个样本2026-10-31

  Oral squamous cell carcinoma (OSCC) is a major oral-maxillofacial tumor with marked effects on facial appearance and high recurrence rate. In addition to tobacco and alcohol consumption, betel nut chewing plays a significant role in promoting the occurrence of OSCC, highlighted by the prevalence of oral cancer in East Asia, Southeast Asia, and South Asia. However, the specific underlying mechanisms are unclear. By analyzing clinical data, we first noted that habitual betel nut chewing only affect occurrence of second primary tumors, indicated that it induces tumorigenic changes in the normal tumor-adjacent mucosa tissues. Tumorigenesis relies on the combined effect of genetic and environmental changes, with epigenetic changes, primarily methylation, serving as a key link connecting genetics and the environment. Herein, we analyzed global DNA methylation in the oral mucosa and found that habitual betel nut chewing leads to significant hypomethylation in the normal tumor-adjacent mucosa. This change makes the normal mucosa more similar to OSCC tissues than other normal tissues at the molecular pathological level. Our multiomics analysis revealed that habitual betel nut chewing may facilitate tumorigenesis by reducing the global DNA methylation level of normal mucosa, suppressing antitumor immunity, and promoting abnormal cell proliferation. Through experimental verification and screening, we identified five key genes involved in this process: DEPDC1B, ANLN, ECT2, SPC25, and PLK1. Our study revealed that habitual betel nut chewing can promote OSCC tumorigenesis by regulating global DNA methylation. Early detection of global DNA methylation and key gene markers may reveal potential targets for assessing OSCC risk.

  多组学
• Spatial genome and transcriptome co-mapping reveals clonal heterogeneity in tumor tissue [DNA-Seq]
  GSE276212Homo sapiens; Mus musculus11 个样本2026-10-31

  Tumor heterogeneity arises from the sequential acquisition of somatic mutations and the selection of fitter clones, leading to distinct genotypes and phenotypes. Joint mapping of genome and transcriptome in the same tumor tissue can directly link clonoal relation to transcriptional state enabling a more in-depth understanding of intrinsic and extrinct tumor heterogeneity in the tissue context. Here, we introduce Spatial-GT-seq, a spatial multi-omic technology capable of genome-wide co-profiling of the genome and transcriptome at near single-cell resolution. We demonstrated in situ identification of tumor subclones in a mouse model of lung metastasis, with parallel transcriptomic profiles indicating that the gene expression profile of the same tumor clone is altered by the tumor microenvironment. Furthermore, analysis of primary and recurrent human pancreatic neuroendocrine tumors reveals both persistent and newly emerging tumor subclones, exhibiting transcriptional changes in both the original and recurrence sites. These findings highlight Spatial-GT-seq as a valuable platform for studying genotype-phenotype-microenvironment associations, providing new insights into cancer evolution and heterogeneity.

  单细胞空间转录组多组学
• Spatial genome and transcriptome co-mapping reveals clonal heterogeneity in tumor tissue [RNA-Seq]
  GSE276211Homo sapiens; Mus musculus11 个样本2026-10-31

  Tumor heterogeneity arises from the sequential acquisition of somatic mutations and the selection of fitter clones, leading to distinct genotypes and phenotypes. Joint mapping of genome and transcriptome in the same tumor tissue can directly link clonoal relation to transcriptional state enabling a more in-depth understanding of intrinsic and extrinct tumor heterogeneity in the tissue context. Here, we introduce Spatial-GT-seq, a spatial multi-omic technology capable of genome-wide co-profiling of the genome and transcriptome at near single-cell resolution. We demonstrated in situ identification of tumor subclones in a mouse model of lung metastasis, with parallel transcriptomic profiles indicating that the gene expression profile of the same tumor clone is altered by the tumor microenvironment. Furthermore, analysis of primary and recurrent human pancreatic neuroendocrine tumors reveals both persistent and newly emerging tumor subclones, exhibiting transcriptional changes in both the original and recurrence sites. These findings highlight Spatial-GT-seq as a valuable platform for studying genotype-phenotype-microenvironment associations, providing new insights into cancer evolution and heterogeneity.

  单细胞空间转录组多组学
• RNA-seq of clear cell renal cell carcinoma tumor and adjacent normal kidney tissue samples.
  GSE346548Homo sapiens10 个样本2026-10-30

  Renal cell carcinoma (RCC) is among the most common urological malignancies, yet the transcriptomic landscape underlying its pathogenesis remains incompletely characterized, particularly for non-coding regions that may harbor functional non-canonical open reading frames (ncORFs). Here we performed whole-transcriptome RNA-seq on 5 clear cell RCC tumor tissues and 5 adjacent normal kidney tissues to systematically profile mRNA, lncRNA, and circRNA expression. This dataset serves as the transcriptomic layer of an integrative multi-omics study aimed at identifying dysregulated ncORF-encoded micropeptides in RCC, with lncRNAs representing a predominant source of tumor-associated cryptic peptides. The data provide a reference for translational activity assessment when combined with matchedribosome profiling and immunopeptidomics datasets.

  多组学
• Time series analysis of transcriptomic responses to iron and zinc stress in Poplar
  GSE344088Populus trichocarpa173 个样本2026-10-30

  Extending our understanding of iron (Fe) and zinc (Zn) homeostasis beyond annual model plants is essential for improving plant productivity, nutritional quality, and food safety. However, the mechanisms coordinating metal acquisition, systemic signaling, and detoxification remain poorly understood in woody perennials. We generated a 21-d time-series multi-omics resource integrating transcriptomic, ionomic, and physiological measurements from roots and leaves of black cottonwood (Populus trichocarpa) exposed to Fe or Zn deficiency or excess. Temporal analyses revealed tissue-specific metal partitioning, extensive nutrient crosstalk, and restriction of Zn accumulation during prolonged Zn excess. Gene regulatory network inference identified bHLH38/39.2 as a hub associated with root Fe uptake and leaf Fe signaling. Fe deficiency rapidly induced five C-TERMINALLY ENCODED PEPTIDE (CEP) genes in roots. A fluorescently labeled CEP peptide supplied to roots accumulated in leaves, where CEP treatment induced IRON MAN (IMA) genes. Receptor-dependent protoplast assays further demonstrated CEP-mediated activation of IMA promoters. These findings support a model in which root-derived CEP peptides convey Fe status to leaf IMA signaling. Under Zn excess, declining Zn accumulation coincided with increased root suberization and induction of suberin-biosynthetic genes. NAC058.1 and NAC058.2 emerged as regulatory hubs and activated most tested suberin gene promoters. These findings suggest that NAC-regulated suberization restricts Zn entry during prolonged exposure. Our study identifies systemic and barrier-based mechanisms of micronutrient homeostasis in a woody perennial.

  多组学
• Acquired resistance to anti-PD-1 therapy is associated with tumor intrinsic macrophage reprogramming.
  GSE344292Mus musculus19 个样本2026-10-29

  Immune checkpoint inhibitors targeting the PD-1/PD-L1 axis can produce durable tumor responses, but acquired resistance remains a major clinical problem. To define tumor-intrinsic transcriptional changes associated with acquired resistance, we generated independently derived anti-PD-1-resistant MC-38 colon adenocarcinoma cell lines (MC38-PR) by serial in vivo selection in immunocompetent C57BL/6 mice. Isotype-control-passaged MC38-ISO lines and the parental MC-38 line served as controls. Bulk RNA sequencing was performed to compare parental, isotype-control-passaged, and acquired anti-PD-1-resistant cell lines. These data support a multi-omic investigation of resistance in which independently derived resistant tumors converged on an immunosuppressive, macrophage-skewing tumor program despite retaining antigen-presentation machinery, interferon-gamma responsiveness, and most predicted neoantigens.

  多组学
• Multi-omics analysis reveals an EXOSC10-lncRNA-dependent checkpoint in nucleolar proteostasis recovery
  GSE329077Homo sapiens12 个样本2026-10-29

  Proteotoxic stress induced by heat shock drives the formation of nucleolar aggresomes. However, the mechanisms governing their resolution during recovery remain poorly understood. Here, we combine temporal quantitative proteomics, transcriptomics and live imaging to define the dynamics of the detergent-insoluble fraction during heat shock and recovery. We find that nucleolar aggresome recovery follows a multiphasic lag–burst–resolution kinetic program that tightly couples the recruitment of protein quality-control factors and remobilization of ribosomal proteins. We identify stress-induced long non-coding RNA IGS16 as a critical regulator of this process. IGS16 accumulates in the nucleolus upon heat shock where it restrains chaperone engagement. Clearance of IGS16 by the nucleolar exonuclease EXOSC10 is required to initiate nucleolar remodeling and enable HSP70-dependent restoration of ribosomal protein mobility. Notably, IGS16 degradation occurs independently of HSP70 ATPase activity, indicating that RNA turnover precedes and licenses chaperone-mediated aggregate resolution. Together, our findings uncover an RNA-dependent regulatory checkpoint that coordinates RNA metabolism and protein quality control to regulate nucleolar proteostasis recovery. This work also reveals a previously unknown function for EXOSC10 in stress-induced condensate dynamics control potentially through long non-coding RNA degradation.

  多组学
• AP-1 Family Member Transcription Factors Play a Critical Role in Human Beta Cell Replication and Differentiation [Multiome]
  GSE326458Homo sapiens2 个样本2026-10-29

  Insulinomas are a rare and benign type of pancreatic neuroendocrine tumor. They consist of pancreatic beta cells that are able to replicate as opposed to their human islet counterparts. They are also able to secrete insulin. Although we know epigenetics is a critical factor, it is unclear which exact pathways play a role in the control of replication and differentiation. Here we performed multiome assay to delineate open accessible chromatin regions and single cell transcriptomic profiles in various insulinoma cell types.

  单细胞多组学
• Single-cell Characterization of DNA Hydroxymethylation of the Mouse Brain [scRNA-seq]
  GSE314217Mus musculus491 个样本2026-10-29

  DNA methylation, particularly CpG methylation, plays a pivotal role in brain development, function, and aging. While recent single-cell brain methylome atlases have been mapped, they cannot distinguish between 5-hydroxymethylcytosine (5hmC) and 5-methylcytosine (5mC) due to their reliance on bisulfite conversion. This limitation is particularly problematic in the brain, where postmitotic neurons accumulate abundant 5hmCG, which may exert functions opposite to 5mCG. Consequently, how CpG modifications regulate neuronal gene expression remains incompletely understood. To address this, we present Joint-Cabernet, a bisulfite-free single-cell platform enabling simultaneous profiling of 5hmC, 5mC, and transcriptomes. Applying Joint-Cabernet to nuclei from adult mouse brains, we resolved cell-type-specific DNA hydroxymethylation landscapes, revealing elevated 5hmCG and 5hmCH levels in transcriptionally active genes and regulatory elements across diverse brain cell types and spatial gradients in cortical layers. This single-cell multi-omic atlas (DNA methylation, hydroxymethylation, and transcriptome) of the mouse brain provides a framework for studying methylation-driven regulation in the brain organization and neurodegenerative diseases.

  单细胞空间转录组细胞图谱多组学
• Single-cell Characterization of DNA Hydroxymethylation of the Mouse Brain [5mC]
  GSE314211Mus musculus479 个样本2026-10-29

  DNA methylation, particularly CpG methylation, plays a pivotal role in brain development, function, and aging. While recent single-cell brain methylome atlases have been mapped, they cannot distinguish between 5-hydroxymethylcytosine (5hmC) and 5-methylcytosine (5mC) due to their reliance on bisulfite conversion. This limitation is particularly problematic in the brain, where postmitotic neurons accumulate abundant 5hmCG, which may exert functions opposite to 5mCG. Consequently, how CpG modifications regulate neuronal gene expression remains incompletely understood. To address this, we present Joint-Cabernet, a bisulfite-free single-cell platform enabling simultaneous profiling of 5hmC, 5mC, and transcriptomes. Applying Joint-Cabernet to nuclei from adult mouse brains, we resolved cell-type-specific DNA hydroxymethylation landscapes, revealing elevated 5hmCG and 5hmCH levels in transcriptionally active genes and regulatory elements across diverse brain cell types and spatial gradients in cortical layers. This single-cell multi-omic atlas (DNA methylation, hydroxymethylation, and transcriptome) of the mouse brain provides a framework for studying methylation-driven regulation in the brain organization and neurodegenerative diseases.

  单细胞空间转录组细胞图谱多组学
• Single-cell Characterization of DNA Hydroxymethylation of the Mouse Brain [5hmC]
  GSE314195Mus musculus479 个样本2026-10-29

  DNA methylation, particularly CpG methylation, plays a pivotal role in brain development, function, and aging. While recent single-cell brain methylome atlases have been mapped, they cannot distinguish between 5-hydroxymethylcytosine (5hmC) and 5-methylcytosine (5mC) due to their reliance on bisulfite conversion. This limitation is particularly problematic in the brain, where postmitotic neurons accumulate abundant 5hmCG, which may exert functions opposite to 5mCG. Consequently, how CpG modifications regulate neuronal gene expression remains incompletely understood. To address this, we present Joint-Cabernet, a bisulfite-free single-cell platform enabling simultaneous profiling of 5hmC, 5mC, and transcriptomes. Applying Joint-Cabernet to nuclei from adult mouse brains, we resolved cell-type-specific DNA hydroxymethylation landscapes, revealing elevated 5hmCG and 5hmCH levels in transcriptionally active genes and regulatory elements across diverse brain cell types and spatial gradients in cortical layers. This single-cell multi-omic atlas (DNA methylation, hydroxymethylation, and transcriptome) of the mouse brain provides a framework for studying methylation-driven regulation in the brain organization and neurodegenerative diseases.

  单细胞空间转录组细胞图谱多组学
• The Circadian Clock controls Hepatic Inflammation in Metabolic dysfunction-Associated Steatotic Liver Disease (MASLD) [Multi-omics]
  GSE327440Mus musculus6 个样本2026-10-28

  The circadian clock dictates time-of-day dependent gene, protein expression, and metabolite levels to ensure liver homeostasis. Circadian misalignment is implicated in the development of various metabolic disorders, but its contribution to the progression of Metabolic dysfunction-Associated Steatotic Liver Disease (MASLD) toward Metabolic dysfunction-Associated Steatohepatitis (MASH) remains poorly understood. Here, we aimed to dissect the role of the circadian clock in MASH development. Using an environmental model of chronic circadian misalignment, combined with metabolic and immune phenotyping, single nuclei transcriptomics and lipidomic profiling, we investigated the role of the clock in MASLD development and hepatic inflammation. To dissect the specific contribution of the immune clock, we used a genetic model overexpressing the clock component Rev-erbα in myeloid cells. Chronic circadian misalignment combined with a high-fat, high-sucrose, cholesterol-enriched (HFHSC) diet markedly amplified hepatic inflammation, characterized by the upregulation of pro-inflammatory genes and increased immune cell infiltration, including the expansion of lipid-associated macrophages (LAMs). Although circadian misalignment did not worsen glucose intolerance or hepatic steatosis, it altered hepatic metabolic gene expression, reflecting a broad reprogramming of immune and metabolic pathways. The circadian clock controls both FA profile and inflammatory process, and its misalignment aggravates MASLD by increasing liver inflammation. Targeting circadian regulators such as Rev-erbα in myeloid cells may offer a promising therapeutic avenue for controlling liver inflammation in MASLD.

  多组学
• sn-multiome of psoriasis skin
  GSE294957Homo sapiens18 个样本2026-10-27

  We simultaneously profile the gene expression and chromatin accessibility of lesional skin of psoriasis to understand the epigenetic landscape that regulates gene expression in the psoriatic skin

  多组学
• Single Cell multi-omics identifies VEGFA-mediated angiogenesis results in relapse in Sonic Hedgehog Medulloblastoma [snRNA-seq]
  GSE287109Homo sapiens12 个样本2026-10-27

  Relapse in Sonic Hegdehog Medulloblastoma (SHH-MB) a common pediatric brain tumor, remain a significant clinical challenge due to its poor prognosis and limited therapeutic intervention. Understanding the underlying molecular mechanisms driving relapse is critical for developing targeted interventions. Here, we utilize single-cell multi-omics, combining single-nucleus RNA sequencing (snRNA-seq), single-nucleus ATAC sequencing (snATAC-seq), and spatial omics to comprehensively characterize the cellular landscape and regulatory networks associated with SHH medulloblastoma relapse. Our integrative analysis identifies distinct GCP population enriched with angiogenic activity characterized high expression of Vascular Endothelial Growth Factor A (VEGFA) regulated by the transcription factor HIF1A. Notably, we find that VEGFA-mediated angiogenesis is a critical driver of tumor recurrence, promoting a microenvironment that supports tumor revascularization and growth in the endothelial cells. Furthermore, we uncover potential therapeutic targets within the VEGFA signaling axis that could disrupt angiogenesis and reduce relapse rates. Our findings provide new insights into the molecular and cellular dynamics of SHH medulloblastoma relapse and highlight VEGFA as a key mediator of angiogenesis-driven recurrence, offering a promising avenue for therapeutic intervention.

  单细胞空间转录组多组学
• Single Cell multi-omics identifies VEGFA-mediated angiogenesis results in relapse in Sonic Hedgehog Medulloblastoma
  GSE287108Homo sapiens13 个样本2026-10-27

  Relapse in Sonic Hegdehog Medulloblastoma (SHH-MB) a common pediatric brain tumor, remain a significant clinical challenge due to its poor prognosis and limited therapeutic intervention. Understanding the underlying molecular mechanisms driving relapse is critical for developing targeted interventions. Here, we utilize single-cell multi-omics, combining single-nucleus RNA sequencing (snRNA-seq), single-nucleus ATAC sequencing (snATAC-seq), and spatial omics to comprehensively characterize the cellular landscape and regulatory networks associated with SHH medulloblastoma relapse. Our integrative analysis identifies distinct GCP population enriched with angiogenic activity characterized high expression of Vascular Endothelial Growth Factor A (VEGFA) regulated by the transcription factor HIF1A. Notably, we find that VEGFA-mediated angiogenesis is a critical driver of tumor recurrence, promoting a microenvironment that supports tumor revascularization and growth in the endothelial cells. Furthermore, we uncover potential therapeutic targets within the VEGFA signaling axis that could disrupt angiogenesis and reduce relapse rates. Our findings provide new insights into the molecular and cellular dynamics of SHH medulloblastoma relapse and highlight VEGFA as a key mediator of angiogenesis-driven recurrence, offering a promising avenue for therapeutic intervention.

  单细胞空间转录组多组学
• Single Cell multi-omics identifies VEGFA-mediated angiogenesis results in relapse in Sonic Hedgehog Medulloblastoma [Visium]
  GSE287107Homo sapiens6 个样本2026-10-27

  Relapse in Sonic Hegdehog Medulloblastoma (SHH-MB) a common pediatric brain tumor, remain a significant clinical challenge due to its poor prognosis and limited therapeutic intervention. Understanding the underlying molecular mechanisms driving relapse is critical for developing targeted interventions. Here, we utilize single-cell multi-omics, combining single-nucleus RNA sequencing (snRNA-seq), single-nucleus ATAC sequencing (snATAC-seq), and spatial omics to comprehensively characterize the cellular landscape and regulatory networks associated with SHH medulloblastoma relapse. Our integrative analysis identifies distinct GCP population enriched with angiogenic activity characterized high expression of Vascular Endothelial Growth Factor A (VEGFA) regulated by the transcription factor HIF1A. Notably, we find that VEGFA-mediated angiogenesis is a critical driver of tumor recurrence, promoting a microenvironment that supports tumor revascularization and growth in the endothelial cells. Furthermore, we uncover potential therapeutic targets within the VEGFA signaling axis that could disrupt angiogenesis and reduce relapse rates. Our findings provide new insights into the molecular and cellular dynamics of SHH medulloblastoma relapse and highlight VEGFA as a key mediator of angiogenesis-driven recurrence, offering a promising avenue for therapeutic intervention.

  单细胞空间转录组多组学
• Gene Expression Data of Neuroendocrine Tumors from Different Primary Sites
  GSE305904Homo sapiens194 个样本2026-10-26

  Neuroendocrine tumors (NETs) represent a unique group of tumors with diverse anatomical origins but share common clinical and molecular characteristics. Despite their low mutational burden and limited number of recurrent mutations, epigenetic mechanisms play a crucial role in their biology. This study aims to establish a universal molecular classification of NETs, independent of their site of origin, by integrating gene expression and methylation data. The objective is to uncover shared vulnerabilities to support the development of improved diagnostic, prognostic, and predictive biomarkers, as well as innovative treatment strategies to enhance patient outcomes. Transcriptomic and methylomic profiles were examined from paraffin-embedded tumor samples of 194 patients diagnosed with G1-G3 neuroendocrine tumors (NETs) originating in the gastrointestinal-pancreatic (GEP) tract and lungs. Using these integrated datasets, a Multi-Omics Factor Analysis (MOFA) model comprising eight factors was developed. This model facilitated the application of unsupervised clustering algorithms, resulting in a consensus molecular classification for neuroendocrine tumors.

  多组学计算与 AI