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。

• Overexpression of desmin and vimentin in primary human bladder smooth muscle cells
  GSE127725Homo sapiens9 个样本2026-10-28

  Desmin and Vimentin overexpression differentially regulates smooth muscle gene expression in primary human bladder smooth muscle (HBSM) cells
• Detailed characterization of the immune response to Epstein-Barr virus in multiple sclerosis and following B cell depleting treatment
  GSE352228Homo sapiens24 个样本2026-10-27

  B-cell-depleting therapies are increasingly used for the treatment of multiple sclerosis (MS). Here, we characterize the impact of BCDT on humoral and cellular immune response to Epstein-Barr virus (EBV) in persons with MS (pwMS). We find that EBV viral load does not differ between pwMS and HC. By contrast, distinct differences are found in both humoral and cellular EBV-specific immunity in MS. EBV-specific antibody titres are increased in pwMS, whereas cellular immunity diverges toward lower CD8+ T cell reactivity against lytic antigens, including BZLF1. Notably, during periods of disease activity, both CD4+ and CD8+ T cell responses to lytic antigens tend to be higher. In addition, BZLF1-specific T cell clones recognizing the peptide RAKFKQLL were the most clonally expanded population in the intrathecal compartment of a pwMS with high CSF T cell counts. BCDT reduces EBV viral load and is associated with pronounced reduction in CD8+ T cell responses to all lytic EBV antigens. These findings delineate distinct alterations in EBV-specific immunity in MS and demonstrate that BCDT modulates both viral load and T cell responses. The data support a potential role for CD8+ T cell clones targeting lytic EBV proteins in MS pathogenesis.
• Transcriptome-wide mapping reveals an RNA-dependent mechanism of platinum cancer drugs. [ptRNAseq_A2780_Fractionation]
  GSE352212Homo sapiens24 个样本2026-10-27

  Clinically used small molecules have been predicted to off-target to RNAs. However, the extent of this interaction is small molecule cancer therapeutics have not been characterized. Here, we screened for anticancer small molecules for their RNA interactions and uncovered widespread RNA off-targeting. Cisplatin was found to be one among the RNA binders. We used it as a model agent to identify the specific transcripts it interacts with. To accomplish this, we developed Plat-RNAseq, a click-chemistry-mediated transcriptome-wide assay. Our results revealed that cisplatin binding was enriched at guanine-rich regions capable of forming RNA G-quadruplexes (rG4s). We found that the recruitment of cisplatin to rG4s partially contributed to its cytotoxicity, revealing a noncanonical mechanism of action for this widely used chemotherapeutic agent. This experiment applied PlatRNA-seq to chromatin-associated, nuclear and cytoplasmic RNA fractions to assess whether platinum binding occurs co-transcriptionally or on mature RNA.
• Transcriptome-wide mapping reveals an RNA-dependent mechanism of platinum cancer drugs. [ChIP-Seq_Spike-In]
  GSE352210Homo sapiens6 个样本2026-10-27

  Clinically used small molecules has been predicted to off-target to RNAs. However, the extend of this interaction is small molecule cancer therapeutics has not been characterized. Here, we screened for anticancer smalll molecules for their RNA interactions and uncovered widespread RNA off-targeting. Cisplatin was found to be one among the RNA binders. We used it as a model agent to identify the specific transcripts it interact with. To accomplish this, we developed Plat-RNAseq, a click-chemistry-mediated transcriptome-wide assay. Our results revealed that cisplatin binding was enriched at guanine-rich regions capable of forming RNA G-quadruplexes (rG4s) .We found that the recruitment of cisplatin to rG4s partially contributed to its cytotoxicity, revealing a noncanonical mechanism of action for this widely used chemotherapeutic agent. To assess the prevalence of RNA Pol II stalling in the cisplatin-target RNA we used RNA Pol II ChIP-seq and caculated the genome-wide stalling. This experiment uses RNA Pol II ChIP-seq with a Drosophila chromatin spike-in for quantitative normalization, unlike the previously deposited Pol II ChIP-seq (GSE309934), which was normalized to library size without a spike-in.
• GRHL2 loss alters redox homeostasis and attenuates erastin-induced ferroptosis in colorectal cancer cells
  GSE352117Homo sapiens6 个样本2026-10-27

  Redox homeostasis critically determines ferroptosis sensitivity, but the role of grainyhead-like 2 (GRHL2) in colorectal cancer remains unclear. RNA sequencing was performed to compare parental HCT116 cells with a CRISPR/Cas9-generated B8 GRHL2-KO clone and to define GRHL2-associated transcriptional changes relevant to redox homeostasis and ferroptosis sensitivity.
• Micro-C-TALE: BAC-based targeted high-resolution measurement of 3D chromatin interactions [Micro-C-TALE]
  GSE351910Homo sapiens2 个样本2026-10-27

  Chromosome conformation capture methods have greatly advanced our understanding of genome organization, but obtaining high-resolution interaction maps of selected genomic regions remains costly due to the sequencing requirements. Here, we introduce Micro-C-TALE, a new chromosome conformation capture method that combines Micro-C, which uses micrococcal nuclease to the resolution and sensitivity of chromatin interaction measurements, and C-TALE, which uses probes generated from bacterial artificial chromosomes (BACs) for targeted enrichment. This combination enables the generation of high-resolution interaction maps without requiring custom synthesis of capture oligonucleotides. We applied Micro-C-TALE to a 214 kb region in human HAP1 cells, obtaining detailed interaction maps with approximately ~5-6 million sequenced read pairs. Compared with published genome-wide Micro-C data, Micro-C-TALE yielded a higher amount of informative interactions within the targeted region despite ~550-fold lower sequencing depth. To evaluate the sensitivity of the method to fine-scale changes in genome organization, we introduced a CTCF binding site into the targeted region using CRISPR-Cas9. Comparing Micro-C-TALE to the restriction enzyme-based C-TALE, we found Micro-C yielded a ~5-fold higher fraction of informative reads and detected novel CTCF-mediated point interactions associated with the inserted CTCF site, which were barely discernible using C-TALE. Our results demonstrate that Micro-C-TALE provides a flexible and cost-effective approach for targeted high-resolution measurement of chromatin interactions, facilitating the investigation of fine-scale genome organization and its response to genetic perturbations.

  扰动筛选
• Micro-C-TALE: BAC-based targeted high-resolution measurement of 3D chromatin interactions [C-TALE]
  GSE351909Homo sapiens1 个样本2026-10-27

  Chromosome conformation capture methods have greatly advanced our understanding of genome organization, but obtaining high-resolution interaction maps of selected genomic regions remains costly due to the sequencing requirements. Here, we introduce Micro-C-TALE, a new chromosome conformation capture method that combines Micro-C, which uses micrococcal nuclease to the resolution and sensitivity of chromatin interaction measurements, and C-TALE, which uses probes generated from bacterial artificial chromosomes (BACs) for targeted enrichment. This combination enables the generation of high-resolution interaction maps without requiring custom synthesis of capture oligonucleotides. We applied Micro-C-TALE to a 214 kb region in human HAP1 cells, obtaining detailed interaction maps with approximately ~5-6 million sequenced read pairs. Compared with published genome-wide Micro-C data, Micro-C-TALE yielded a higher amount of informative interactions within the targeted region despite ~550-fold lower sequencing depth. To evaluate the sensitivity of the method to fine-scale changes in genome organization, we introduced a CTCF binding site into the targeted region using CRISPR-Cas9. Comparing Micro-C-TALE to the restriction enzyme-based C-TALE, we found Micro-C yielded a ~5-fold higher fraction of informative reads and detected novel CTCF-mediated point interactions associated with the inserted CTCF site, which were barely discernible using C-TALE. Our results demonstrate that Micro-C-TALE provides a flexible and cost-effective approach for targeted high-resolution measurement of chromatin interactions, facilitating the investigation of fine-scale genome organization and its response to genetic perturbations.

  扰动筛选
• Spatial transcriptomic profiling of human left ventricular tissue in ischaemic heart disease and dilated cardiomyopathy
  GSE351778Homo sapiens2 个样本2026-10-27

  Spatially resolved single-cell gene expression profiling was performed on fresh-frozen human left ventricular tissue from one ischaemic heart disease (IHD) and one dilated cardiomyopathy (DCM) specimen. The Xenium Human Multi-Tissue and Cancer Gene Expression panel supplemented with 100 custom probes was used to characterise cardiomyocytes and cardiac fibroblasts and investigate spatial relationships between fibroblast subpopulations and cardiomyocyte.

  单细胞空间转录组
• Transcriptomics of human fetal microglia infected with HIV-1
  GSE351613Homo sapiens36 个样本2026-10-27

  This SuperSeries is composed of the SubSeries listed below.

  SuperSeries
• Transcriptomics of human fetal microglia infected with HIV-1 [V8 RNA-Seq]
  GSE351612Homo sapiens12 个样本2026-10-27

  Microglia act as HIV reservoirs in the brain and contribute to the development of HIV-associated neurocognitive disorders. Understanding the pathobiology of HIV-infected microglia is therefore essential. Here, we examined the transcriptome of primary microglia infected ex vivo with HIV-1. Analyses reveal a significant expression modulation of DNA/cell cycle, cellular stress-related, as well as non-membrane bounded organelle assembly-related genes, and a broad effect on microRNA expression. MicroRNA-23b is identified among upregulated microRNAs in HIV-1-infected microglia, and the downregulated g3bp2 mRNA validated as its target. G3BP2 is a component of stress granules (SGs), which serve as antiviral and proinflammatory platforms. MicroRNA-23b mimics reduce both SG assembly and G3BP2 expression in arsenite (As)-treated monocyte-derived microglial cells (MDMi), and few SGs aggregate in infected MDMi in response to As-mediated stress. MicroRNA-23b inhibitors partially re-establish SG formation and reduce HIV-1 replication and spread. Thus, microRNA-23b induction enables HIV-1 to counter SG assembly in infected microglia, a host response that restricts HIV-1 replication and ensuing neuropathogenesis
• Transcriptomics of human fetal microglia infected with HIV-1 [V6 miRNA-Seq]
  GSE351611Homo sapiens24 个样本2026-10-27

  Microglia act as HIV reservoirs in the brain and contribute to the development of HIV-associated neurocognitive disorders. Understanding the pathobiology of HIV-infected microglia is therefore essential. Here, we examined the transcriptome of primary microglia infected ex vivo with HIV-1. Analyses reveal a significant expression modulation of DNA/cell cycle, cellular stress-related, as well as non-membrane bounded organelle assembly-related genes, and a broad effect on microRNA expression. MicroRNA-23b is identified among upregulated microRNAs in HIV-1-infected microglia, and the downregulated g3bp2 mRNA validated as its target. G3BP2 is a component of stress granules (SGs), which serve as antiviral and proinflammatory platforms. MicroRNA-23b mimics reduce both SG assembly and G3BP2 expression in arsenite (As)-treated monocyte-derived microglial cells (MDMi), and few SGs aggregate in infected MDMi in response to As-mediated stress. MicroRNA-23b inhibitors partially re-establish SG formation and reduce HIV-1 replication and spread. Thus, microRNA-23b induction enables HIV-1 to counter SG assembly in infected microglia, a host response that restricts HIV-1 replication and ensuing neuropathogenesis
• Synapse-seq reveals cytotoxic CD4+ T cell suppression of human antibody responses
  GSE351507Homo sapiens22 个样本2026-10-27

  Deciphering the molecular dialogue between cells is central to understanding how immune responses are orchestrated. Here we applied Synapse‐seq, a new image‐enabled cell interaction sorting and transcriptomic profiling approach, to characterize CD4+ T-B cell synaptic interactions in human spleen organoids. We identified B cells synapsing with FOXP3+ regulatory T cells (Tregs) expressing high levels of perforin and granzymes A and B, indicating that cytotoxicity is a major mechanism of CD4+ Treg suppression of specific B cells. Antigen-specific Synapse-seq revealed opposing phenotypes of viral and autoreactive T-B interactions and identified a hemagglutinin-specific TCR-BCR pair in a human immune system. Both CD3+ and CD4+ T cell-specific knockouts of cytotoxic genes robustly increased antibody responses against both nuclear autoantigens and viral antigens. Consistent with these findings, patients with systemic lupus erythematosus (SLE) exhibited a significant enrichment of cytotoxic CD4+ Tregs. Our findings support cytotoxicity as a dominant way CD4+ T cells regulate B cells and antibody responses. More broadly, we suggest Synapse-seq as a generalizable method to characterize cell interactions without requiring cell engineering.
• Study of LETT@MVs‑induced ferroptosis in tumor cells via supplementation of PUFA
  GSE351467Homo sapiens4 个样本2026-10-27

  Ferroptosis represents a promising therapeutic strategy for cancer, yet its anti‑tumor efficacy is largely limited by insufficient polyunsaturated fatty acids (PUFA) within the tumor microenvironment (TME). Aloe vera thylakoid membranes, naturally rich in PUFA, are an ideal source to facilitate robust lipid peroxidation. To address biological delivery obstacles, we constructed tumor‑targeting biomimetic microvesicles (LETT@MVs) by engineering aloe‑thylakoid‑derived microvesicles (TDMVs) with the multifunctional peptide LETT, which enables tumor‑targeted delivery and lysosomal escape. We systematically characterized the influences of LETT@MVs on hepatocellular carcinoma (HCC) cells, including cell viability, vasculogenic mimicry (VM) formation, lipid peroxidation and ferroptosis in vitro. Antitumor potency and biosafety were further validated using an orthotopic HCC mouse model. Mechanistically, multi‑omics strategies combining bulk RNA‑seq, metabolomics and scRNA‑seq were applied to decipher underlying molecular events. LETT@MVs were effectively internalized by HCC cells and successfully escaped lysosomal degradation. Taking advantage of endogenous PUFA stored in thylakoid components, LETT@MVs triggered potent lipid peroxidation and ferroptosis, meanwhile remodelled the extracellular matrix (ECM) to suppress vasculogenic mimicry. In orthotopic HCC mice, LETT@MVs markedly retarded tumor growth via ferroptosis induction and VM repression without obvious safety risks. Integrated multi‑omics data demonstrated that LETT@MVs rewired transcriptional and metabolic profiles of HCC cells, driving highly‑metabolic tumor cells toward ferroptotic stress status and generating near‑death cell subpopulations. Collectively, our work validates that aloe‑thylakoid‑originated biomimetic nanoplatform can trigger robust tumor ferroptosis through PUFA supplementation, providing new clues to conquer ferroptosis resistance and advance therapeutic interventions for hyper‑metabolic tumors.

  单细胞
• Genomic and Immune Profiling Characterizes Immune Heterogeneity and a TIGIT-Associated Subtype in Intrahepatic Cholangiocarcinoma
  GSE350183Homo sapiens164 个样本2026-10-27

  Background and Aims: Intrahepatic cholangiocarcinoma (iCCA) is characterised by marked molecular and microenvironmental heterogeneity and moderate response to immunotherapy. We aimed to define the genomic and spatial determinants of immune checkpoint activity in iCCA and their association with clinical outcome. Approach and Results: We performed integrated transcriptomic, DNA panel sequencing, and multiplex immunohistochemistry analyses in a cohort of 144 patients with iCCA. Tumors were classified according to STIM-defined microenvironmental subtypes. Spatially resolved immune profiling was conducted across tumor core, stroma, invasive margin, and adjacent liver. Immune checkpoint expression, cellular proximity, and clinical outcome were analysed using Cox regression and Kaplan-Meier methods. TIGIThigh tumors were further characterised by differential gene expression and pathway enrichment analyses. STIM classification stratified tumors into inflamed (47%) and non-inflamed (53%) subtypes with distinct survival outcomes and genomic profiles. Recurrent alterations in CDKN2A/B, TP53, MTAP, and BAP1 showed subtype-specific enrichment and prognostic relevance. Spatial immune profiling revealed compartment-specific distributions of T cells and immune checkpoints, with predominance of TIGIT and PD-1 expression in stromal and marginal regions. Most tumor-infiltrating T cells lacked inhibitory receptor expression, while co-expression of multiple checkpoints was uncommon. TIGIThigh tumors displayed coordinated activation of immune effector, antigen presentation, and interferon signalling pathways, alongside enrichment of distinct genomic alterations, defining an immune-activated molecular subtype. Conclusions: Integrated genomic and spatial immune profiling reveals pronounced context-dependent heterogeneity of immune checkpoint regulation in iCCA. TIGIT delineates an immune-activated subtype with distinct molecular features, providing a potential biomarker framework for patient stratification and rational immunotherapeutic targeting.

  空间转录组
• ScRNA-seq reveals cellular heterogeneity in urethral stricture
  GSE347480Homo sapiens6 个样本2026-10-27

  Urethral strictures are characterized by fibrotic scar tissue formation in the urethra, leading to difficulties in urination and potential renal dysfunction. The cellular microenvironment contributes to stenosis. However, the heterogeneity of key cell types hinders our understanding of this disease. Single-cell RNA sequencing was performed on three urethral scar tissues and three normal urethral tissues. First, the main cell types and sample heterogeneity were identified. Transcription factor (TF) and enrichment analyses were used to characterize the transcriptional regulation and metabolic patterns of fibroblasts and mast cells. Finally, CellChat was used to elucidate intercellular communication networks in urethral scar tissues. Of the eight cell types detected, fibroblasts, mast cells, and macrophages were major contributors to urethral scar tissue. These cells were categorized into seven (FB0–FB6), two (Mast0 and Mast1), and nine (Macro0-Macro8) subclusters, respectively, based on heterogeneity. Urethral scar tissue exhibited increased proportions of FB3 fibroblast, Mast1 mast cell, Macro1, and Macro7 counts. Marker genes of these subclusters facilitated the dysregulation of fibrosis through various biological processes, including cell adhesion and extracellular matrix organization. Additionally, screening of the dysregulation of multiple TFs and metabolic pathways revealed potential candidate TFs—ETS1 (from FB3) and SMAD3 (from Mast1)—associated with fibrosis. Furthermore, communication substantially increased between fibroblasts and other cells, and between Macro1 or Macro7 and other macrophage subclusters or fibroblasts in urethral scar tissue. We revealed the transcriptional characteristics of key cells involved in the fibrogenesis of urethral stricture, which elucidates the pathogenesis of urethral stenosis and advances the exploration of therapeutic targets.

  单细胞
• Hi-C analysis of HCT-116 and K562 cells
  GSE339260Homo sapiens2 个样本2026-10-27

  We performed Hi-C analysis on two common cancer cell lines.
• Regulatory T Cell Instability Facilitates Blood-Brain Barrier Disruption via the β-catenin-Tight Junctions Axis, Leading to Perioperative Neurocognitive Disorders
  GSE337348Homo sapiens12 个样本2026-10-27

  Perioperative neurocognitive disorders (PND) are significant neurological complications in elderly surgical patients, yet the underlying immune-mediated mechanisms remain elusive. Blood-brain barrier (BBB) disruption is increasingly recognized as a critical neurovascular event in PND and may result from perioperative immune dysregulation. Regulatory T cells (Tregs) are key mediators of neurovascular homeostasis and BBB integrity. We therefore investigated whether perioperative Treg instability contributed to BBB disruption and PND. Single-cell transcriptomic profiling of perioperative PBMCs from elderly surgical patients revealed marked remodeling of the CD4+ T cell compartment, characterized by disproportionate Treg loss and functional destabilization. Tregs shifted from resting and immunosuppressive states toward an inflammatory phenotype, accompanied by reduced expression of regulatory and tissue-reparative genes, including FOXP3, CTLA4, PDCD1, and AREG. Comparative transcriptomic analysis of Tregs identified 34 dexmedetomidine-corrected genes, with CTNNB1, encoding β-catenin, emerging as the dominant hub within the protein-protein interaction network. These findings implicated impaired β-catenin signaling as a central driver of perioperative Treg destabilization. Mouse hippocampal scRNA-seq revealed postoperative endothelial remodeling characterized by reduced S1pr1 and Cldn5 and increased Icam1 expression. In a murine PND model, β-catenin activation restored postoperative Treg abundance and regulatory gene expression while preserving hippocampal endothelial barrier programs, as evidenced by increased S1PR1 and Claudin-5 and reduced ICAM1 expression. These protective effects were abolished by PC61-mediated Treg depletion, indicating a Treg-dependent mechanism. Furthermore, restoration of Treg homeostasis with recombinant PD-L1 preserved ultrastructural BBB integrity, reduced Evans blue-defined BBB leakage, attenuated hippocampal neuroinflammation, and improved cognitive function. These findings identify perioperative Treg instability as a key immune driver of BBB disruption and cognitive dysfunction in PND, and establish Treg β-catenin signaling as a potential therapeutic target for preserving neurovascular integrity.

  单细胞
• T and B cells recognize splicing-derived neutrophil neoantigens in lupus
  GSE327018Homo sapiens100 个样本2026-10-27

  This SuperSeries is composed of the SubSeries listed below.

  SuperSeries
• Bulk RNA-seq of neutrophils from systemic lupus erythematosus, rheumatoid arthritis, Sjogren syndrome, and healthy control samples
  GSE326777Homo sapiens78 个样本2026-10-27

  This study profiled bulk RNA-seq from human neutrophil samples derived from individuals with systemic lupus erythematosus, rheumatoid arthritis, Sjogren syndrome, and healthy controls. Total RNA was extracted and sequenced to characterize transcriptomic features across disease groups. Raw and normalized gene-level count matrices, gene annotation, and sample-level metadata are provided.
• Bulk RNA-seq of monocytes from systemic lupus erythematosus samples
  GSE326771Homo sapiens10 个样本2026-10-27

  This study profiled bulk RNA-seq from human monocyte samples derived from individuals with systemic lupus erythematosus. Total RNA was extracted and sequenced to characterize transcriptomic features in SLE monocytes. Raw gene-level count matrices, gene annotation, and sample-level metadata are provided.
• Bulk RNA-seq of IFN-treated and untreated healthy control neutrophils
  GSE326770Homo sapiens12 个样本2026-10-27

  This study profiled bulk RNA-seq from human neutrophils derived from healthy control donors under untreated and IFN-treated conditions. Total RNA was extracted and sequenced to characterize transcriptional responses associated with IFN exposure. Raw and normalized gene-level count matrices, along with sample-level metadata and gene annotation files, are provided.
• 3D genome remodeling directs in vitro human hematopoietic development and predicts disease trait genetics
  GSE311714Homo sapiens14 个样本2026-10-27

  The 3D genomic architecture provides a regulatory scaffold for cell fate transitions, yet how chromatin architecture directs human hematopoietic development remains poorly understood. The endothelial-to-hematopoietic transition (EHT) is the developmental gateway by which specialized hemogenic endothelial cells generate definitive hematopoietic stem and progenitor cells (HSPCs), which go on to support blood cell production throughout mammalian life. Understanding mechanisms that regulate EHT is critical for blood disease modeling and regenerative medicine applications. Using a human induced pluripotent stem-cell (iPSC) hematopoiesis model, we combined single-nucleus RNA-seq, ATAC-seq, and Hi-C to chart chromatin reorganization during hemogenic specification and EHT. Hierarchical reorganization of topologically associating domains (TADs) and sub-TAD structures accompany the morphological conversion of endothelial sheets into HSPCs. Dynamic TAD and sub-TAD reorganization precedes transcriptional activation of key hematopoietic regulators (e.g., RUNX1, CEBPA), revealing a structural logic by which genome topology anticipates formation of cis-regulatory elements and transcription factor programs that control hematopoietic development. For example, we identify modulation of dynein and kinesin molecular motor genes during EHT. Functional dynein inhibition promotes EHT, likely through unopposed activities of kinesin motors. Integration of single cell data with Hi-C and genome-wide association study (GWAS) loci reveals enrichment for blood and immune trait variants, connecting 3D genome remodeling during in vitro hematopoiesis to in vivo human disease genetics. Together, these findings define the regulatory architecture of blood cell emergence and establish iPSC differentiation as a tractable platform for interrogating 3D genome principles in human development and disease. More broadly, our integrated data across rare developmental cell types helps define 3D chromatin regulatory architecture that underlies human GWAS variation.

  单细胞
• p53 preserves chromosome stability in dividing cells under hypo-osmotic stress
  GSE311220Homo sapiens30 个样本2026-10-27

  Cells respond to frequent osmotic stress to maintain structural integrity and function. Whereas acute volume regulation is well-known, the cellular response to prolonged osmotic stress and its long-term consequences remain poorly understood. In this study, we investigate how lasting hypo-osmotic stress influences cell proliferation and the associated cellular response. We observe that cells undergoing their first division under hypo-osmotic stress experience delayed mitotic entry, lengthened mitotic duration, elevated mitotic errors and aneuploidy formation. However, continued cell division is halted through a p53/p21-dependent G1 arrest. p53 activation occurs post-mitotically and is associated with loss of perichromosomal layer (PCL), defective chromosome decondensation and impaired nuclear expansion in daughter cells after mitotic exit. We show that the altered nuclear size dynamics lead to nuclear accumulation of p53 and activation of downstream gene expression. These findings uncover a mechanosensitive, p53-mediated mechanism that safeguards chromosome integrity by suppressing erroneous mitosis under hypo-osmotic stress.
• Chemically Defined Differentiation of Human PSCs to Definitive Hematopoietic Progenitors
  GSE304432Homo sapiens21 个样本2026-10-27

  This study investigates hematopoietic differentiation of human pluripotent stem cells (hPSCs) using a chemically defined differentiation system. RNA-seq was used to characterize cell populations generated during differentiation, including adherent supportive cells and suspension hematopoietic populations. The newly submitted samples provide additional transcriptomic profiling of FACS-sorted CD34+CD38-CD45RA-CD90+CD49f+ cells isolated from the suspension hematopoietic population and complement the other samples .
• SAA-expressing hepatocytes as a key liver cell population in Alcohol associated Hepatitis
  GSE304325Homo sapiens13 个样本2026-10-27

  This study describes the dynamics of cellular heterogeneity during the progression of ALD to AH at a single cell level. Moreover, we have identified the specific subpopulations enriched in AH. This condition is characterized by an expansion of proinflammatory SAA+ hepatocytes, which strongly interact with hyperactivated neutrophils, suggesting a potential mechanism that could contribute to the exacerbated inflammation that characterizes this disease.

  单细胞
• Effect of senescent cells on macrophage polarisation
  GSE296922Homo sapiens10 个样本2026-10-27

  Senescent cells (SCs) accumulate with age and injury and express a pro-inflammatory/pro-fibrotic secretome, termed the senescence-associated secretory phenotype (SASP). Hence, accumulation of senscent cells can lead to inflammation and organ fibrosis. To investigate effects of SASP factors on macrophage polarisation macrophages matured from healthy donor blood monocytes were exposed to control or senescent cell conditioning media for 24 hours. Senescent cell media was derived from human proximal tubular epithelial cells (PTECs) exposed to 10 Gy of ionising radiation to induce senescence in vitro.
• 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