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。

• Microglial lipid signaling drives glioblastoma invasion and represents a therapeutic vulnerability
  GSE348401Mus musculus8 个样本2026-10-27

  Glioblastoma (GBM) is characterized by diffuse infiltration into the surrounding brain, limiting complete surgical resection, the strongest determinant of patient survival. The mechanisms driving this invasive growth remain incompletely understood. Here, we identify a lipid-mediated paracrine signaling axis through which tumor-associated microglia/macrophages promote glioma invasion. Integrating single-cell transcriptomics, spatial lipidomics, and functional perturbation across mouse models and human GBM samples, we show that invading tumor cells engage and reprogram myeloid cells via CSF1R–PI3K signaling. This induces lipid metabolic reprogramming and secretion of bioactive lipids, including lysophosphatidylcholines (LPCs) and lysophosphatidic acids (LPAs), which promote GBM invasion through distinct downstream pathways. Disruption of this myeloid–GBM axis, reduces lipid secretion and suppresses invasion. Targeting downstream LPA–LPAR or YAP/TAZ signaling further constrains invasion in a context-dependent manner. Together, these findings define a lipid-driven circuit linking the tumor microenvironment to glioma invasion and identify strategies to reduce infiltration and improve surgical resection.

  单细胞空间转录组扰动筛选
• Macrophage lipid signaling drives glioblastoma invasion and represents a therapeutic vulnerability
  GSE348147Mus musculus16 个样本2026-10-27

  Glioblastoma (GBM) is characterized by diffuse infiltration into the surrounding brain, limiting complete surgical resection, the strongest determinant of patient survival. The mechanisms driving this invasive growth remain incompletely understood. Here, we identify a lipid-mediated paracrine signaling axis through which tumor-associated microglia/macrophages promote glioma invasion. Integrating single-cell transcriptomics, spatial lipidomics, and functional perturbation across mouse models and human GBM samples, we show that invading tumor cells engage and reprogram myeloid cells via CSF1R–PI3K signaling. This induces lipid metabolic reprogramming and secretion of bioactive lipids, including lysophosphatidylcholines (LPCs) and lysophosphatidic acids (LPAs), which promote GBM invasion through distinct downstream pathways. Disruption of this myeloid–GBM axis, reduces lipid secretion and suppresses invasion. Targeting downstream LPA–LPAR or YAP/TAZ signaling further constrains invasion in a context-dependent manner. Together, these findings define a lipid-driven circuit linking the tumor microenvironment to glioma invasion and identify strategies to reduce infiltration and improve surgical resection.

  单细胞空间转录组扰动筛选
• Glioma regulates GABAergic signaling to drive hyperactivity and tumor progression [RNA-seq]
  GSE348105Mus musculus6 个样本2026-10-27

  Recent studies identified bi-directional communication between neurons and glioma tumors as a key driver of hyperexcitability and malignant progression. While much of this work has focused on the activity of excitatory neurons, roles for inhibitory neurons remain poorly defined. Using in-vivo screening approaches in autochthonous glioma models, we found that loss of a GABA transporter (Slc6a1) enhanced glioma progression, promoted network hyperactivity, and influenced tonic GABA release by tumors. Mechanistically, we show that glioma tumors influence the activity of inhibitory neurons and their subsequent stimulation suppresses tumor growth. Further screening of these phenomena identified Diazepam Binding Inhibitory (DBI), a secreted negative allosteric modulator of GABA-A, as a link between glioma related hyperexcitability and proliferation that functions through modulating inhibitory neuronal signaling. Collectively, our findings indicate that glioma tumors utilize multiple mechanisms to manipulate the activity of inhibitory neurons as a means to drive network hyperactivity, which ultimately facilitates malignant progression.
• Glioma regulates GABAergic signaling to drive hyperactivity and tumor progression
  GSE348034Mus musculus4 个样本2026-10-27

  Recent studies identified bi-directional communication between neurons and glioma tumors as a key driver of hyperexcitability and malignant progression. While much of this work has focused on the activity of excitatory neurons, roles for inhibitory neurons remain poorly defined. Using in-vivo screening approaches in autochthonous glioma models, we found that loss of a GABA transporter (Slc6a1) enhanced glioma progression, promoted network hyperactivity, and influenced tonic GABA release by tumors. Mechanistically, we show that glioma tumors influence the activity of inhibitory neurons and their subsequent stimulation suppresses tumor growth. Further screening of these phenomena identified Diazepam Binding Inhibitory (DBI), a secreted negative allosteric modulator of GABA-A, as a link between glioma related hyperexcitability and proliferation that functions through modulating inhibitory neuronal signaling. Collectively, our findings indicate that glioma tumors utilize multiple mechanisms to manipulate the activity of inhibitory neurons as a means to drive network hyperactivity, which ultimately facilitates malignant progression.
• 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
• Molecular Imaging of the TGF-β Activating Integrin avb6 Detects Chronic Lung Allograft Dysfunction
  GSE346597Mus musculus2 个样本2026-10-27

  TGF-β-activating integrins promote solid-organ fibrosis, suggesting their potential as disease markers. Chronic lung allograft dysfunction (CLAD), a progressive fibrotic complication that limits lung transplant survival, is driven by intragraft TGF-β activation. However, TGF-β-activating integrin expression patterns remain undefined in lung transplants. Single-cell RNA sequencing and proteomic analysis of tissue specimens from a mouse CLAD model and human explanted lungs with CLAD revealed high levels of the TGF-β-activating integrin αvβ6, primarily localized to fibrosis-associated Keratin 8+ alveolar transitional epithelial cells, which were greatly reduced in tolerant lungs. Molecular imaging with a newly optimized positron emission tomography radiotracer specific for avb6, [64Cu]Cu-DOTA-A20-K16R, showed significantly higher uptake in CLAD than in tolerant transplants. [64Cu]Cu-DOTA-A20-K16R activity was also reduced by experimental treatments that lowered avb6 expression and inhibited CLAD severity. Finally, [64Cu]Cu-DOTA-A20-K16R autoradiographic analysis of human explanted lungs with CLAD showed elevated activity that correlated with increased avb6 expression. Collectively, these findings illustrate the potential utility of αvβ6 molecular imaging for detecting CLAD pathogenesis.

  单细胞
• A single-cell RNA sequencing atlas of postnatal ovarian development in dairy goats
  GSE345824Capra hircus10 个样本2026-10-27

  Postnatal ovarian development is a critical process that establishes ovarian reserve and determines female reproductive capacity. However, the cellular and molecular dynamics underlying early folliculogenesis in livestock species remain poorly characterized. Here, we generated a single-cell RNA sequencing dataset of dairy goat ovaries collected at postnatal days 4, 20, and 60, representing distinct stages of follicular development. This dataset comprises 90,770 high-quality single cells and 20,412 gene features, including six major ovarian cell populations with distinct transcriptional signatures. The dataset provides comprehensive transcriptomic profiles of oocytes, granulosa cells, theca cells, stromal cells, endothelial cells, and immune cells during early ovarian development. Cell-level annotations, sample information, and gene expression count matrices are provided to facilitate investigation of ovarian cellular heterogeneity, folliculogenesis, and cell-cell communication.

  单细胞细胞图谱
• YS-10 Exerts Therapeutic Effects on Radiation-Induced Testicular Damage
  GSE345816Rattus norvegicus9 个样本2026-10-27

  This study comparatively analyzed RNA‑sequencing data of rat testicular tissues from the control group, radiation‑induced injury model group, and treatment group
• Single-cell profiling of microglia transcriptomes transduced by the AAV-MSRE tool
  GSE345675Mus musculus9 个样本2026-10-27

  This study profiles the transcriptomic responses of microglia transduced with the AAV-MSRE tool at single-cell resolution. Single-cell RNA sequencing was used to characterize transduced microglial populations, assess their molecular identities, and evaluate transcriptional changes associated with AAV-MSRE delivery. These data provide a resource for examining the cellular specificity and transcriptomic impact of AAV-MSRE-mediated targeting in microglia.

  单细胞
• Transcriptomic profiling of M1-like and M2-like mouse bone marrow-derived macrophages
  GSE344431Mus musculus6 个样本2026-10-27

  Macrophage activation states are involved in intestinal inflammation and tissue remodeling, but the transcriptional programs linking macrophage polarization to ulcerative colitis-associated molecular changes remain incompletely characterized. In this study, primary bone marrow-derived macrophages from mice were polarized toward M1-like or M2-like states and subjected to bulk RNA sequencing. M1-like polarization was induced using lipopolysaccharide and interferon-gamma, whereas M2-like polarization was induced using interleukin-4 and interleukin-13. Three biological replicates were analyzed per group. The resulting transcriptomes were used to identify macrophage polarization-related genes and were subsequently integrated with ulcerative colitis macrophage single-cell transcriptomic and circulating proteomic evidence to prioritize disease-associated macrophage candidates.

  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.
• VIPP1/pTAC4 indirectly supports PEP accumulation and RpoB occupancy on chloroplast DNA
  GSE339035Arabidopsis thaliana108 个样本2026-10-27

  Chloroplast DNA together with proteins and RNAs form nucleoids, where genomes are stored, replicated and expressed. VIPP1/pTAC4 is a conserved membrane-associated protein previously identified in chloroplast nucleoid fractions, suggesting a possible role of this protein in linking plastid DNA, thylakoid membranes, and transcription. Here, we used plastid ChIP-seq to test whether VIPP1/pTAC4 directly affects plastid-encoded RNA polymerase (PEP) association with chloroplast DNA. Loss of VIPP1/pTAC4 caused a genome-wide reduction in RpoB occupancy, but we found no evidence of VIPP1/pTAC4 binding to chloroplast DNA. Likewise, the VIPP1-interacting protein VIA1 did not detectably bind chloroplast DNA, but was not required for normal RpoB occupancy. Comparison with other non-photosynthetic mutants and immunoblot analyses indicated that reduced PEP occupancy in ptac4 is likely an indirect consequence of impaired chloroplast development and reduced PEP core subunit accumulation. These findings challenge a direct role of VIPP1/pTAC4 in the chloroplast nucleoid and highlight the pleiotropic effects of chloroplast biogenesis defects on plastid transcription.
• RNA-seq data from hypothalamic tissues of male and female Japanese quail embryos.
  GSE338413Coturnix japonica12 个样本2026-10-27

  Total RNA was extracted from E12 hypothalamic tissues of male, female, vehicle-treated male, and EB-treated male embryos. Transcriptomes were analyzed by RNA sequencing.
• 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.
• C-Met controls CD8+ T cell-mediated anti-tumor immunity
  GSE319458Mus musculus12 个样本2026-10-27

  The hepatocyte growth factor (HGF)/c-Met axis is a major oncogenic pathway, yet how it shapes cytotoxic T cell function remains unclear. Here, we show that c-Met identifies a transcriptionally and functionally distinct subset of tumor-reactive CD8⁺ T cells, while HGF suppresses their effector function. Using Pmel-1 CD8⁺ T cells and a CD8⁺ T cell–specific c-Met knockout, RNA sequencing revealed c-Met⁺ CTLs are enriched for cytotoxic, interferon, TCR signaling, and inflammatory programs, whereas HGF induces immunoregulatory pathways, including IL-13–STAT3/STAT6, and downregulates effector genes. Functionally, c-Met⁺ CTLs displayed enhanced antigen-specific killing and superior tumor control, with increased degranulation and lower inhibitory checkpoint expression. HGF or c-Met deficiency restrained these responses. These findings identify c-Met as a marker of highly cytotoxic CD8⁺ T cells and reveal HGF as a key suppressor of CTL function in cancer providing a mechanistic framework for HGF-driven immune suppression in cancer.
• A single cell atlas defines perinatal factors that drive murine bone marrow development
  GSE318094Mus musculus2 个样本2026-10-27

  Processes that direct initial colonization and maturation of the bone marrow remain elusive, despite their importance to lifelong hematopoiesis. Bone marrow mesenchymal and stromal cell (BMSC) maturation must establish supportive hematopoietic niches prior to the recruitment and colonization of hematopoietic stem cells (HSCs). Here, we define the identity of murine BMSC progenitors and temporal nature of marrow colonization through a single cell atlas spanning late gestation through 18 months of age. We define progenitor cells and developmental trajectories for Cxcl12-abundant reticular (CAR) cells and osteoblasts within the marrow, including the emergence of direct and secreted signaling modalities that impact HSC quiescence and regenerative capacity. We further identify temporal changes in Early B Cell Factor (Ebf) 1-3 transcription factor expression and activity that correlate with niche establishment. These transcriptional activities relate to change to changes in systemic physiology, including metabolic, inflammatory, and hypoxic signaling, that direct CAR cell emergence after birth in mice. These findings provide unprecedented resolution to the colonization and maturation of the murine bone marrow environment.

  单细胞细胞图谱
• CEBPA-Induced Trophectoderm-like Cells from Pluripotent Stem Cells Enable Modeling of Trophoblast Lineage Specification [scRNA-Seq]
  GSE315752Mus musculus1 个样本2026-10-27

  Trophoblast lineages are essential for placental development and play indispensable roles in mammalian development. However, the regulatory mechanisms governing trophoblast lineage specification, particularly trophectoderm formation, remain elusive. Here, we show that transient overexpression of the transcription factor Cebpa in mouse pluripotent stem cells efficiently generates trophectoderm-like cells that recapitulate key transcriptional features of trophectoderm. These trophectoderm-like cells can be further induced to form trophoblast organoids and exhibit developmental competence to generate all trophoblast lineages in vitro. Mechanistically, Cebpa overexpression drives extensive epigenetic reprogramming toward a trophectoderm-like state, including global remodeling of chromatin accessibility and coordinated changes in H3K4me3 and H3K27me3 histone modifications. CUT&RUN analyses further reveal binding of CEBPA to multiple trophectoderm-specific enhancers. Together, our findings identify Cebpa as a potent inducer of trophectoderm potential and establish a new platform for modeling trophectoderm lineage specification in vitro.

  单细胞
• CEBPA-Induced Trophectoderm-like Cells from Pluripotent Stem Cells Enable Modeling of Trophoblast Lineage Specification
  GSE315751Mus musculus28 个样本2026-10-27

  Trophoblast lineages are essential for placental development and play indispensable roles in mammalian development. However, the regulatory mechanisms governing trophoblast lineage specification, particularly trophectoderm formation, remain elusive. Here, we show that transient overexpression of the transcription factor Cebpa in mouse pluripotent stem cells efficiently generates trophectoderm-like cells that recapitulate key transcriptional features of trophectoderm. These trophectoderm-like cells can be further induced to form trophoblast organoids and exhibit developmental competence to generate all trophoblast lineages in vitro. Mechanistically, Cebpa overexpression drives extensive epigenetic reprogramming toward a trophectoderm-like state, including global remodeling of chromatin accessibility and coordinated changes in H3K4me3 and H3K27me3 histone modifications. CUT&RUN analyses further reveal binding of CEBPA to multiple trophectoderm-specific enhancers. Together, our findings identify Cebpa as a potent inducer of trophectoderm potential and establish a new platform for modeling trophectoderm lineage specification in vitro.
• CEBPA-Induced Trophectoderm-like Cells from Pluripotent Stem Cells Enable Modeling of Trophoblast Lineage Specification [RNA-Seq]
  GSE315750Mus musculus14 个样本2026-10-27

  Trophoblast lineages are essential for placental development and play indispensable roles in mammalian development. However, the regulatory mechanisms governing trophoblast lineage specification, particularly trophectoderm formation, remain elusive. Here, we show that transient overexpression of the transcription factor Cebpa in mouse pluripotent stem cells efficiently generates trophectoderm-like cells that recapitulate key transcriptional features of trophectoderm. These trophectoderm-like cells can be further induced to form trophoblast organoids and exhibit developmental competence to generate all trophoblast lineages in vitro. Mechanistically, Cebpa overexpression drives extensive epigenetic reprogramming toward a trophectoderm-like state, including global remodeling of chromatin accessibility and coordinated changes in H3K4me3 and H3K27me3 histone modifications. CUT&RUN analyses further reveal binding of CEBPA to multiple trophectoderm-specific enhancers. Together, our findings identify Cebpa as a potent inducer of trophectoderm potential and establish a new platform for modeling trophectoderm lineage specification in vitro.
• 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.
• Endogenous variability in transcription factor concentrations shapes their genome-wide occupancy [ATAC-seq]
  GSE308326Mus musculus8 个样本2026-10-27

  The control of transcription factor (TF) concentrations is crucial for the precise regulation of gene expression and cell fate decisions during development. Yet, TF concentrations can display substantial temporal fluctuations and intercellular variations. How TF levels quantitatively shape genome-wide occupancy patterns remains largely unexplored. Here, we systematically investigate how physiological fluctuations in the concentrations of the pluripotency TFs OCT4, SOX2, and NANOG impact their genomic binding profiles in mouse embryonic stem cells. We uncover distinct concentration-dependent binding behaviors for each TF. NANOG occupancy increased monotonously with its concentration, even though a common set of regions made accessible by OCT4 and SOX2 were highly and uniformly bound at all NANOG concentrations. In contrast, SOX2 occupancy does not increase with its concentrations, while OCT4 displayed an intermediate behavior. Our results challenge the notion that TF binding follows simple mass-action dynamics and reveal a core set of pluripotency regions that are bound by all three TFs at all TF concentrations, revealing how pluripotency can be maintained despite marked fluctuations in core pluripotency TFs.
• Endogenous variability in transcription factor concentrations shapes their genome-wide occupancy [ChIP-seq]
  GSE308325Mus musculus44 个样本2026-10-27

  The control of transcription factor (TF) concentrations is crucial for the precise regulation of gene expression and cell fate decisions during development. Yet, TF concentrations can display substantial temporal fluctuations and intercellular variations. How TF levels quantitatively shape genome-wide occupancy patterns remains largely unexplored. Here, we systematically investigate how physiological fluctuations in the concentrations of the pluripotency TFs OCT4, SOX2, and NANOG impact their genomic binding profiles in mouse embryonic stem cells. We uncover distinct concentration-dependent binding behaviors for each TF. NANOG occupancy increased monotonously with its concentration, even though a common set of regions made accessible by OCT4 and SOX2 were highly and uniformly bound at all NANOG concentrations. In contrast, SOX2 occupancy does not increase with its concentrations, while OCT4 displayed an intermediate behavior. Our results challenge the notion that TF binding follows simple mass-action dynamics and reveal a core set of pluripotency regions that are bound by all three TFs at all TF concentrations, revealing how pluripotency can be maintained despite marked fluctuations in core pluripotency TFs.
• 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.