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。

• Overlapping MHC class I/II epitopes program monocyte-derived dendritic cells toward a cDC1-like state via mTORC1 pathway inhibition [RNA-Seq]
  GSE325601Homo sapiens66 个样本2026-10-26

  Viral infection polarizes monocyte derived dendritic cells (moDC) to initiate type 1 immune responses. The availability of homologous (overlapping) MHC class I and II epitopes, an occurrence associated with viral infection, significantly enhances this process; however, the underlying mechanism(s) remain unclear. We demonstrate that moDC loaded with homologous MHC epitopes acquire a cDC1-like phenotype in a process governed by mTORC1. mTORC1 pathway inhibition among cDC1-like cells leads to NF-B-mediated expression of IL-12 and other type I immune polarizing genes. The cDC1-like signature was also significantly enhanced in clinical moDC vaccine products for glioblastoma and PDAC made through methodologies that enforced class I and II antigenic homology. Collectively, these findings reveal a novel mechanism of immune governance that may also be exploited in cancer immunotherapy.
• Overlapping MHC class I/II epitopes program monocyte-derived dendritic cells toward a cDC1-like state via mTORC1 pathway inhibition [scRNA-seq]
  GSE325592Mus musculus6 个样本2026-10-26

  Viral infection polarizes monocyte derived dendritic cells (moDC) to initiate type 1 immune responses. The availability of homologous (overlapping) MHC class I and II epitopes, an occurrence associated with viral infection, significantly enhances this process; however, the underlying mechanism(s) remain unclear. We demonstrate that moDC loaded with homologous MHC epitopes acquire a cDC1-like phenotype in a process governed by mTORC1. mTORC1 pathway inhibition among cDC1-like cells leads to NF-B-mediated expression of IL-12 and other type I immune polarizing genes. The cDC1-like signature was also significantly enhanced in clinical moDC vaccine products for glioblastoma and PDAC made through methodologies that enforced class I and II antigenic homology. Collectively, these findings reveal a novel mechanism of immune governance that may also be exploited in cancer immunotherapy.

  单细胞
• Overlapping MHC class I/II epitopes program monocyte-derived dendritic cells toward a cDC1-like state via mTORC1 pathway inhibition [ChIP-Seq]
  GSE324817Mus musculus12 个样本2026-10-26

  Viral infection polarizes monocyte derived dendritic cells (moDC) to initiate type 1 immune responses. The availability of homologous (overlapping) MHC class I and II epitopes, an occurrence associated with viral infection, significantly enhances this process; however, the underlying mechanism(s) remain unclear. We demonstrate that moDC loaded with homologous MHC epitopes acquire a cDC1-like phenotype in a process governed by mTORC1. mTORC1 pathway inhibition among cDC1-like cells leads to NF-kB-mediated expression of IL-12 and other type I immune polarizing genes. The cDC1-like signature was also significantly enhanced in clinical moDC vaccine products for glioblastoma and PDAC made through methodologies that enforced class I and II antigenic homology. Collectively, these findings reveal a novel mechanism of immune governance that may also be exploited in cancer immunotherapy.
• RNA Polymerase II Dynamics in Antiviral NK Cell Responses [Pol IIS5P CUT&RUN]
  GSE318335Mus musculus22 个样本2026-10-26

  Natural killer (NK) cells are innate lymphocytes that uniquely exhibit both innate and adaptive responses towards certain pathogens. During cytomegalovirus (CMV) infection, antigen-specific NK cells will generate a long-lived pool of memory cells with enhanced responses to secondary infection. The underlying molecular mechanisms that regulate early innate effector functions and delayed adaptive proliferation followed by longevity during antiviral NK cell differentiation remain to be fully understood. Here, we investigated the dynamics of serine-5 phosphorylated RNA Polymerase II (Pol IIS5P) occupancy in NK cells ex vivo during mouse CMV (MCMV) infection. During the initial NK cell antiviral response, Pol IIS5P occupancy increased broadly across the genome, at both upregulated and downregulated genes relative to NK cells at rest. NK cells across response states showed distinct enrichment of Pol IIS5P at transcriptional start sites (TSS) versus non-promoter regions with select genes maintaining Pol IIS5P occupancy throughout MCMV infection to the memory phase. Thus, our findings illustrate the dynamic Pol IIS5P genomic occupancy in NK cells during antiviral immunity.
• NFIC condensates partition NMNAT1 to limit nuclear NAD+ synthesis and promote cellular senescence
  GSE317403Homo sapiens6 个样本2026-10-26

  In this study, two groups of human-derived U2OS cells were subjected to transcriptome comparative analysis, including the control group (ctrl) and the gene knockout group (KO), with three biological replicates set for each group. Using eukaryotic UID-mRNA sequencing technology, the characteristics of transcriptomic changes in cells after gene knockout were systematically identified and analyzed.
• Spatially Decoding Interactypes of Vascular and Synaptic Remodeling in the Glioblastoma Tumor Microenvironment by Surprisal Information-Theoretic Analysis
  GSE317289Homo sapiens10 个样本2026-10-26

  Glioblastoma (GBM) is a highly heterogeneous and invasive brain cancer, where interactions between tumor cells, vasculature, and neurons shape disease progression and therapeutic resistance. To better understand the spatial organization of these processes, we profiled ten tumor samples from five patients, one sample from T1-constrast-enhanced and one from non-contrast enhanced regions using spatial transcriptomic sequencing and multiplexed protein imaging. While each patient’s tumor presents a unique landscape, together these samples capture all major histological and spatial niches of GBM, enabling a complete picture of the tumor microenvironment and cell–cell “interactypes.” By applying surprisal analysis, an information-theoretic framework, for the first time to spatial omics data, we decomposed gene expression into orthogonal constraint modes that uncovered distinct processes such as extracellular matrix remodeling, vascular-associated invasion, and neuron–tumor synaptic interactions, each with well-defined molecular mechanism. Complementing this approach, a spatial ligand–receptor interactype analysis mapped specific communication events across niches. Within the perivascular niche, we observed collagen–integrin signaling linked to a trajectory from astrocyte-like to mesenchymal-like tumor states. At neuron–tumor interfaces, synaptic remodeling emerged, characterized by NLGN1–NRXN1 and SEMA5A–MET interactions together with enrichment of neuronal gene modules including MAP2 and CALM1. These findings suggest that surprisal analysis can reveal vascular remodeling and neuron-tumor crosstalk are critical mechanisms of GBM progression. This study demonstrates the use of surprisal information-theoretic analysis of spatial omics data to expose hidden spatial programs with mechanistic insights and the interactype mapping to decode the GBM biology across all major tumor niches, pointing toward the discovery of potential therapeutic vulnerabilities mediated by cell-cell interaction and microenvironments.

  空间转录组
• Placental insufficiency causes fetal growth restriction in mice lacking Delta-like homologue 1
  GSE313753Mus musculus31 个样本2026-10-26

  Fetal growth restriction (FGR) affects between 3-7% of pregnancies, is associated with increased perinatal morbidity and mortality, and linked to failure of placental function. The placenta is the key transient organ in pregnancy that makes direct contact with the maternal circulation and directs nutrient transfer, intermediary metabolism and the production of hormones that drive maternal metabolic adaptations essential for pregnancy and lactation. The exchange surface of the placenta is formed in early development by the interaction between trophoblast cells that enclose the maternal blood and extraembryonic mesodermal cells that comprise the fetal vasculature. Despite recent insights into trophoblast development derived from novel in-vitro approaches, the processes driving extraembryonic mesoderm development are not well explored. This is due to a dearth of studies employing unbiased approaches to interrogate extraembryonic mesoderm cell populations. Here we use genetic labelling techniques to separate molecular events occurring in the trophoblast from those in the mesodermal layers of the placenta. In combination with conditional targeting, we show that the imprinted gene Dlk1 is a key player in providing nutrients to the embryo by controlling the placental surface area available for nutrient exchange, and by modulating the production of placental hormones that promote maternal nutrient provision in pregnancy.
• Non-enzymatic functions of CBP/EP300 are harnessed by gene-targeted inducers of proximity [ChIP-seq]
  GSE313540Homo sapiens82 个样本2026-10-26

  Friedreich’s ataxia (FRDA) is a rare neurodegenerative disease caused by an expansion of GAA-trinucleotide repeats within the frataxin (FXN) gene. These GAA repeat expansions are enriched in repressive chromatin marks that accompany near complete silencing of the gene. Restoring FXN expression is thus a curative therapeutic goal. Here, we report the development of bifunctional synthetic gene regulators (SynGR-KATs) that recruit lysine acetyl transferases CBP/KAT3A and EP300/KAT3B to GAA repeat expansions. The GAA-targeted enzymes install transcriptionally conducive acetyl marks on proximal chromatin and restore FXN expression. Proximity-induced pharmacology of CBP/EP300 focuses solely on the enzymatic activity of these multi-domain proteins; however, we find that the non-enzymatic protein scaffolding functions contribute in equal measure to FXN expression. Highlighting the importance of protein scaffolding, co-treatment of patient-derived FRDA cells with BRD4/BET-binding SynGRs (SynGR-BETs) along with SynGR-KATs enhanced FXN expression beyond what can be achieved by either class of molecules on their own. Thus, SynGR-KATs serve as invaluable probes of transcriptional regulation while also providing a new path to therapeutic restoration of FXN expression.
• A Novel Syngeneic Mouse Model of Metastatic Hormone-Sensitive Prostate Cancer Provides a Platform for Studying Combination Immunotherapy II
  GSE312299Mus musculus2 个样本2026-10-26

  Immunocompetent, hormone-sensitive models of metastatic prostate adenocarcinoma remain limited. We established PL051, a syngeneic luciferase-labeled cell line derived from a Pten^pc-/-;Lkb1^pc-/- (PTEN/LKB1-deficient) mouse background, and profiled its genome and transcriptome alongside tumors from the progenitor GEMM. Whole-exome sequencing (WES) of matched samples shows that PL051 is genetically near-identical to the primary tumor: we detected only one high-confidence somatic coding variant, and copy-number alterations (CNAs) were minimal, with <20% of the captured exome altered. CNAs were predominantly focal (~1–3 kb) and gene-sparse. To map androgen-receptor (AR) signaling at the transcript level, we performed RNA-seq on PL051 following vehicle, dihydrotestosterone (DHT), enzalutamide, and the DHT+enzalutamide combination. The dataset captures agonist-induced AR target activation and antagonist-associated transcriptional shifts (including cell-cycle effects), providing a resource to interrogate AR pathway dynamics in an immune-competent, metastatic context. Together, these data benchmark PL051 as a faithful, transplantable derivative of the GEMM and supply harmonized genomic and transcriptomic profiles suitable for comparative and mechanistic analyses.
• A Novel Syngeneic Mouse Model of Metastatic Hormone-Sensitive Prostate Cancer Provides a Platform for Studying Combination Immunotherapy
  GSE312104Mus musculus16 个样本2026-10-26

  Immunocompetent, hormone-sensitive models of metastatic prostate adenocarcinoma remain limited. We established PL051, a syngeneic luciferase-labeled cell line derived from a Pten^pc-/-;Lkb1^pc-/- (PTEN/LKB1-deficient) mouse background, and profiled its genome and transcriptome alongside tumors from the progenitor GEMM. Whole-exome sequencing (WES) of matched samples shows that PL051 is genetically near-identical to the primary tumor: we detected only one high-confidence somatic coding variant, and copy-number alterations (CNAs) were minimal, with <20% of the captured exome altered. CNAs were predominantly focal (~1–3 kb) and gene-sparse. To map androgen-receptor (AR) signaling at the transcript level, we performed RNA-seq on PL051 following vehicle, dihydrotestosterone (DHT), enzalutamide, and the DHT+enzalutamide combination. The dataset captures agonist-induced AR target activation and antagonist-associated transcriptional shifts (including cell-cycle effects), providing a resource to interrogate AR pathway dynamics in an immune-competent, metastatic context. Together, these data benchmark PL051 as a faithful, transplantable derivative of the GEMM and supply harmonized genomic and transcriptomic profiles suitable for comparative and mechanistic analyses.
• IGF2 regulates postnatal adipocyte progenitor proliferation and differentiation
  GSE309372Mus musculus2 个样本2026-10-26

  Functional adipose tissue is critical to metabolic homeostasis, the development of which occurs through a combination of hyperplastic expansion of adipocyte number and hypertrophic adipocyte growth. The relative contribution of these two fundamental growth mechanisms shifts in favor of hypertrophy with advancing age, suggesting stage specific regulatory mechanisms. Here, we merged stable isotope tracer measurements of adipogenesis with cell cycle analyses of primary murine adipocyte progenitor (AP) cells and defined an early hyperplastic-to-hypertrophic growth switch in the first 2 postnatal weeks. Through integration of bulk and single cell transcriptomics, we identified insulin-like growth factor 2 (IGF2) as lead candidate regulator, the expression of which was largely limited to the early post-natal period in AP cells. Using mouse models of AP-targeted Igf2 genetic manipulation, loss of function impaired postnatal AP proliferation and adipose growth leading to adipose dysfunction that persisted into adulthood and with diet-induced obesity. Conversely, AP-targeted gain of Igf2 preserved systemic metabolic function despite increased diet-induced weight gain and adiposity. This study establishes that AP cells early in life integrate genetic and metabolic cues through IGF2 to control their proliferation and resultant development of functional adipose, critical for long term metabolic resilience.

  单细胞
• VisiumHD of EVOV treated GSCs
  GSE308834Homo sapiens4 个样本2026-10-26

  Humanized mice were implanted with patient-derived glioblastoma stem-like cells (GSCs) tumor and treated with control (EV) or treatment (EVOV).

  空间转录组
• cinedathodes experiment-Cinedathodes experiment.
  GSE308406Arabidopsis thaliana42 个样本2026-10-26

  2023_03_qs_cinedathodes-cinedathodes experiment-Transcriptomic Profiling of Differentiating Hydathodes after LAM (laser microdissection)-Transcriptome of hydathode development (H samples) kinetics compared to leaf mesophyll (C control samples) using the first leaf of Arabidopsis thaliana, 5 to 11 days after germination.
• SCAF1 driven polyadenylation site usage regulates mRNA isoform expression and neuronal differentiation
  GSE307416Homo sapiens; Mus musculus117 个样本2026-10-26

  This SuperSeries is composed of the SubSeries listed below.

  SuperSeries
• DNA Methylation Patterns in Neuroendocrine Tumors from Different Primary Sites
  GSE305905Homo 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.
• 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
• Oxidative Stress Potentiates a STAT1–APOL1 Feedforward Loop and Governs Disease Severity in APOL1-Mediated Kidney Disease
  GSE300326Mus musculus8 个样本2026-10-26

  Introduction: Apolipoprotein L1 (APOL1) risk variants (G1 and G2) confer immunity against Trypanosoma infection but markedly increase susceptibility to progressive kidney disease. However, only a subset of biallelic risk-variant carriers develops disease progression, distinct from murine models. Here, we evaluated molecular drivers of progressive disease using a model that reflected the low human disease penetrance. Methods: To investigate the heterogeneity of APOL1-mediated kidney disease, we generated novel APOL1 bacterial artificial chromosome transgenic mice with doxycycline-inducible systemic IFNγ expression (G0- or G1-IFNγ mice). Podocyte-specific transcriptomics using translating ribosome affinity purification (TRAP-seq) and single-cell spatial transcriptomics via 10x Genomics Xenium In Situ platform were performed. Mechanistic validation and analysis of factors regulating APOL1 upregulation were conducted in primary podocytes and subsequently validated in human and mouse kidney biopsy specimens via immunofluorescence. Results: A subset of G1-IFNγ mice developed severe albuminuria and focal segmental glomerulosclerosis, which strongly correlated with the magnitude of APOL1 upregulation. By pairing TRAP-seq with single-cell spatial transcriptomic data, we identified mitochondrial dysfunction and JAK-STAT signaling as a central mediator of podocyte injury. In primary podocytes, APOL1 risk variants triggered mitochondrial-derived oxidative stress, establishing a self-amplifying STAT1-APOL1 feedforward loop that further enhances APOL1 expression and APOL1 oligomerization. This pathogenic loop was consistently enriched in podocytes from both G1-IFNγ mice and in kidney biopsy specimens from patients with APOL1-mediated focal segmental glomerulosclerosis, demonstrating translational relevance. Conclusions: Our findings suggest that biallelic risk variants initiate an oxidative stress-induced positive feedback loop which promotes APOL1 upregulation and STAT1 phosphorylation, thereby contributing to disease susceptibility and outcome.

  单细胞空间转录组
• Glial Fatp1 mediates chenodeoxycholic acid signaling in brain aging
  GSE295894Drosophila melanogaster9 个样本2026-10-26

  Aging is shaped by interorgan metabolic communication, yet the mechanism linking peripheral metabolism to brain aging remain poorly understood. Here, we identify a fat body–brain pathway connecting age-associated accumulation of chenodeoxycholic acid (CDCA) to glial inflammation and functional decline. In Drosophila, the fat body cytochrome P450 enzyme Cyp6w1 contributes to cholesterol-derived CDCA production, while the fatty acid transporter Fatp1 facilitates CDCA uptake into glial cells. Intracellular CDCA accumulation activates mTOR and JAK-STAT signaling, promoting neuroinflammation. Fatp1 knockdown in ensheathing glia reduces CDCA accumulation, attenuates inflammatory signaling, and improves healthspan in wild-type and Alzheimer’s disease model flies. Pharmacological inhibition of FATP1 or mTOR also reduces CDCA-induced neuroinflammatory responses and behavioral impairment in mice. The findings link peripheral bile acid metabolism to glial signaling and identify Fatp1-mediated CDCA transport as a potential target for modulating brain aging.
• Organoids and cortical tubers in Tuberous Sclerosis Complex show non-cell autonomous effects of second hit variants
  GSE294081Homo sapiens10 个样本2026-10-26

  Structural abnormalities are common causes of refractory epilepsy, and while progress has been made in understanding the genetic changes associated with these malformations, the pathogenic mechanisms often remain unclear. Dysregulation of the mechanistic target of rapamycin pathway has been found to contribute to a group of focal cortical dysplasia, and patients with Tuberous Sclerosis Complex often have several of these malformations. We used organoids generated from heterozygous patient-derived induced pluripotent stem cells and added isogenic stem cells with second hit variants to determine whether there are non-cell autonomous effects of the null cells. We found that the presence of null cells during differentiation led to abnormalities in neuronal development, which was due to secreted factors. Furthermore, null cells secreted extracellular vesicles containing proteins that inhibit the transcriptional coactivator, YAP1, and knockdown of one specific factor, AMOT, in null cells rescued neuronal differentiation and YAP1 expression. Finally, we analyzed cell type specific gene expression in malformations in patients with TSC and observed similar patterns of gene expression dysregulation. These data define a novel pathogenic mechanism underlying the development of focal brain malformations.
• EGR1 Binding to a Promoter G-Quadruplex Supports Early TNF Expression
  GSE292945Homo sapiens16 个样本2026-10-26

  G-quadruplexes (G4s) influence chromatin and transcription, but their roles in stimulus-induced rapid gene activation remain incompletely understood. Integration of public transcription-factor ChIP-seq, genome-wide G4 maps, and G4 pull-down/MS identified EGR1 as a G4-associated transcription factor. In vitro binding assays further demonstrated that EGR1 directly interacts with multiple G4 conformations, including parallel MYC G4, hybrid BCL2 G4, and antiparallel telomeric hTel21T18 G4. RNA-seq revealed an EGR1-dependent early LPS-induced inflammatory program. Integration with EGR1 ChIP-seq and G4access profiles prioritized TNF as a promoter-proximal EGR1–G4-associated target. A TNF promoter G4 showed BG4 enrichment and a parallel-like CD signature, and its mutation reduced BG4 signal, EGR1 occupancy, reporter activation, and early LPS-induced TNF expression. G4 ligands further disrupted EGR1 binding to the TNF G4 and reduced TNF expression. These findings reveal a promoter G4-dependent layer of EGR1-mediated TNF activation.