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。

• METTL16-associated RNAs in human Jurkat cells profiled by RIP-seq
  GSE347246Homo sapiens4 个样本2026-10-26

  This study aimed to identify RNAs associated with METTL16 in human Jurkat cells using RNA immunoprecipitation followed by high-throughput sequencing (RIP-seq). METTL16-immunoprecipitated RNA and matched input RNA were profiled from two untreated biological replicates. Gene-level read counts were generated to assess RNA enrichment in METTL16 immunoprecipitates relative to input controls.
• Recordanelles for transcriptome-wide single-cell RNA recording in human cells [dataset_4 scRNA-seq]
  GSE344737Homo sapiens2 个样本2026-10-26

  Transcriptomic measurement technologies provide powerful approaches to understand biology but are limited to providing either a high-resolution snapshot at a moment in time or a low-resolution history of transcription constrained to a few genes over a narrow time range. Here, we introduce the “recordanelle”, a single-component synthetic organelle capable of recording the transcriptome in human cells. Recordanelles are composed of a mitochondrial membrane anchor, a condensate assembler and a poly-A-binding protein. We demonstrate that the recordanelle can be engineered to recruit engineered RNAs or a sampling of up to 90% of all endogenous mRNAs and protect them over several days. We further show that transient and dynamic transcriptional responses resulting from inducible promoters or interferon signaling are preserved throughout time within the recordanelle at the single-cell level. This work provides a non-disruptive and unbiased transcriptome-wide single-cell RNA recording technology to enable a deeper understanding of biology.

  单细胞
• Transcriptomic profiling of C17orf58 knockdown in Jurkat T cells
  GSE343757Homo sapiens9 个样本2026-10-26

  C17orf58 is a poorly characterized gene implicated in the survival and proliferation of T-cell malignancies. To characterize transcriptional changes associated with C17orf58 depletion, RNA sequencing was performed in Jurkat T cells following lentiviral transduction with shRNAs targeting C17orf58. Two independent C17orf58-targeting shRNA constructs were evaluated, with scrambled shRNA and luciferase-targeting shRNA serving as negative controls. RNA was collected 72 hours after lentiviral transduction and subjected to RNA sequencing to identify gene-expression changes and molecular pathways associated with C17orf58 depletion.

  扰动筛选
• Attenuation of DOK3 re-programs tumor-associated macrophages to enhance anti-PD-1-mediated cancer immunotherapy
  GSE343606Homo sapiens1 个样本2026-10-26

  Downstream of Kinase 3 (DOK3) is an adaptor protein that binds and modulates Caspase recruitment domain-containing protein 9 (CARD9) signaling but the role for DOK3 during tumor immune escape remains unclear. Here, we revealed immunosuppressive Osteopontin (SPP1+) tumor-associated macrophages (TAMs) to highly express DOK3 while DOK3low/neg TAMs express CARD9 and T cell-homing chemokines within the tumor microenvironment (TME). Interestingly, Dok3-/- mice showed decreased tumor growth and improved response to anti-PD-1 therapy. While DOK3 is constitutively expressed by macrophages, blocking its interaction with CARD9 enhances JNK signaling to reprogram TAMs for improved homing and activation of T cells. Further spatial studies clarified the localization of DOK3high TAMs within the TME and an association of DOK3 expression with progressive disease in an ongoing Phase II study of Lenvatinib/Pembrolizumab in recurrent clear cell gynecological carcinomas. Overall, targeting DOK3-CARD9 axis may represent a new avenue to overcome resistance in cancer immunotherapy by driving the emergence of favorable response-associated TAM states.

  空间转录组
• The antioxidant (+)-Catechin reduces inflammation and promotes a stable plaque phenotype in female LDL receptor deficient mice fed a high-fat diet via anti Inflammatory and smooth muscle cell regulatory pathways [human]
  GSE343575Homo sapiens6 个样本2026-10-26

  Nutraceuticals such as (+)-Catechin are emerging as promising agents for the prevention and treatment of atherosclerotic cardiovascular disease. A large prospective study of 34,492 participants previously demonstrated an inverse association between (+)-Catechin intake and risk for coronary heart disease. Our recent work further showed that (+)-Catechin inhibits several atherosclerosis related processes in vitro, induces beneficial metabolic changes in male C57BL/6J mice fed a high fat diet (HFD), and reduces plaque burden and inflammation in male low-density lipoprotein (LDL) receptor deficient (LDLr / ) mice fed a HFD. Given known sex specific differences in atherosclerosis, it is essential to extend these investigations to female mice. The objective of this study was therefore to investigate the effects of (+)-Catechin in female LDLr / mice in vivo. (+)-Catechin lowered plasma cholesterol levels, reduced circulating T cell populations, and increased several beneficial short chain fatty acids in both the plasma and the faeces. It also decreased plaque size, lipid content, macrophage accumulation, and CD3⁺ T cell infiltration in the aortic root, while enhancing markers of plaque stability. RNA sequencing (RNA seq) of the thoracic aorta revealed modulation of key pathways involved in inflammatory signalling, hypertension and immune responses. Complementary studies in human aortic smooth muscle cells demonstrated that (+)-Catechin attenuated macropinocytosis and oxidised LDL uptake, processes linked to plaque progression, without promoting calcification. RNA seq identified several genes and pathways consistent with the compound’s anti atherogenic and plaque stabilising actions. Collectively, these findings provide new mechanistic insights into the beneficial cardiovascular effects of (+)-Catechin in female mice and support further evaluation of this flavanol in human clinical trials.
• T cell Mechanomemory Takes Training
  GSE341175Homo sapiens8 个样本2026-10-26

  Biomaterials provide a powerful tool for directing the function of T cells, mediators of adaptive immunity and cellular immunotherapy. As an intriguing facet of biomaterial design, modulating the mechanical stiffness of biomaterials provides control over T cell activation, optimizing expansion through a parameter that is orthogonal to and can be combined with other approaches. A key question is whether mechanosensing is limited to immediate impacts on cell function or includes long-lasting imprints on cell function. This report demonstrates such a mechanomemory in the context of expansion of T cells for immunotherapy; populations activated on mechanically soft surfaces exhibit an extended proliferative phase for multiple generations following removal from the substrate. Using media manipulation, this report shows that mechanomemory is mediated by both intrinsic, epigenetic changes and extrinsic factors associated with cell-cell signaling. Moreover, the impact of extrinsic factors decreases over the course of expansion. The development and solidification of mechanomemory in T cells over multiple cell divisions provides new design rules for optimization and insights into how these agents interpret mechanically complex microenvironments.
• Attenuation of DOK3 re-programs tumor-associated macrophages to enhance anti-PD-1-mediated cancer immunotherapy [scRNA-seq]
  GSE341136Homo sapiens6 个样本2026-10-26

  Downstream of Kinase 3 (DOK3) is an adaptor protein that binds and modulates Caspase recruitment domain-containing protein 9 (CARD9) signaling but the role for DOK3 during tumor immune escape remains unclear. Here, we revealed immunosuppressive Osteopontin (SPP1+) tumor-associated macrophages (TAMs) to highly express DOK3 while DOK3low/neg TAMs express CARD9 and T cell-homing chemokines within the tumor microenvironment (TME). Interestingly, Dok3-/- mice showed decreased tumor growth and improved response to anti-PD-1 therapy. While DOK3 is constitutively expressed by macrophages, blocking its interaction with CARD9 enhances JNK signaling to reprogram TAMs for improved homing and activation of T cells. Further spatial studies clarified the localization of DOK3high TAMs within the TME and an association of DOK3 expression with progressive disease in an ongoing Phase II study of Lenvatinib/Pembrolizumab in recurrent clear cell gynecological carcinomas. Overall, targeting DOK3-CARD9 axis may represent a new avenue to overcome resistance in cancer immunotherapy by driving the emergence of favorable response-associated TAM states.

  单细胞空间转录组
• Non-enzymatic functions of CBP/EP300 are harnessed by gene-targeted inducers of proximity [RNA-seq]
  GSE337925Homo sapiens8 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.
• 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.
• 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