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。

• RNA Immunoprecipitation Sequencing (RIP-seq) of RNAs associated in vivo with the FopA protein performed in Escherichia coli J53 or CFT073
  GSE290169Escherichia coli J53; Escherichia coli CFT07336 个样本2026-10-31

  This SuperSeries is composed of the SubSeries listed below.

  SuperSeries
• Identification of RNAs interacting with protein FopA in Escherichia coli [RIP-Seq]
  GSE290168Escherichia coli CFT073; Escherichia coli J5324 个样本2026-10-31

  The goal of this analysis was to identify the RNAs interacting with protein FopA which is encoded on IncI1 plasmid in two E. coli strains J53 and CFT073
• Social Stress Differentially Affects the Behavior and the Transcriptome of the adBNST between Male and Female Mice.
  GSE287634Mus musculus20 个样本2026-10-31

  Stress can be broken down into systemic and processive stressors with processive stressors requiring higher limbic processing. These are also often called social stressors as they require an understanding of social dynamics as opposed to physical based stressors. This differing of processing necessitates we study both phenomena. Additionally, sex is an important aspect of stress research as men and women show differing responses to stress and mood disorder development. To study this, we used a chronic social instability stress (CSIS) paradigm to stress male and female mice. This paradigm is approximately 7-weeks long and involves changing the cage mates of a mouse every 3 days so stable social dynamics cannot form. Afterwards, one cohort was used for avoidance behavior testing using the open field test, the elevated plus maze, the light/dark box emergence test, and the novelty suppressed feeding test. A second cohort was used for bulk RNA-Sequencing of the anterodorsal bed nucleus of the stria terminalis which is a limbic structure known to be related to chronic stress signaling. In the behavior assays, CSIS caused the females to be less avoidant, while the males became more avoidant. Additionally, we found that a low estrogen state in the females caused them to be less avoidant than in a high estrogen state. In the transcriptome, we found major differences between the males and females with the males expressing more genes related to transcription whereas the females expressed more genes related to synaptic transmission. We also found that the transcriptome in the males is more sensitive to the stress than the females. In summary, we have found how social stress is differentially regulated between males and females and how this may be related to the development of stress-related behavioral changes.
• Comparative analysis of RLR-specific RNA ligands during influenza virus infection
  GSE287560Homo sapiens; Influenza A virus (A/Guangdong-Maonan/51/2009(H1N1))48 个样本2026-10-31

  RIG-I-like receptors (RLRs) play a critical role in detecting RNA virus infections and initiating antiviral immune responses. This study examined the roles of three RLRs—RIG-I, MDA5, and LGP2—in recognizing wild-type (WT) influenza virus infections and characterized their RNA ligands at both the nucleotide sequence and post-transcriptional modification levels. Our findings indicate that RIG-I and MDA5 are essential for sensing influenza A (IAV) and influenza B (IBV) viruses. RNA ligands isolated from RIG-I and LGP2 demonstrated immunostimulatory activity in type I interferon (IFN) reporter assays. Specifically, RIG-I bound to RNA sequences within the negative-sense NS and M segments of the influenza virus, while LGP2 interacted exclusively with the negative-sense 5′ and 3′ ends of the M segment. Notably, the viral segments were more potent in activating type I IFN signaling than their positive-sense counterparts, which aligns with the IC50 values of the NS and M segments binding to RIG-I. Additionally, in IAV-infected cells, RIG-I selectively recognized RNA polymerase III transcripts, which exhibited decreased 5-methylcytosine (m5C) modification levels upon infection. These results highlight the contributions of both viral and host RLR ligands to anti-influenza virus immunity, emphasizing their specific sequences and the NSUN2-mediated post-transcriptional modification profile. Overall, this study provides a comprehensive view of RLR-mediated sensing mechanisms that regulate antiviral responses to influenza virus infections.
• Nephrin-associated phospho-protein network necessary for filtration at the slit-diaphragm and podocyte adhesion.
  GSE284774Mus musculus25 个样本2026-10-31

  Minimal Change Disease (MCD) is characterized by nephrotic syndrome. In a subgroup of patients, pathogenic antibodies against the slit-diaphragm (SD) protein Nephrin encoded by the gene NPSH1 were identified in blood and biopsy samples. Nephrin is essential for the SD as specific NPHS1 variants result in congenital nephrotic syndrome. Intact Nephrin is a structural component of the SD, but also transmits signals to the actin cytoskeleton of podocyte foot processes (FP) thereby presumably stabilizing podocyte FP morphology. Thus, analyzing the Nephrin signalosome is attractive to identify potential targets for therapeutic intervention in MCD. We employed a model of MCD with antibody-mediated clustering of Nephrin leading to tyrosine phosphorylation-dependent signal transduction in podocyte culture. Phospho-proteome analysis after antibody-mediated Nephrin clustering revealed approx. 180 differentially phosphorylated peptides. Gene set analysis showed that among others the biological process ‘cell matrix adhesion’ was enriched. We verified that two thirds of the identified proteins were necessary for filtration in vivo employing a knockdown approach with consecutive analysis by an in-vivo filtration assay in Drosophila melanogaster nephrocytes. One of the phosphorylated proteins following Nephrin activation in the phospho-proteome analysis was the activating factor of the small GTPase Rap1 – Rapgef1. The significance of this Nephrin effector Rapgef1 for SD and focal adhesion integrity was exemplary studied generating a Rapgef1 knockout (Rapgef1KO) in the metanephric mesenchyme of mice. We confirmed that an early Rapgef1 knockout in podocytes - like transgenic Nephrin mice deficient in tyrosine-dependent signaling – resulted in nephrotic syndrome and an MCD/focal segmental glomerulosclerosis (FSGS) phenotype. RNA sequencing of Rapgef1 knockout mice glomeruli revealed significant regulation of genes involved in cell signaling, cell adhesion, and extracellular matrix organization. Changes in glomerular basement membrane (GBM), focal adhesion (FA) composition, and significant podocyte loss were confirmed by immunofluorescence analysis in Rapgef1 knockout mice glomeruli. Altogether, we identified a Nephrin-associated phospho-protein network necessary for filtration at the slit-diaphragm and podocyte adhesion.
• SUMOylation of SND1 promotes degradation of novel tumor suppressive miRNAs in cancer cells
  GSE281560Homo sapiens16 个样本2026-10-31

  Endonuclease Staphylococcal nuclease domain-containing protein 1 (SND1) was reported mediate miRNA decay of both protein-free and AGO2-loaded miRNAs. We recently found that SUMOylation of SND1 is involved in the regulation of the mature miRNA decay. The in vivo and in vitro SUMOylation assay have proven that SND1 can be modified by SUMO1 at the major site K513, and this modification can be enhanced upon the sodium arsenite and heat shock. Mutation K513R of SND1 inhibits cell proliferation and colony formation of H1299 cells under both normal and sodium arsenite stimulated conditions. Our data demonstrate that miRNA metabolism is connected to cellular stress response and tumorigenesis through the reversible SUMOylation of SND1. The stress-induced SND1 SUMOylation can degrade miRNA to regulate mRNA homeostasis, which may be a key node in the stress survival strategy.
• Deciphering the diversities of CTCF and CTCF-s in human embryonic stem cells [ChIP-seq]
  GSE280302Homo sapiens11 个样本2026-10-31

  In this study, Biotin ChIP-seq was performed to obtain the independent genome binding sites of CTCF-s or CTCF. CTCF ChIP-seq was performed to investigate the influence of the overexpression of CTCF-s on the binding of CTCF in hESCs.
• Habitual betel nut chewing promotes oral squamous cell carcinoma tumorigenesis by inhibiting global methylation in normal oral mucosa
  GSE280233Homo sapiens33 个样本2026-10-31

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

  多组学
• Joint profiling of 5-methylcytosine, 5-hydroxymethylcytosine, and the transcriptome in single cells identifies factors responsible for genome-wide DNA methylation erasure in human primordial germ cell maturation
  GSE280112Homo sapiens23 个样本2026-10-31

  Reprogramming of DNA methylation plays a vital role in the establishment of cell identity during early mammalian development. To gain deeper mechanistic insights into this process requires capturing the entire dynamics of DNA methylation – both 5-methylcytosine (5mC) and its downstream oxidation product 5-hydroxymethylcytosine (5hmC) – in individual cells. Therefore, in this work, we report a new single-cell genome-wide strand-specific sequencing method, scMHT-seq, to jointly profile 5mC, 5hmC, and the transcriptome from individual cells. Using human embryonic stem cells (hESCs), we first show that scMHT-seq can accurately detect both 5mC and 5hmC from the same cell with minimal crosstalk in quantifying these two DNA modifications, and that the multi-modal measurements are in close agreement with individual measurements of 5mC and 5hmC in single cells. After establishing scMHT-seq, we next applied scMHT-seq to gain insights into human primordial germ cell (hPGC) maturation. After specification, hPGCs undergo rapid global demethylation as they mature, and this reprogramming is critical for normal development of gametes. However, it has not been possible to overcome this key epigenetic barrier in a dish, thereby limiting our ability to generate mature hPGC-like cells (hPGCLCs) and accomplish in vitro gametogenesis. To gain a deeper understanding of the molecular factors involved in germ cell maturation, we applied scMHT-seq to an extended in vitro culture system for generating hPGCLCs and observed partial and heterogeneous erasure of the methylome across single cells that is mechanistically predominantly driven by passive demethylation due to reduced DNMT1-mediated maintenance methylation activity. Notably, we discover that hPGCLCs in extended culture can be transcriptionally classified into two distinct states, with one population enriched for more mature hPGCLCs exhibiting genome-wide loss of the methylome. Moreover, we identify DND1 and SOX15 as two critical factors that are potentially key drivers of hPGCLC maturation. Overall, we demonstrate that scMHT-seq is a robust and high-throughput technology that can provide insights into the mechanisms driving DNA methylation dynamics and their effect on cellular states during hPGCLC maturation, thereby providing a platform to advance in vitro gametogenesis in humans.

  单细胞
• Type I regulatory T cells have overlapping phenotypes with circulating Tfh and Th1 in P. falciparum
  GSE279685Homo sapiens16 个样本2026-10-31

  Immunity to P. falciparum malaria develops slowly, requiring repeated infection in areas of high transmission, and wanes rapidly in the absence of parasite exposure. Key to this immunity, is the development of antibodies which is supported by CD4⁺ T follicular helper (Tfh) cells that drive robust germinal centre responses. However, in malaria, the malaria-specific CD4⁺ T cell compartment in peripheral blood is dominated by Type 1 regulatory T cells (Tr1), which produce high levels of IL-10 in response to parasites. Tr1-like Tfh cells (Tfh10) have been reported in several settings of repeated antigen stimulation but have not been investigated in malaria. Here we used single-cell RNA sequencing and multiparameter flow cytometry to characterise malaria-specific Tfh and Tr1 cells in a longitudinal cohort of highly exposed individuals and assessed their persistence after transmission interruption. Malaria-specific Tfh and Tr1 cells shared overlapping profiles, and Tr1 cell-like transcriptional signatures and phenotypes were detectable within the Tfh cell compartment. Tfh10 cell subsets were the dominant phenotype of malaria-specific Tfh cells. Following disruption of malaria transmission, the frequencies of malaria-specific Tr1 and Tfh10 cells declined. These findings highlight a close relationship between Tfh and Tr1 cells and show that the Tfh cell compartment in malaria is dominated by Tfh10 cells. The rapid waning of these cells in the absence of continuous exposure is consistent with requirements of persistent antigen in maintaining regulatory CD4 T cell phenotypes.

  单细胞
• Krüppel-like factor 5 remodels lipid metabolism in exercised skeletal muscle
  GSE279425Mus musculus16 个样本2026-10-31

  Regular physical activity induces a variety of health benefits, preventing and counteracting diseases caused by a sedentary lifestyle. However, the molecular underpinnings of skeletal muscle plasticity in exercise remain poorly understood. We identified a role of the Krüppel-Like Factor 5 (Klf5) in this process, in particular in the regulation of lipid homeostasis. Surprisingly, gain- and loss-of-function studies in muscle in vivo revealed seemingly opposite functions of Klf5 in the response to an acute exercise bout and chronic training, modulating lipid oxidation and synthesis, respectively. Thus, even though only transiently induced, the function of Klf5 is complex and integral for a normal long-term training response. These findings highlight the importance of this mediator of external stress response to adaptive remodeling of skeletal muscle tissue.
• Spatial genome and transcriptome co-mapping reveals clonal heterogeneity in tumor tissue
  GSE276213Mus musculus; Homo sapiens22 个样本2026-10-31

  This SuperSeries is composed of the SubSeries listed below.

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

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

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

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

  单细胞空间转录组多组学
• Collection of CRC cell line grown in vitro
  GSE271191Homo sapiens19 个样本2026-10-31

  Recent studies revealed the presence of an aggressive subgroup of colorectal cancer (CRC) that exhibits a distinct tumor growth pattern, characterized by high abundance of cancer-associated fibroblasts (CAFs). To identify cancer cells-intrinsic traits underlie this phenotype and to characterize its stromal features, we generated mouse xenografts from 19 CRC cell lines, where normal mouse stroma cells are recruited and educated by epithelial cancer cells. The in vivo xenograft growth rate showed high variability between cell lines, revealing a subgroup of slow-paced tumors. Cancer cells of this subgroup display distinctive transcriptional features, only partially captured by previously described CRC molecular subtypes, involving epithelial-mesenchymal transition and cooperation with a specific CAF population in remodeling the extracellular matrix. We therefore called the cancer cell signature “epithelial matrix remodeling” (EMR), and the CAF signature “matrix remodeling CAF” (mrCAF). In pan-cancer analysis, the EMR and mrCAF signatures were co-detected and associated with poor prognosis in multiple tumor types. Altogether, these results highlight the intrinsic capability of cancer cells to recruit, educate and cooperate with CAFs, indicating route toward tumor progression involving the interaction between tumor and its microenvironment.
• Collection of CRC cell line grown in vivo
  GSE267353Homo sapiens38 个样本2026-10-31

  Recent studies revealed the presence of an aggressive subgroup of colorectal cancer (CRC) that exhibits a distinct tumor growth pattern, characterized by high abundance of cancer-associated fibroblasts (CAFs). To identify cancer cells-intrinsic traits underlie this phenotype and to characterize its stromal features, we generated mouse xenografts from 19 CRC cell lines, where normal mouse stroma cells are recruited and educated by epithelial cancer cells. The in vivo xenograft growth rate showed high variability between cell lines, revealing a subgroup of slow-paced tumors. Cancer cells of this subgroup display distinctive transcriptional features, only partially captured by previously described CRC molecular subtypes, involving epithelial-mesenchymal transition and cooperation with a specific CAF population in remodeling the extracellular matrix. We therefore called the cancer cell signature “epithelial matrix remodeling” (EMR), and the CAF signature “matrix remodeling CAF” (mrCAF). In pan-cancer analysis, the EMR and mrCAF signatures were co-detected and associated with poor prognosis in multiple tumor types. Altogether, these results highlight the intrinsic capability of cancer cells to recruit, educate and cooperate with CAFs, indicating route toward tumor progression involving the interaction between tumor and its microenvironment.
• TAF1-dependent transcriptional dysregulation underlies multiple sclerosis
  GSE255578Mus musculus12 个样本2026-10-31

  In the search for new targets for therapeutic intervention, MS-associated common variants provide clues about etiology-relevant molecular mechanisms, but the individual effect of each variant is minimal. A current priority to better understand the molecular basis of MS and to identify targets for designing progression-modifying therapies, is therefore to detect in the CNS of MS patients specific biochemical alterations -likely related to environmental factors and/or GWAS-identified molecular mechanisms- that per se would suffice to cause MS progression.
• Transcriptomic changes from resulting from treatment of KNS42 with drugs of abuse
  GSE246989Homo sapiens28 个样本2026-10-31

  KNS42 cells were treated with drugs of abuse (ethanol, cocaine, morphine, THC, and psilocin) prior to RNA sequencing. A bioinformatics pipeline of Trim Galore, Kallisto, DESeq2 and Qiagen Ingenuity Pathway Analysis was used for pathway analysis.
• Deciphering the interaction between Twist1 and PPARγ during adipocyte differentiation
  GSE246718Mus musculus12 个样本2026-10-31

  Obesity, a worldwide epidemic in recent years, is mainly due to the uncontrolled development of adipose tissues, which includes adipocyte hypertrophy and hyperplasia. Adipocyte differentiation is a process involving multiple transcription factor cascades, and the exact mechanism has not yet been defined. As a bHLH transcription factor, Twist1 exerts its activity by forming homo- or heterodimers with other factors. In this study, we showed Twist1 restricts adipogenesis through PPARγ. Expression of various differentiation markers (including PPARγ and adiponectin) and triglyceride-containing lipid droplets were decreased with overexpression of Twist1. Pathway enrichment analysis of RNA-seq data showed that differentially expressed genes (DEGs) caused by Twist1 overexpression were significantly related to lipolysis and PPARγ signaling. This implicates that Twist1 plays important regulatory roles in these processes. ChIP and dual luciferase assays showed that Twist1 could bind either PPARγ or adiponectin promoter to repress their respective transcription or directly to PPARγ protein to regulate its transcriptional activity. Furthermore, Twist1 directly interacted RXRα, which usually forms heterodimer with PPARγ to regulate adipogenesis. Taken together, our results suggest that Twist1 is an inhibitory modulator of adipogenesis and its function is likely through direct interaction with PPARγ protein or its gene promoter.
• ISL1 and AQP5 complement each other to enhance gastric cancer cell stemness by regulating CD44 expression
  GSE246329Homo sapiens12 个样本2026-10-31

  Gastric cancer, a prevalent and life-threatening malignancy, is believed to involve cancer stem cells as a contributing factor to tumor progression. This study delves into the influence of ISL1 on the stem-like properties of human gastric cancer cells. In human gastric cancer samples, there is an observed elevation in ISL1 expression, which correlates with the expression of stem cell markers, notably LGR5. Functionally, ISL1 fosters the self-renewal, cell proliferation, migration, and the clonogenic potential of gastric cancer cells in vitro. Furthermore, it enhances the ability of these cells to form tumors and metastasize in vivo. Additionally, ISL1 collaborates with AQP5, collectively intensifying the tumorigenicity of gastric cancer cells. Mechanistically, transcriptomic analysis of cells overexpressing ISL1 unveils a notable activation of the FOXO pathway. This activation leads to increased nuclear expression of FOXO3, subsequently resulting in elevated expression of the stemness-associated gene CD44 in gastric cancer cells. These findings shed light on the role of ISL1 in promoting the stem-like characteristics of gastric cancer cells and emphasize the connection between ISL1 and AQP5 as a novel therapeutic target for individuals with gastric cancer.
• Identification of RNAs interacting with protein FovB in Escherichia coli
  GSE234102Escherichia coli CFT073; Escherichia coli J5312 个样本2026-10-31

  The goal of this analysis was to identify the RNAs interacting with protein FovB which is encoded on IncI1 plasmid in two E. coli strains J53 and CFT073
• Genome-wide DNA methylation analysis in colorectal tumor and normal tissues
  GSE159670Homo sapiens24 个样本2026-10-31

  The current risk stratification system defined by clinicopathological features do not accurately identify the risk of disease recurrence in patients with stage I-II colorectal cancer (CRC). We aimed to investigate whether the CpG sites from newly established genome-wide methylation profiles could serve as biomarkers to improve prognosis prediction.
• The metabolic reprogramming of T cells controls airway remodeling in severe asthma
  GSE352552Mus musculus10 个样本2026-10-30

  Background: Mixed granulocytic asthma (MGA) is a severe Th2-low endotype, characterized by high Th17/neutrophilic burden and exacerbated airway remodeling. Both features confer resistance to inhaled corticosteroids and typical asthma treatments. Objective: We aimed to address gaps in knowledge, including how Th17 cells induce pathological tissue remodeling and how Th17 differentiation occurs in response to allergens. Methods: We generated a Th2-low murine model of asthma on the Il4rα-/- background that mimics the decrease in type 2 response seen in corticosteroid-resistant patients. We monitored major features of human disease including heightened airway reactivity to methacholine, Th17/neutrophilic inflammation, airway remodeling, and resistance to corticosteroid treatment. Comparative transfer of Th2 versus Th17 cells were analyzed. We further investigated how the mitochondrial oxidative phosphorylation (OXPHOS) pathway modulates pathogenic Th17 cell reprogramming by in vitro T cell cultures and in vivo therapeutic blockades. Results: LIGHT (aka TNFSF14) and the OXPHOS pathway are enriched in human MGA and likewise upregulated in this mouse model. We show OXPHOS promotes the metabolic reprograming of Th17 cells, to sustain their survival despite steroid treatment and produce LIGHT that controls airway remodeling. Mechanistically, OXPHOS regulates RORγt expression and the subsequent transcriptional network to program differentiation of Th17 cells, whereas LIGHT drives airway remodeling by activating the MMP9-dependent TGFβ pathway. Additionally, OXPHOS+Th17 cells promote the expression of osteopontin necessary for fibroblast activation. LIGHT antagonistic blockade reduces airway remodeling, whereas OXPHOS inhibition kills Th17 cells and subsequent neutrophilia. Importantly, the dual blockade of LIGHT and OXPHOS reverses all features of MGA back to baseline and reciprocally increases the numbers of Treg cells. Conclusions: The dual blockade of LIGHT and OXPHOS constitutes a promising target for clinical interventions in human MGA, possibly extending to other Th17-driven fibrotic diseases.
• Cilengitide limits the progression of both syndromic and sporadic thoracic aortic aneurysms by targeting alpha V integrins
  GSE352523Homo sapiens11 个样本2026-10-30

  Spatial transcriptomics was used to characterize gene expression patterns in human ascending aortic tissue from healthy controls, patients with Marfan syndrome (MFS), and patients with sporadic thoracic aortic aneurysm (sTAA). Carnoy-fixed, paraffin-embedded ascending aortic tissue sections were profiled using the 10x Genomics Visium platform. Spatially resolved gene expression profiles were analyzed to investigate transcriptional heterogeneity, pathway-associated signatures, and inferred cellular composition across disease groups.

  单细胞空间转录组
• T cell responses distinguish the subset of oral dysplasia that progressed to cancer
  GSE351967Homo sapiens16 个样本2026-10-30

  The factors that determine which oral premalignant lesions progress to cancer while others do not remain unclear. Immune responses to early lesions result in cancer immunoediting, so variability in their nature and strength may influence risk of cancer progression. Here, we show that T cell-mediated immune responses arise in oral premalignant dysplasia years before invasive cancer develops and distinguish lesions that progress from those that do not. Progressing lesions were characterized by robust infiltration of CXCL13+ CD8 T cells in proximity to dysplastic epithelial cells and macrophages expressing interferon-stimulated genes (ISGs), including the T cell-recruiting chemokines CXCL9, CXCL10, and CXCL11. Infiltrating CXCL13+ CD8 T cells were clonally expanded and persisted through malignant transformation. Over time, their frequency and transcriptional profile remained stable, while myeloid cells accumulated and basal epithelial cells upregulated an extracellular matrix-associated transcriptional program partly induced by IFNγ. The transition to invasive cancer was subsequently marked by tissue remodeling accompanied by a shift of the CXCL13+ CD8 T cells from the epithelium to the underlying stroma. Our results provide evidence that IFNγ-driven immune signatures are detectable early and distinguish progressing oral lesions.
• Elucidation of the anti-neuroinflammatory effect of M4FQA in HMC3 cells
  GSE351949Homo sapiens12 个样本2026-10-30

  These study demonstrate that M4FQA attenuates LPS-induced microglial inflammation through coordinated modulation of NF-κB-associated transcriptional networks and suggest that interaction with the TLR4/MD-2 system may contribute to its anti-inflammatory activity. M4FQA therefore emerges as a promising CQA-derived therapeutic candidate for further investigation in the treatment of neuroinflammatory disorders. Pretreatment of 1µM M4FQA significantly attenuated LPS-induced expression of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6. Transcriptomic analysis demonstrated that pretreatment of M4FQA markedly modulated the LPS-induced transcriptional profile, with prominent regulation of genes associated with NF-κB-related inflammatory signaling, cytokine and chemokine responses, cellular homeostasis, and MAPK-associated pathways. M4FQA also reduced the expression of NF-κB-associated inflammatory chemokines, including CCL2, CXCL8, and CXCL6, while functional analyses identified additional modulation of genes associated with synaptic organization and signaling. Molecular docking predicted favourable interaction of M4FQA with the TLR4/MD-2 complex, and SPR analysis further supported interaction with the TLR4 target.
• White Collar proteins AoLreA and AoLreB coordinate light-responsive conidiation and pathogenicity in Arthrobotrys oligospora
  GSE350352Orbilia oligospora12 个样本2026-10-30

  Light is a major environmental cue for filamentous fungi, yet the contribution of canonical White Collar proteins to the specialized development of nematode-trapping fungi remains poorly understood. Here, we characterized the White Collar homologs AoLreA and AoLreB in Arthrobotrys oligospora using gene deletion, light-dependent phenotyping, microscopy, protein-interaction assays, and transcriptomics. Both deletion mutants produced few conidia in darkness but abundant conidia under white light, accompanied by altered conidial morphology and spore-related gene expression. Furthermore, AoLreA interacted with AoLreB, whereas AoLreB also interacted with the velvet regulator AoVeA, linking the White Collar module to a broader developmental network. Beyond sporulation, ΔAolreA formed more traps and displayed enhanced pathogenicity, while ΔAolreB had comparatively limited effects on nematode predation. Cellular analyses further revealed altered vacuolar organization in ΔAolreA and an accumulation of autophagy-associated structures in ΔAolreB. Transcriptomic comparisons of WT and ΔAolreA strains under light and dark conditions revealed extensive transcriptional changes associated with carbohydrate and polysaccharide metabolism, cell-wall organization, hydrolase and oxidoreductase functions, and secondary metabolism. Together, these results identify AoLreA and AoLreB as functionally distinct light-responsive developmental regulators in A. oligospora.
• Empowering multiplexed ultra-throughput ribosome profiling with RiboWich
  GSE350000Homo sapiens; Mus musculus33 个样本2026-10-30

  Ribosome profiling has improved the understanding of mRNA translation, enabling single-nucleotide resolution mapping of ribosome positioning along transcripts. However, most ribosome profiling methods remain labor-intensive, inefficient, and low-throughput, limiting scalability and broader adoption. Here, we develop RiboWich (Ribosome sandWich), a streamlined approach that directly ligates adaptors to ribosome-embedded RNA fragments, bypassing the need for ribosome purification and footprint size-selection, tackling two major bottlenecks. Through a dual-step multiplexing strategy, RiboWich supports automated 384-well profiling while retaining sensitivity and capturing condition-specific differences in translation. By enabling scalable, low-input, and automated translatome profiling, RiboWich provides a versatile and accessible platform for ultra-throughput and future single-cell ribosome profiling applications.

  单细胞
• Ribosome profiling of clear cell renal cell carcinoma tumor and adjacent normal kidney tissue samples
  GSE346551Homo sapiens10 个样本2026-10-30

  Despite growing recognition that non-canonical open reading frame (ncORF)-encoded micropeptides constitute a hidden layebiological functions, and therapeutic relevance in renal cell carcinoma (RCC) remain entirely undefined. Through integrative transcriptomic, translatomic, and proteomic profiling of clinical RCC specimens, we systematically mapped the dysregulated ncORF-encoded micropeptidome and identified long non-coding RNAs (lncRNAs) as a predominant source of tumor-associated cryptic peptides. These findings illuminate a therapeutically actionable micropeptide-mediated regulatory network in RCC and establish ncORF-encoded tumor suppressors as a druggable class of biologics for precision oncology.r of functional regulators in cancer, their translational landscape,
• RNA-seq of clear cell renal cell carcinoma tumor and adjacent normal kidney tissue samples.
  GSE346548Homo sapiens10 个样本2026-10-30

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

  多组学