Ask about this productRelated genes to: TNFRSF10C Blocking Peptide
- Gene:
- TNFRSF10C NIH gene
- Name:
- TNF receptor superfamily member 10c
- Previous symbol:
- -
- Synonyms:
- DcR1, TRAILR3, LIT, TRID, CD263
- Chromosome:
- 8p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2016-10-05
Related products to: TNFRSF10C Blocking Peptide
Related articles to: TNFRSF10C Blocking Peptide
- Background Glioblastoma (GBM) is characterized by immune dysregulation and epigenetic alterations that contribute to tumor progression. Although tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) signaling has been implicated in tumor biology, the transcriptional and immunological relevance of its decoy receptors, TNF receptor superfamily member 10C and 10D (TNFRSF10C and TNFRSF10D), in gliomas remains incompletely characterized. Methods An integrative multi-omic analysis was performed using The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and Chinese Glioma Genome Atlas (CGGA) datasets in combination with Gene Expression Profiling Interactive Analysis 3 (GEPIA3), University of Alabama at Birmingham Cancer database (UALCAN), Tumor Immune Estimation Resource 3.0 (TIMER3.0), Search Tool for the Retrieval of Interacting Genes/Proteins (STRING), and MEXPRESS platforms. Gene expression, promoter methylation, molecular subtype distribution, immune infiltration patterns, and clinical associations were evaluated using harmonized analytical workflows and cross-validation across datasets. Results Both receptors demonstrated progressive upregulation from normal brain to lower-grade glioma (LGG) and GBM, with higher expression observed in isocitrate dehydrogenase (IDH)-wildtype tumors. Promoter methylation analysis revealed inverse correlations between CpG methylation and gene expression, suggesting potential epigenetic associations. Immune deconvolution analyses showed consistent associations with myeloid cell populations, including macrophages, neutrophils, and dendritic cells (DCs), alongside limited correlations with T-cell subsets. Protein-protein interaction network analysis indicated that these receptors interact with multiple components of inflammatory and TNF/TRAIL signaling systems. Higher expression showed trends toward shorter progression-free intervals (PFI). Conclusions TNFRSF10C and TNFRSF10D demonstrate reproducible associations with methylation patterns and immune microenvironment characteristics in GBM. These findings highlight potential links between TRAIL decoy receptors and inflammatory tumor states and support further mechanistic investigation. - Source: PubMed
Publication date: 2026/03/25
Khurana Kartik MSaoji AjeetPahuja Heena - This study aimed to screen the specific modules and hub genes of hyperlipidemia. - Source: PubMed
Publication date: 2025/12/10
Zhao ZhiyiCao YinGu AnnaYao Hanxin - Air pollution disproportionately affects individuals with asthma, triggering asthma exacerbations and morbidity. We hypothesized that children with and without asthma have distinct airway transcriptome networks associated with ozone and particulate matter ≤ 2.5 µm (PM) exposure. - Source: PubMed
Publication date: 2025/12/22
Chun YoojinIrizar HaritzZhang LingdiReed KyleGrishina GalinaGrishin AlexanderVicencio AlfinBunyavanich Supinda - Type 1 diabetes (T1D) results from a chronic autoimmune disease that leads to pancreatic beta cell death and states of dysfunction such as senescence. Cellular senescence is a programmed stress response involving cell cycle arrest, apoptosis resistance and secretion of immunogenic molecules referred to as the senescence-associated secretory phenotype (SASP). Histologic evidence indicates the accumulation of senescent beta cells in T1D, however, there are no biomarkers to noninvasively detect senescent beta cells. Circulating SASP factors have been used as a biomarker for senescent cell accumulation in age-related diseases, but a similar approach has not been explored in T1D. Here, we measured a panel of 7 previously identified human islet-secreted SASP factors (GDF15, CXCL1, CXCL5, CXCL8, CCL20, IGFBP4 and TNFRSF10C) in a blinded cohort of pediatric and young adult plasma samples from TrialNet including autoantibody-negative controls, single autoantibody-positive, and clinical stages of T1D progression (n = 20 donors per group). SASP factor concentrations were higher in stages 1, 2 and 3 recent onset T1D donors versus controls and effectively discriminated stages 2 and 3 disease status. SASP factor concentration did not associate with the extent of beta cell dysfunction, autoantibody titre or donor age. Analysis of matched plasma and pancreas samples from an independent cohort of control donors supported a relationship between senescent beta cells and circulating SASP markers. These results suggest that senescent beta cell burden may be reflected by the circulating levels of specific islet-associated SASP factors and could represent a novel biomarker for senescence in T1D. - Source: PubMed
Publication date: 2025/11/19
Préfontaine CamillePipella JasmineHeidinger IanAlcasid NicoleThompson Peter J - This study aims to investigate the potential role of B cells in the pathogenesis of Primary Sjögren's Syndrome (pSS) by analyzing cell types, differentially expressed genes, and associated signaling pathways using single-cell RNA sequencing. - Source: PubMed
Publication date: 2025/10/16
Zhang XiaoyuHan YuanweiZhang JingSong YuZhou YanWang JiaTian JinhaiXin XinranLiu BinFang LiZhu Hong