CD264 _ TRAIL_R4
- Known as:
- CD264 _ TRAIL_R4
- Catalog number:
- 10-519-C025
- Product Quantity:
- 0.025 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD264 _ TRAIL_R4
Related genes to: CD264 _ TRAIL_R4
- Gene:
- TNFRSF10D NIH gene
- Name:
- TNF receptor superfamily member 10d
- Previous symbol:
- -
- Synonyms:
- DcR2, TRUNDD, TRAILR4, CD264
- Chromosome:
- 8p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2016-10-05
Related products to: CD264 _ TRAIL_R4
Related articles to: CD264 _ TRAIL_R4
- Ovarian endometriosis (OE) is a chronic, inflammatory gynecological disorder associated with sterility and an elevated risk of ovarian cancer. Despite its high prevalence, the complex molecular mechanisms governing OE pathogenesis remain poorly investigated. We conducted a comprehensive histopathological and molecular investigation of OE in a cohort of 188 Saudi women (88 patients with OE and 100 healthy controls) using histopathological, qRT-PCR, immunostaining, and Western blot techniques. Histopathological analysis confirmed significant stromal fibrosis and chronic inflammation in endometriotic lesions. Gene expression profiling revealed a pro-proliferative, anti-apoptotic signature, marked by the upregulation of and the downregulation of , , and . Interestingly, we identified a post-transcriptional regulatory paradox in the inflammatory response: while mRNA was significantly upregulated, its corresponding protein level was downregulated, suggesting a novel, tightly controlled mechanism to limit excessive local inflammation. Besides the increased autophagic activity and decreased Ubiquitin mRNA levels, epigenetic dysregulation was prominent, characterized by the upregulation of DNA methyltransferase DNMT3B and the downregulation of the histone variant H3.1. These findings elucidate novel molecular pathways underlying OE pathogenesis as evidenced by a post-transcriptional paradox in IL-6 expression, and uncover key dysregulations spanning cell proliferation, apoptosis, inflammation, autophagy, and epigenetic regulation. - Source: PubMed
Publication date: 2026/05/20
Nahdi SaberArafah MariaPetraglia FeliceJalouli MarouaAlamri AbdullahAlanazi MohammadRahman Md AtaurAlwasel SalehHarrath Abdel Halim - 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 - Odontogenic keratocyst (OKC) is a locally aggressive jaw cyst with a high recurrence rate. This study evaluated the efficacy of topical 5-fluorouracil (5-FU) as an adjunct to enucleation in 12 OKC patients. After cyst removal, residual bone cavities were packed with 5% 5-FU-coated iodoform gauze for 72 hours. Over a mean follow-up of 14 months, all patients healed uneventfully, and one recurrence occurred (8.3%; 95% CI: 0.2%-38.5%) at 12 months. Bulk RNA sequencing revealed enrichment of necroptosis and cellular senescence pathways, with upregulation of pro-apoptotic genes (FAS, TNFRSF10A, TNFRSF10D) and downregulation of proliferation-related genes (TOP2A, CDK1, CDK5) after 5-FU treatment in OKC tissues. These findings support topical 5-FU as a safe, cost-effective, adjuvant therapy that potentially reducing recurrence risk. Validation in larger multicenter studies with extended follow-up is warranted. - Source: PubMed
Publication date: 2025/10/14
Yi Jing-RuiDeng Shu-HangMan Qi-Wen - Proper testicular development is essential for spermatogenesis, a complex biological process that depends on the continuous proliferation and differentiation of spermatogonial stem cells (SSCs). These processes are tightly regulated by the SSC niche. Understanding the developmental mechanisms of SSCs is therefore critical for elucidating the basis of male fertility. Recent studies have shown that members of the G-protein-coupled receptor (GPCR) superfamily play key roles in ion and water balance in the epididymis, development of efferent ductules, blood-epididymal barrier formation, and sperm maturation. To investigate SSC development in humans, we performed microarray analysis to examine G-protein gene expression in single cells from six human testes. Our analysis revealed that genes such as LEPROT, LRRC15, LPAR1, SSR1, BMPR2, TNFRSF11B, TNFRSF10D, DDR2, SSR3, SIGMAR1, GRIA3, OGFRL1, GRIK2, TMEM87A, GPR108, TNFRSF1A, S1PR2, and VASN were down-regulated, while FLT1, ADGRG6, CSF1R, IL7R, ADGRL3, OR4N4, MMD, SIRPB1, OR5I1, PTGDR, MPL, and GPR107 were up-regulated. Single-cell transcriptomic and bioinformatic analyses were used to validate SSC-specific gene expression and assist in SSC isolation and sorting. Additionally, immunofluorescence labeling at different developmental stages provided insights into the spatial and temporal dynamics of spermatogonia. Our findings offer new insights into the molecular mechanisms governing human SSC development and provide a valuable foundation for advancing SSC-based fertility research and therapeutic applications. - Source: PubMed
Publication date: 2025/07/22
Hashemi Karoii DanialBavandi SobhanAbroudi Ali ShakeriDjamali MelikaAzizi HosseinSkutella Thomas - Childhood obesity (OB) is influenced by complex gene-environmental interaction. While genetics of adult OB have been extensively studied, polygenic childhood OB in non-European populations is still underexplored. Furthermore, in a developing nation such as India, how the environmental component strongly modulated by the socioeconomic status (SES) shapes the genetic susceptibility is crucial to understand. - Source: PubMed
Publication date: 2025/02/25
Nair Janaki MChauhan GaneshPrasad GauriBandesh KhushdeepGiri Anil KChakraborty ShraddhaMarwaha Raman KMathur SandeepChoudhury DevapriyaTandon NikhilBasu AnalabhaBharadwaj Dwaipayan