Hamster Anti-Mouse CD262
- Known as:
- Hamster Antibody toMouse CD262
- Catalog number:
- 129-10130
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Hamster Anti-Mouse CD262
Related genes to: Hamster Anti-Mouse CD262
- Gene:
- TNFRSF10B NIH gene
- Name:
- TNF receptor superfamily member 10b
- Previous symbol:
- -
- Synonyms:
- DR5, KILLER, TRICK2A, TRAIL-R2, TRICKB, CD262, TRAILR2
- Chromosome:
- 8p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2018-01-25
Related products to: Hamster Anti-Mouse CD262
Related articles to: Hamster Anti-Mouse CD262
- Cardiovascular-kidney-metabolic (CKM) stages 0-2 represent a potentially modifiable period before overt cardiovascular complications, yet molecular markers that identify individuals at higher downstream risk remain insufficiently defined. We investigated whether plasma proteomic signatures could characterize early CKM-related molecular risk and improve prediction of incident cardiovascular, kidney and mortality outcomes. - Source: PubMed
Publication date: 2026/09/30
Li XingyuZhang HongqiangWang SuijianShi JieZhang JunhaoChen MinghuiZhao MinzheYue TongZheng Xueying - Osteoarthritis (OA) is a chronic inflammatory and degenerative joint disease that commonly affects the aging population. This study was designed to decipher gene-metabolite regulatory networks driving OA progression via combined computational prediction and experimental validation. Differential gene expression analysis, weighted gene coexpression network analysis, and machine learning algorithms were integrated to screen for key regulatory genes. To infer causal associations between these candidates and OA susceptibility, we performed Mendelian randomization (MR) using cis-expression quantitative trait loci (cis-eQTL) as genetic instruments and identified significant associations between TNFRSF10B and OA. In parallel, single-nucleus RNA sequencing (snRNA-seq) was used to map the cell-type-specific expression profile of TNFRSF10B, and its expression was validated in human knee synovial tissues. The protective effect of TNFRSF10B on OA was statistically mediated in part by the alpha-tocopherol-to-sulfate ratio, as inferred from Mendelian randomization analysis, with the indirect effect accounting for 16.85% (95% CI: 2.96-30.74%) of the total protective effect. snRNA-seq data revealed that TNFRSF10B was widely expressed across synovial cell populations but reduced in OA samples. Collectively, this study identified TNFRSF10B as a candidate protective factor in OA, supported by genetic evidence from MR analysis and reduced expression in OA synovial tissues, offering statistical evidence for gene-metabolite interplay in OA pathogenesis. - Source: PubMed
Publication date: 2026/09/20
Gao QichangShao TuoMa YimingYu ZhangeGu JiaaoYuan Keying - Upper tract urothelial carcinoma (UTUC) is characterized by a high incidence of muscle invasion and distinct molecular heterogeneity, with tumor microenvironment (TME) heterogeneity playing a pivotal role in its malignant progression. However, the spatial distribution patterns of functional cell populations in UTUC and their regulatory mechanisms driving high-grade (HG) and muscle-invasive (MI) progression remain largely unelucidated. Herein, we integrated single-cell RNA sequencing (scRNA-seq) and spatial transcriptome sequencing (ST-seq) to systematically characterize the cellular landscape, spatial molecular network, and intercellular communication profile of UTUC tissues. Six tumor cell subpopulations were identified in UTUC, among which SLC14A1⁺ tumor cells were correlated with favorable clinical prognosis, whereas S100A8/9⁺ tumor cells were associated with poor clinical outcomes. Mechanistically, SLC14A1⁺ tumor cells decelerated UTUC progression via modulating cell apoptosis mediated by the FASLG-TNFRSF10B ligand-receptor pair. In contrast, S100A8/9⁺ tumor cells promoted the malignant progression of UTUC by regulating extracellular matrix remodeling and epithelial-mesenchymal transition (EMT) via the CCL19-CCR7, CCN2-EGFR, ADAM28-ITGA4 and CD14-ITGB2 ligand-receptor pairs. Collectively, our study uncovers the cellular and spatial heterogeneity of the UTUC TME, identifies SLC14A1⁺ tumor cells as a tumor-suppressive subpopulation and S100A8/9⁺ tumor cells as a key driver of UTUC malignant progression, and further delineates the core spatial signaling pathways underlying HG and MI progression of UTUC. These findings provide novel prognostic biomarkers and potential therapeutic targets for UTUC, and advance our mechanistic understanding of spatial TME regulation in urothelial carcinoma. - Source: PubMed
Publication date: 2026/09/03
Liu JiangWei YangyangLiu YiSun ShiweiDilixiati DiliyaerZhou ZhouLu XiangyunLu PingZhao YangZhang YuShi - Epithelial ovarian cancer (EOC) is typically diagnosed at an advanced stage and is associated with high mortality due to metastasis and chemoresistance. Cancer stem cells (CSCs) are central to EOC progression, recurrence, and treatment resistance, with their functional behavior shaped by the tumor immune microenvironment. While M1 and M2 macrophages have been well-characterized, the role of interferon-stimulated gene-enriched subpopulations, particularly interferon-induced protein with tetratricopeptide repeats 1 tumor-associated macrophages (IFIT1 TAMs), in regulating CSC properties in EOC remains largely unexplored. - Source: PubMed
Liu RuiFang YilinZheng RuxiLin LiyaHuang DaZhai LingyunHe QionghuaZhang ZhigangZhou JianweiZhang Xiaoming - Capsid assembly modulators (CAMs) are promising antiviral agents for chronic hepatitis B virus (HBV) infection. This study investigates the anti-HBV activity and immunomodulatory effects of Class I CAMs (CAM-A) in vitro and in vivo. In HepAD38 cells, CAM-A treatment significantly upregulated the expression of interferon-stimulated genes (IP-10, MX1, OAS1). In AAV-HBV mice, CAM-A (GLS4) induced rapid reductions in HBV DNA and delayed HBsAg decline accompanied by transient ALT elevation, upregulated interferons and Tnfsf10/Tnfrsf10b gene expression, while terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and immunohistochemistry (IHC) experiments indicated caspase-3-independent cell death in HBV-infected hepatocytes. Importantly, the antiviral and HBsAg-lowering effects of CAM-A did not require adaptive immunity. Furthermore, combination of CAM-A with a TLR7 agonist in AAV-HBV mice, or with Peg-IFN-α in primary human hepatocytes (PHH) resulted in synergistic antiviral effects, underscoring the therapeutic potential of these agents to promote sustained HBsAg decline and support functional cure strategies in chronic HBV infection. - Source: PubMed
Publication date: 2026/08/31
Wang PuLiu XinchangXie YongZhang YingjunGu BaohuaLi JingChen Yunfu