Mouse Anti-Human CD262
- Known as:
- Mouse Antibody toHuman CD262
- Catalog number:
- 129-10128
- Product Quantity:
- 25
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Mouse Anti-Human CD262
Related genes to: Mouse Anti-Human 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: Mouse Anti-Human CD262
Related articles to: Mouse Anti-Human CD262
- HIV escapes sterilizing immunity through a variety of mechanisms, including the downregulation of MHC-I expression by HIV Nef and Vpu to counteract CD8 T cell responses. While reduced MHC-I expression would be expected to support targeting by NK cells, a subpopulation of infected CD4 T cells consistently resists multiple rounds of NK cell natural and antibody-dependent cytotoxicity. Studies further reveal that the HIV accessory protein Vpr induces expression of (TRAIL-R2) in CD4 T cells, with 'survivors' of NK cell targeting exhibiting relatively higher MHC-I and weaker expression of TRAIL-R2. In fact, reverse TRAIL signaling in NK cells leads to the release of perforin and granzymes, a pathway limited when TRAIL-R2 expression is diminished. Thus, independent of canonical death receptor signaling, TRAIL-R2 serves as an activating ligand that augments NK cell killing. These observations demonstrate that through Vpr, HIV can regulate the TRAIL/TRAIL-R2 axis to control NK cell functionality. - Source: PubMed
Publication date: 2026/04/19
Grasberger Paula ESondrini Abigail RGlidden NicoleModica AmandaPushlar NatalieBedir SedenBromfield TaraGentling SheldonCheema KomalKucukural AlperOzdemir MilenaZapp MariaBosque AlbertoLeyre LouiseShulkin AaronPiechocka-Trocha AlicjaJones R BradClayton Kiera L - BackgroundTumor necrosis factor receptor superfamily member (10B TNFRSF10B), as a key apoptosis regulator of Oral Squamous Cell Carcinoma (OSCC), exerts a critical effect on its development.MethodsDifferentially expressed genes in OSCC (GSE25099) were screened first. Weighted gene co-expression network analysis identified gene modules, followed by Lasso regression and Cox modeling to pinpoint pivotal genes. Expression was validated in the Cancer Genome Atlas databases and in clinical samples. The Search Tool for the Retrieval of Interacting Genes/Proteins database was used to generate a protein-protein interaction (PPI) network, and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses explored biological functions. Then, for in vitro assays, core gene-targeted siRNAs were introduced into SCC-4 and SCC-9 cell lines to mediate gene knockdown. Cell proliferation was quantified by the CCK-8 method, and apoptotic activity was assessed via flow cytometry, TUNEL staining, and Western blotting for apoptosis-associated proteins.ResultsAmong the 10 core genes that were further screened, TNFRSF10B was most notably linked to unfavorable OSCC prognosis and showed strong diagnostic power. Additionally, its overexpression was associated with clinical stage, nodal metastasis, and chemoresistance. PPI and enrichment analyses revealed its role in extrinsic and necroptotic apoptosis. Moreover, the knockdown of TNFRSF10B suppressed viability and induced apoptosis by upregulating Bax, downregulating Bcl-2, and activating Caspase-3/PARP.ConclusionsTNFRSF10B drives OSCC progression by impairing apoptosis. Its overexpression correlates with poor prognosis and represents a potential diagnostic and therapeutic target. Furthermore, targeting TNFRSF10B may restore apoptosis, thus making precision therapy achievable. - Source: PubMed
Publication date: 2026/03/02
Yang YingshunZhuang ZhizhengHu YanLiu JilunGuo JieJin LinyuQiu Yongle - Benzo[a]pyrene (BaP), a ubiquitous environmental carcinogen predominantly found in tobacco smoke and air pollution, plays a pivotal role in head and neck squamous cell carcinoma (HNSC) pathogenesis. However, the molecular networks governing BaP-induced toxicity and programmed cell death (PCD) mechanisms in HNSC remain poorly characterized, limiting the development of targeted therapeutic interventions. We systematically analyzed PCD patterns in HNSC using the GSE30784 dataset and identified BaP toxicity targets through comprehensive database mining. Machine learning algorithms, including RF and SVM, were employed to identify core toxic targets. Target validation was performed using the TCGA-HNSC cohort, followed by the construction of a prognostic nomogram. Mechanistic insights were obtained through spatial transcriptomics, single-cell RNA sequencing (scRNA-seq), gene set enrichment analysis (GSEA), molecular docking, and molecular dynamics simulations to elucidate BaP-protein interactions. We identified ten distinct PCD modes significantly dysregulated in HNSC compared to normal tissues. Among 260 putative BaP targets, 24 demonstrated significant associations with PCD pathways in HNSC. Machine learning analysis revealed SERPINE1, TNFRSF10B, and STK3 as core mediators of BaP toxicity, with SERPINE1 emerging as the predominant driver of BaP-induced cellular dysfunction. The integrated nomogram achieved robust performance in cancer risk stratification. Spatial transcriptomic analysis demonstrated preferential enrichment of these targets in malignant epithelial cells, while scRNA-seq revealed cell type-specific expression patterns. GSEA identified enrichment in apoptotic signaling, TGF-β pathway activation, and DNA damage response mechanisms. Molecular docking studies revealed high-affinity binding interactions, with molecular dynamics simulations confirming stable BaP-protein complexes. This integrative multi-omics analysis elucidates the complex molecular architecture underlying BaP-induced toxicity in HNSC, establishing SERPINE1 and STK3 as promising prognostic biomarkers and potential therapeutic targets. Our findings provide mechanistic insights into environmental carcinogen-mediated HNSC pathogenesis and offer a rational framework for developing precision medicine approaches targeting BaP-associated malignancies. - Source: PubMed
Publication date: 2026/02/11
Guo YanZhang JiaruiGe JingchunLi LiangLiu MingTian Linli - Pasteurella multocida toxin (PMT) is a key virulence factor produced by some strains of the zoonotic respiratory pathogen Pasteurella multocida (P. multocida). The role of PMT in inducing damage and apoptosis in respiratory epithelial cells remains unclear. In this study, we investigated the molecular mechanism through which PMT induces apoptosis in porcine tracheal epithelial cells (NPTr). It was found that high concentrations of PMT specifically induced caspase-3-dependent apoptosis, an effect absent in its mutant form. Mechanistic analysis demonstrated that PMT activated the NF-κB signaling pathway via the PERK pathway associated with Endoplasmic Reticulum (ER) stress, significantly upregulating the expression of the death receptor 5 (DR5) which subsequently activated caspase-3, triggering apoptosis. Crucial validation experiments showed that knocking out the DR5-encoding gene TNFRSF10B nearly completely inhibited PMT-induced apoptosis and significantly restored cell viability. In summary, this study identifies the PERK-NF-κB-DR5 signaling axis as the principal regulatory pathway for PMT-induced apoptosis in porcine tracheal epithelial cells. - Source: PubMed
Publication date: 2026/02/02
Wang FeiLei YuhaoChen MenghanBi HaixinLuo YayuanBai FangfangHua LinChen HuanchunHe QigaiWu BinPeng Zhong - Cardiac Arrest (CA) is a serious event that threatens life. However, the early proteomic characteristics of CA remain poorly understood. We sought to systematically identify CA-related proteins in a prospective cohort and construct a predictive model. - Source: PubMed
Publication date: 2026/01/29
Wang NingGuo YanLu SonglinSun ChenWang ChangRen QinduoXu YuanLiu QinghuaHu JingyangYan ChiZhou TianyuLiu ChuanwuLv WenhuaJiang YongshuaiShang ZhenweiZhang MingmingLv Hongchao