CD261 _ TRAIL_R1
- Known as:
- CD261 _ TRAIL_R1
- Catalog number:
- 10-403-C025
- Product Quantity:
- 0.025 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD261 _ TRAIL_R1
Related genes to: CD261 _ TRAIL_R1
- Gene:
- TNFRSF10A NIH gene
- Name:
- TNF receptor superfamily member 10a
- Previous symbol:
- -
- Synonyms:
- DR4, Apo2, TRAILR-1, CD261, TRAILR1
- Chromosome:
- 8p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2018-01-25
Related products to: CD261 _ TRAIL_R1
Related articles to: CD261 _ TRAIL_R1
- VPS37A, a subunit of ESCRT-I involved in endosomal sorting and autophagy, is frequently downregulated in diverse human cancers. In this study, we showed that VPS37A downregulation, as part of a large chromosome 8p deletion, arises early during tumorigenesis and persists throughout tumor progression. Integrative analysis of VPS37A gene copy number and CRISPR dependency revealed that VPS37A deficiency creates a synthetic lethal dependency on the MAP3K7-NF-κB-CFLAR axis, and targeting this axis triggered CASP8-mediated apoptosis and suppressed tumor growth. This synthetic vulnerability depends on ATG8ylated membranes, which serve as a platform for CASP8 activation upon inhibition of phagophore closure, and can be triggered without disrupting receptor sorting. Consistently, despite frequent co-deletion of VPS37A and the death receptors TNFRSF10A/B, inhibition of the MAP3K7-NF-κB-CFLAR axis selectively induced apoptosis in spheroid tumors with 8p deletion. These results uncover a selective vulnerability in cancer cells harboring VPS37A/8p loss, providing a mechanistic rationale for targeted therapeutic intervention. - Source: PubMed
Publication date: 2026/07/07
Hattori TatsuyaChen LongguiLiang XinwenHamamoto KoutaWang Hong-GangTakahashi Yoshinori - Clear cell renal cell carcinoma (ccRCC) is the most common subtype of renal malignancy and remains a major cause of cancer-related mortality worldwide. Although advances in surgery, targeted therapy, and immunotherapy have improved outcomes for patients, reliable biomarkers for predicting prognosis remain limited. Therefore, robust gene-based prognostic models are urgently needed to improve risk stratification and guide individualized treatment strategies. - Source: PubMed
Publication date: 2026/06/22
Deng YuyouHao ChangzhenYang XiaobingYu ChengfanXia MingWang Tian - Chronic inflammation drives vascular aging and stroke risk, yet circulating proteins linking immune activation to cerebrovascular events remain elusive. People with HIV (PWH) face elevated stroke risk beyond traditional vascular risk factors, even under antiretroviral therapy. We aimed to identify circulating proteomic signatures of HIV-associated stroke, characterize underlying biological pathways, and assess their longitudinal stability. We conducted a nested case-control study of 135 PWH with stroke (HIV + /Stroke + , mean age 64.2 years, 85.9% ischemic) and two matched control groups (HIV + /Stroke- and HIV - /Stroke - , n = 135 each), with longitudinal validation in 37 PWH who subsequently developed stroke (78.4% ischemic). Among 184 plasma proteins measured using Olink Cardiovascular panels, 16 were associated with stroke in PWH, centrally involving the tumor necrosis factor receptor superfamily (TNFRSF). TNFRSF proteins (TNFRSF10A, TRAIL-R2, TNFRSF14, and TNF-R1) were strongly inter-correlated (ρ > 0.77), with their co-expression module associated with stroke (adjusted OR = 1.75, P = 0.018). TNFRSF expression increased monotonically across HIV - /Stroke - , HIV + /Stroke - , and HIV + /Stroke+ groups. Longitudinal analysis confirmed post-stroke upregulation of these TNFRSF members, alongside MMP12 and TFF3, particularly in ischemic subtypes. These findings suggest coordinated TNFRSF upregulation as a potential signature associated with both HIV-related inflammation and cerebrovascular events, providing candidate biomarkers for future investigation. - Source: PubMed
Publication date: 2026/06/09
Chen TailinLin HaijiangChen XiaoxiaoWang MiaochenZhang HaijunWang ShanlingWang LiangyouWang TingtingXie YaliWang YatingRen JiyuanZhang ZhiyiHe Na - To define CSC genetic architecture and identify implicated ocular tissues, cell types, genes, and circulating proteins. - Source: PubMed
Publication date: 2026/05/22
Chen LiyinKim Soo HyunTruong BuuRämö Joel TGorman Bryan Rvan Dijk Elon H CBrinks JoostNikopensius TiitChoi Seung HoanKajanne RistoMehtonen JuhaKaarniranta KaiSobrin LuciaKurki MitjaYzer Suzanne Wu Wen-ChihTurunen Joni ASegrè Ayellet JMercader Josep MariaHuerta AliciaDaly Mark JPalotie AarnoEllinor Patrick TBoon Camiel JfIyengar Sudha KPeachey Neal SNatarajan PradeepRossin Elizabeth J - We evaluated the serum expression profiles of proteins encoded by AMD-related genes in age-related macular degeneration patients and controls. - Source: PubMed
Publication date: 2026/06/03
Battu PriyaSharma SureshSingh RamandeepAnand Akshay