TNFR1 antibody
- Known as:
- TNFR1 (anti-)
- Catalog number:
- orb100329
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- TNFR1 antibody
Related genes to: TNFR1 antibody
- Gene:
- TNFRSF1A NIH gene
- Name:
- TNF receptor superfamily member 1A
- Previous symbol:
- TNFR1
- Synonyms:
- TNF-R, TNFAR, TNFR60, TNF-R-I, CD120a, TNF-R55
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1991-01-15
- Date modifiied:
- 2019-04-23
Related products to: TNFR1 antibody
Related articles to: TNFR1 antibody
- Multiple sclerosis (MS) is a heterogeneous autoimmune disorder of the central nervous system of polygenic nature. Uncovering the genetic predictors of MS phenotype can help to explain the nature of the disease's clinical heterogeneity, and contribute to the development of novel tools for precise disease prognosis. We conducted a retrospective genetic association study of 35 polymorphic variants in immune-related genes with MS severity assessed using the Multiple Sclerosis Severity Score (MSSS) in a sample of 548 Russian relapsing-onset MS patients who have not previously received immunomodulatory therapy. Variants in the , , , , , , , , , and genes were identified as MSSS-associated in at least two of the three models analyzed (MSSS > 3.5 versus ≤3.5; MSSS > 5.0 versus <2.5; MSSS as a continuous variable). Among them, variants in , and genes were associated with MSSS only in women, while variants in the and genes only in men. The variant in was MSSS-associated both in the total sample and in subgroups of female and male MS patients. Thus, we demonstrate that several GWAS-identified MS risk genes, along with other immunological loci, act as modifiers of the MS phenotype. - Source: PubMed
Publication date: 2026/06/13
Kulakova OlgaBaulina NataliaKozin MaximMatveeva NataliaBoyko AlexeyFavorova OlgaKiselev Ivan - Clear cell renal cell carcinoma (ccRCC) is notorious for its clinical unpredictability. While Aquaporin-1 (AQP1) is a major water channel in healthy kidneys, its specific role and regulatory mechanisms in ccRCC remain unclear. Using bioinformatics analysis of 610 TCGA-KIRC patients (RNA sequencing and DNA methylation), single-cell transcriptomics of 27,402 cells, and experimental validation (CCK-8, scratch, Transwell, and xenograft assays, with Western blotting, HE staining, and immunohistochemistry), we systematically characterized AQP1 expression, regulation, and function. AQP1 was significantly downregulated in ccRCC via promoter hypermethylation, with single-cell analysis confirming tumor cell-specific loss. Low AQP1 correlated with worse prognosis; multivariate Cox regression identified AQP1 as an independent protective factor (HR = 0.510, < 0.001), and a prognostic nomogram showed good predictive accuracy for 1-, 3-, and 5-year survival. AQP1 overexpression suppressed proliferation, migration, invasion, and xenograft growth, accompanied by upregulation of TNF-α, TNFRSF1A, Bax, and Cleaved Caspase-3 and reduced Vimentin, suggesting activation of TNF-related pro-apoptotic signaling. AQP1 is epigenetically silenced in ccRCC and suppresses tumor growth via TNF-mediated apoptosis, establishing it as an independent prognostic biomarker and candidate therapeutic target. - Source: PubMed
Publication date: 2026/06/09
Pang ShuoBi YingweiLiu YuxinWang ShimingYi BolinZhu LiangWang Jianbo - Gliomas are highly aggressive brain tumors that pose significant challenges in terms of prognosis and treatment. The precise expression patterns and prognostic significance of necroptosis-related genes (NRGs) in gliomas remain poorly understood, despite necroptosis demonstrating promise as a therapeutic target in cancer. - Source: PubMed
Publication date: 2026/06/11
Wu KaixiangCao LuYang HongchuanSun WenwenWu Kaifu - The tumor microenvironment plays a critical role in therapeutic resistance in diffuse large B-cell lymphoma (DLBCL), yet actionable targets within the immune cells remain largely undefined. Through integrative multiomics profiling, we identified tumor necrosis factor receptor superfamily member 1A () as a key prognostic determinant associated with predicted R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) resistance, specifically localizing its expression to tumor-associated macrophages (TAMs). Mechanistic investigation via ligand-receptor network analysis and in silico perturbation revealed that TNFRSF1A TAMs sustain a pro-oncogenic and immunosuppressive niche, by driving nuclear factor-κB (NF-κB)-dependent B-cell activating factor (BAFF) secretion and immune checkpoint ligand (programmed death-ligand 1/programmed death-ligand 2) expression. Pharmacogenomic screening coupled with molecular dynamics simulations identified curcumin as a potential modulator of TNFRSF1A-associated signaling. Subsequent experimental validation using small interfering RNA-mediated knockdown and coculture assays confirmed that disrupting the macrophage-intrinsic TNFRSF1A/NF-κB/BAFF axis eliminated the protective support provided by TAMs to lymphoma cells. Additionally, a novel risk model derived from the TNFRSF1A TAM transcriptional signature demonstrated robust predictive accuracy for patient outcomes across independent cohorts. Our findings elucidate the role of TNFRSF1A TAMs in driving DLBCL progression, highlight the TNFRSF1A/NF-κB/BAFF axis as a vulnerability in the DLBCL microenvironment, and propose curcumin as a viable therapeutic strategy to disrupt this supportive microenvironment. - Source: PubMed
Publication date: 2026/06/01
Yin WenxianWang XingyueChen ZhuoSun MengqiZhang YinpingSu JiahongYuan ZijunXiao TingTima SingkomeHe XiXiao ZhangangDuangmano Suwit - Retinal degeneration involves complex interactions among diverse cell types, yet the dynamic cellular responses and intercellular communication remain incompletely characterized. Here, we generated a temporal single-cell RNA sequencing atlas of the mouse retina following sodium iodate-induced oxidative injury to characterize cell type-specific trajectories and stage-dependent interactions. Our analysis identified a distinct inflammatory-reactive Müller glia subpopulation enriched for Il1r1, Tnfrsf1a, and C3, which exhibited early activation of TNF/NF-κB/MAPK signaling and later engagement in chemokine signaling, ECM-receptor interaction, and synaptic regulation. Photoreceptor profiling further revealed two rod subclusters with differential vulnerability, in which the more susceptible Rod1 subpopulation displayed marked downregulation of phototransduction genes and selective enrichment of tumor necrosis factor (TNF) signaling. Microglia exhibited early expansion and upregulation of inflammatory gene programs, including Il1b, Tnf, and Ccr2, while in vitro assays confirmed that conditioned medium from sodium iodate-activated microglia reduced photoreceptor viability. Together, we show a conceptual model in which sodium iodate-induced oxidative stress is associated with early microglial inflammation and subsequent glia-photoreceptor crosstalk, suggesting a potential pathway that may contribute to selective rod degeneration. This study provides a comprehensive resource for dissecting retinal degenerative mechanisms and highlights critical temporal windows for therapeutic intervention. - Source: PubMed
Publication date: 2026/05/29
Zhao ZhenzhenZhou YeLiu YingWang QianXu Guo-TongTian HaibinBi YanlongCui TingtingOu Qingjian