TNFR1 antibody
- Known as:
- TNFR1 (anti-)
- Catalog number:
- orb100329
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- TNFR1 antibody
Ask about this productRelated 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
- Hashimoto's Thyroiditis (HT) is the leading cause of primary hypothyroidism, characterized by progressive thyroid follicular cell (TFC) loss and diffuse lymphocytic infiltration. While apoptosis dominates TFC death in HT, the role of pro-inflammatory necroptosis in TFC destruction, especially its cellular heterogeneity, spatial distribution, and inflammatory microenvironmental regulation, remains incompletely elucidated. - Source: PubMed
Publication date: 2026/08/03
Yang DongyuLu CihangTeng WeipingZhao LeiWang XichangSun YingZhang HaonanFan ShutingShi Xiaoguang - Heart failure with preserved ejection fraction (HFpEF) involves interacting immune, vascular, and stromal abnormalities. We asked whether macrophage genes showing opposite diet-associated and dapagliflozin-associated effects could identify regulatory and signaling programs relevant to HFpEF. Genes were ranked in a 2 × 2 × 2 dataset of sorted murine cardiac macrophages, and the locked signatures were evaluated in cardiac single-cell and single-nucleus datasets. Regulon analysis and network-constrained sensitivity testing identified BHLHE40 as the more robust program-level candidate. NFKB1, in turn, was linked to the broadest curated communication network, including TNF-, IL1B-, and PDGFB-related endothelial and fibroblast branches. External evidence varied across datasets and cell compartments. In myocardium from 19 HFpEF and 24 control donors, the CCR2- and cross-subset signatures were higher in macrophages, and the CCR2- signature was also higher in fibroblasts. PDGFB-related fibroblast branches received broader external evidence than the discovery-ranked TNF-TNFRSF1A endothelial branch, whose direction was not retained in human myocardium. These results nominate testable macrophage regulatory and signaling hypotheses for HFpEF but do not establish drug-specific reversal or cross-model conservation. - Source: PubMed
Publication date: 2026/08/17
Wang DingkunCai WenyaoWang RuonanLuo WenboLiu YangZhou QuanJiang Yu - Aging is characterized by a decline in function of intestinal stem cells (ISCs), but the extent to which this is shaped by systemic factors is unclear. Here we show that the ISC aging phenotype can be propagated from old to young mice utilizing heterochronic parabiosis, and implicate a role for inflammation in these effects, as anti-inflammatory drugs, including TNF antibodies, restored function. Parabiotic rescue experiments demonstrate that TNFR1 knockout protected young ISCs from the old environment. In young organoids, TNF downregulated crypt budding, while impairing mitochondrial pathways and fatty acid oxidation (FAO). However, aged ISC function was enhanced by boosting mitochondrial fusion, whereas FAO in aged crypts was improved by countering inflammation with salicylate treatment. Thus, these data identify the old environment through the progeronic factor TNF, as a driver of ISC aging phenotypes through intestinal epithelial cell TNF receptor 1 signaling to downregulate FAO, proliferation and regenerative capacity in these cells. - Source: PubMed
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