Polyclonal Rabbit TNFRSF1B Antibody
- Known as:
- Polyclonal Rabbit TNFRSF1B Antibody
- Catalog number:
- abx000702
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- Polyclonal Rabbit TNFRSF1B Antibody
Related genes to: Polyclonal Rabbit TNFRSF1B Antibody
- Gene:
- TNFRSF1B NIH gene
- Name:
- TNF receptor superfamily member 1B
- Previous symbol:
- TNFR2
- Synonyms:
- TNFBR, TNFR80, TNF-R75, TNF-R-II, p75, CD120b
- Chromosome:
- 1p36.22
- Locus Type:
- gene with protein product
- Date approved:
- 1991-01-15
- Date modifiied:
- 2016-06-28
Related products to: Polyclonal Rabbit TNFRSF1B Antibody
Related articles to: Polyclonal Rabbit TNFRSF1B Antibody
- Sepsis is a life-threatening syndrome with dysregulated immune responses and multiple organ dysfunction. However, precise diagnostic biomarkers and effective therapeutic targets for this syndrome are still lacking. Protein ubiquitination modulates inflammatory regulation and immune cell function, but the specific immune cell subsets that drive ubiquitination-associated immune dysregulation in human sepsis have not been clearly identified. - Source: PubMed
Publication date: 2026/04/22
Li ChengHan YimanZheng ZengluHuang ChengyaLiu ZhiyunZhou JianwenYang RuiWu Jingxiang - Mitogen-activated protein kinases (MAPKs) are central to stress and innate immune signaling in fish, but their genomic composition and infection related transcriptional responses remain unclear in bighead carp (Hypophthalmichthys nobilis). - Source: PubMed
Publication date: 2026/04/13
Mao YangYu XueWang WenjingPeng JinWang MinaoZhou JianyunLi Defeng - Previous genetic studies of skeletal variation in threespine stickleback fish () have focused primarily on striking morphological differences. Here, we examine the largely unexplored genetic architecture of internal bone microstructural variation between marine and freshwater stickleback. μCT X-ray analysis revealed differences in the porosity, bone thickness, and bone volume fraction within armor plates and vertebrae from a marine and freshwater stickleback. Quantitative trait locus mapping in F2 progeny from a marine × freshwater stickleback cross identified a significant locus on chromosome 4 influencing multiple aspects of armor plate internal microstructure. This locus overlaps the well-characterized region previously known to control armor plate number and size. Co-mapping of bone microstructure could be due to pleiotropic effects of on multiple aspects of plate development or to changes in closely linked genes including , which also plays a role in bone formation. Most bone microstructure traits in vertebrae showed weak or no genetic signal, consistent with a polygenic architecture. However, we identified a highly significant locus on chromosome 17 that is strongly associated with abnormally thickened "ivory vertebrae" that occurred in 8.4% of F2 offspring. This phenotype resembles Paget's disease in humans, and the major locus region contains , the stickleback ortholog of a human Paget's disease susceptibility gene . Together, our findings identify genetic loci underlying natural variation in bone microstructure in wild fish and reveal a candidate gene associated with a disease-like skeletal phenotype, highlighting stickleback as a model for studying both evolutionary and pathological bone biology. - Source: PubMed
Publication date: 2026/04/14
Behrens Veronica CLee DavidWucherpfennig Julia IKingsley David M - Immune checkpoint blockade (ICB) targeting PD-1/PD-L1 axis has transformed breast cancer treatment, yet how therapy reshapes the tumor microenvironment (TME) through cell-cell communication (CCC) remains unclear. Existing CCC inference methods relying on correlations have difficulty distinguishing genuine signaling from confounded associations. Here, we present a causal inference framework that uses single-cell data and leverages treatment as an instrumental variable to identify genuine CCC networks, referred to as scIVCCC, which infers causal signal transduction across cell types. Applying scIVCCC to single-cell RNA-seq data from 31 breast cancer patients before and after anti-PD-1 therapy, we constructed causal CCC networks linking exhausted T cells to tumor-associated macrophages (TAMs). Our analysis reveals a dual role of T cell-macrophage crosstalk: CD4+ and CD8+ exhausted T cells drive anti-tumor M1-like TAMs activation via TNF-TNFRSF1A, TNFSF14-LTBR, and ICAM1-ITGAL/ITGB2. Conversely, they also induce immunosuppressive M2-like polarization through pathways such as TNF-TNFRSF1B (TNFR2), TNFSF14-TNFRSF14 (HVEM), and RPS19-C5AR1, which likely contribute to therapeutic resistance. Our causal modeling suggests that receptors within these networks, such as C5AR1, TNFR2, and CSF1R, may serve as potential candidates for combination therapies to enhance anti-PD-1 efficacy. Collectively, these findings demonstrate that scIVCCC offers a robust framework for dissecting treatment-induced CCC dynamics and prioritizing actionable targets for clinical translation. - Source: PubMed
Qiu AodongZhang HanRamsey Joseph DAndrews BryanSun BoyangRen ShuangxiaLu MengyaoZhang KunCooper Gregory FLu BinfengChen LujiaLu Xinghua - Soluble tumor necrosis factor receptor 2 (sTNFR2) is a member of the TNF superfamily whose normal bodily distribution is largely limited to low level expression on lymphoid cells. It has emerged as an important inducible receptor that activates a signaling pathway for cancer growth. We evaluated sTNFR2 as a prognostic biomarker for overall survival (OS) in newly diagnosed lymphoma using a prospective cohort study with banked pretreatment serum samples. sTNFR2 was higher in 1513 lymphoma patients compared to 499 age and sex matched controls (p < 0.0001). Using Kaplan-Meier curves and Cox proportional hazards models to estimate hazard ratios [HR] (high vs. low tertile), higher levels of sTNFR2 at diagnosis were associated with inferior OS across all seven major lymphoma subtypes: Hodgkin lymphoma (p < 0.0001; HR = 12.6), diffuse large B-cell lymphoma (p < 0.0001; HR = 2.6), follicular lymphoma (p = 0.00017; HR = 2.5), mantle cell lymphoma (p < 0.0001; HR = 4.2), small lymphocytic lymphoma (p = 0.012; HR = 2.4), marginal zone lymphoma (p = 0.0012; HR = 3.1), and T-cell lymphoma (p < 0.0001; HR = 3.1). Using CITE-seq profiling of tumor microenvironment tissue, we sought to identify cellular source(s) of circulating sTNFR2. In tumor tissue from follicular lymphoma, high TNFR2-expressing cells were found to be T-regulatory (Treg) cells, suggestive of a Treg-driven cancer. In tissue from a case of marginal zone lymphoma, high TNFR2 expression was found on CD4+ and CD8+ T cells, B cells, and monocytes but also directly on tumor cells. We conclude sTNRF2 is a strong prognostic biomarker of OS across major lymphoma subtypes and may be useful to guide therapeutic choices, including targeted therapies against immunosuppressive TNFR2-expressing Tregs. - Source: PubMed
Publication date: 2026/03/27
Khurana ArushiHayashi HikaruThach BethanyYang Zhi ZhangNegaard Brianna JCerhan James RNovak Anne JLink Brian KHabermann Thomas MFeldman Andrew LParikh Sameer ASlager Susan LAnsell Stephen MMaurer Matthew JFaustman Denise L