CD32B (phospho-Tyr292) antibody
- Known as:
- CD32B (phosphorilated-Tyr292) (anti-)
- Catalog number:
- orb100316
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- CD32B (phospho-Tyr292) antibody
Ask about this productRelated genes to: CD32B (phospho-Tyr292) antibody
- Gene:
- FCGR2B NIH gene
- Name:
- Fc fragment of IgG receptor IIb
- Previous symbol:
- FCG2, FCGR2
- Synonyms:
- CD32, CD32B
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-21
- Date modifiied:
- 2016-10-05
Related products to: CD32B (phospho-Tyr292) antibody
Related articles to: CD32B (phospho-Tyr292) antibody
- High-throughput sequencing of B and T cell repertoires provides unprecedented insights into adaptive immunity but generates high-dimensional feature sets that are challenging to interpret. Standard dimensionality reduction techniques are often suboptimal for adaptive immune receptor repertoire (AIRR) data, which exhibits multi-collinearity, heterogeneous data types, and missingness. - Source: PubMed
Amin SakinaOverend LaurenTucci FeliciaSun BoWhalley JustinDustin Michael LKnight Julian CBashford-Rogers Rachael - Rheumatoid factor (RF) autoantibodies are highly prevalent, yet the molecular determinants of RF development and its progression to rheumatoid arthritis (RA) remain poorly understood. Here, we define the genetic, phenotypic, and molecular architecture of RF and its progression to RA. - Source: PubMed
Publication date: 2026/06/30
Hocaoglu MehmetSawalha Amr H - FCGR2B, the only inhibitory receptor in the Fcγ receptor family, plays a crucial role in both innate and adaptive immunity. In this study, we observed high FCGR2B expression in tumor-associated macrophages (TAMs) induced by B16 melanoma cells. Knockdown of in these TAMs suppressed their M2 polarization, as evidenced by decreased expression of immunosuppressive factors, including Arg-1, IL-10, and Fizz1. Furthermore, knockdown enhanced the phagocytic and antigen-presenting capacities of TAMs, promoted ROS production, and improved their ability to kill melanoma cells in vitro. Transcriptomic analysis revealed that knockdown predominantly affected key metabolic and signaling pathways, including the JAK-STAT and PPAR-γ pathways. Using classic pharmacological inhibitors (2-DG and C75), we confirmed that FCGR2B interference remodels glycolipid metabolism in TAMs, which is characterized primarily by attenuated fatty acid metabolism, accompanied by increased glycolysis and intracellular free fatty acid accumulation. Moreover, FCGR2B interference downregulated the fatty acid oxidation key enzyme CPT1a by inhibiting the JAK/STAT6/PPAR-γ signaling axis, thereby reducing fatty acid oxidation. Concomitantly, it alleviated endoplasmic reticulum stress via the IRE1/XBP1 pathway, ultimately attenuating the tumor-promoting phenotype of TAMs. Our findings delineate a mechanism by which FCGR2B integrates metabolic and signaling pathways to regulate TAM function, providing a mechanistic basis for targeting FCGR2B in cancer immunotherapy. - Source: PubMed
Publication date: 2026/06/14
Han ZexuRao PeiWang FuzhouXing YunyingGuo XuelingDu ChaoWang Yingze - African swine fever (ASF) remains a persistent threat to global pig production, with no licensed vaccines or effective treatments available. Observations of surviving individuals within low-virulence infected herds suggest that host genetic resistance plays a crucial role. - Source: PubMed
Ye XiaoweiXie QinqinCao CaiyunLiu ShuangSun WenboZhang ZheWang QishanPan YuchunWang Zhen - Pemphigus vulgaris (PV) is a rare autoimmune blistering disease mediated by pathogenic autoantibodies. Although both HLA and non-HLA loci contribute to disease susceptibility, their combined roles in immune regulation remain incompletely understood. This study investigated the joint contribution of HLA-DRB1 and FCGR2B variants to PV susceptibility within an integrative immunogenetic framework. Genotype data from 286 individuals (200 controls and 86 PV patients) were analyzed using bias-reduced association models, two-locus genotype combination analyses, and cumulative genetic risk modeling. Gene-gene relationships were explored through epistasis testing, while functional relevance was examined using biological annotation approaches. HLA-DRB1*04:02 and *14:01 were significantly associated with increased PV risk, whereas *11:01 and *16:01 demonstrated protective effects after multiple testing correction (q < 0.05). The FCGR2B c.671T > C (I232T) variant showed a modest effect in single-locus analyses but did not remain statistically significant after correction for multiple testing. Several two-locus genotype combinations involving FCGR2B and HLA-DRB1 were enriched among patients; however, interaction analyses supported an additive immunogenetic architecture rather than epistasis. Genetic risk modeling demonstrated improved discrimination with weighted scores, and explainable machine-learning analysis identified HLA-DRB1 as the dominant predictor, with FCGR2B contributing a secondary modulatory signal. These findings delineate an additive immunogenetic framework underlying PV susceptibility, emphasizing the central role of HLA-DRB1. Although FCGR2B did not retain independent statistical significance after multiple-testing correction, the results suggest a potential modulatory contribution within the broader immunogenetic architecture of PV. - Source: PubMed
Publication date: 2026/05/20
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