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
Related 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
- Atopic dermatitis (AD) is a common pediatric skin disorder with early onset and complex pathophysiology. Tape-strip sampling has enabled minimally invasive molecular profiling of skin lesions in children, yet approaches that verify and standardize stratum corneum (SC) sampling depth have remained limited. - Source: PubMed
Publication date: 2026/07/12
Andersen DanielYélamos OriolCombalia MarcIglesias PabloPotrony MiriamDanneskiold-Samsøe Niels BKristiansen KarstenThysen Anna HGuy Richard HMalvehy JosepRøpke MadsPont MercèPuig SusanaBrix Susanne - 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 - The inhibitory human Fc gamma receptor, hFcγRIIB, is a key mediator of humoral immunity and regulator of antibody-mediated effector function. hFcγRIIB function can be modulated by anti-hFcγRIIB antibodies. We demonstrate that agonistic, but not antagonistic, antibodies reduce hFcγRIIB mobility in the plasma membrane, associated with receptor clustering and redistribution into lipid rafts. Agonists display lower affinity binding with higher off rates compared with antagonists. Using crystallographic structure determination and alanine-scanning mutagenesis, we show that epitopes targeted by agonistic and antagonistic antibodies are overlapping but distinct. Using small-angle X-ray scattering (SAXS) and molecular dynamics simulations, we demonstrate that agonists nucleate more compact receptor complexes. Through their high off rates, we propose that agonists facilitate a catch-and-release mechanism that promotes receptor clustering and subsequent activation. By contrast, antagonists adopt a binding geometry that prevents effective clustering, with their low off rate reducing receptor disengagement and subsequent clustering. These findings provide key principles underpinning agonism versus antagonism of immunomodulatory receptors. - Source: PubMed
Publication date: 2026/06/25
Fisher HaydenSutton Emma JOldham Robert JBradshaw Richard TDuriez Patrick JFrendéus BjörnLarsson GunillaManfredi GiusiMartin-Fernandez Marisa LMockridge IanNeedham Sarah RRolfe Daniel JOrr Christian MPatel KallumRoghanian AliSimpson AlexTully Mark DTeige IngridTornberg Ulla-CarinTynan Christopher JPendower AbigailKim JinnyTennenhouse ArielFleishman Sarel JEssex Jonathan WTews IvoCragg Mark S - 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