CD32B pTyr292 antibody Ab
- Known as:
- CD32B pTyr292 (anti-) Antibody
- Catalog number:
- 1488034
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- CD32B pTyr292 antibody
Related genes to: CD32B pTyr292 antibody Ab
- 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 pTyr292 antibody Ab
Related articles to: CD32B pTyr292 antibody Ab
- 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
Kasap Burak KaanToraman BayramKurt BurçinErmis HandeArıca Deniz Aksu - Platelet-rich fibrin (PRF) is extensively utilized to enhance localized tissue healing, a process that critically depends on the transient polarization of macrophages toward a pro-inflammatory phenotype. Given that PRF, like other blood clot derivatives, may intrinsically modulate macrophage behavior, we conducted a comprehensive screening assay to characterize the global macrophage response to PRF exposure. To this end, we employed two widely used monocytic cell lines-U937 (histiocytic lymphoma) and THP-1 (acute monocytic leukemia)-as models to investigate macrophage responses. Cells were exposed to lysates derived from PRF, and transcriptomic alterations were profiled using bulk RNA sequencing. Differential gene expression analysis was performed, with significance determined by an adjusted p-value threshold of <0.05. In U937-derived macrophages, gene expression profiling revealed a transcriptional signature consistent with inflammatory activation. Clustering of upregulated genes highlighted pathways associated with chemokine activity (e.g., CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL20, CCL23, CCL26, CXCL5, CXCL6, CXCL8, CXCL16, and PPBP), RAGE receptor binding (FPR1, S100A8, S100A9, and S100A12), IgG binding (FCGR1A, FCGR2A, FCGR2B, and FCGR3A), prostaglandin biosynthesis (CBR1, CD74, EDN1, FABP5, IL1B, MIF, PTGES, and PTGS1), and collagen catabolism (CTSL, FAP, MMP3, MMP7, MMP9, MMP12, MMP14, MMP19, and MRC2). In contrast, PRF exposure in THP-1 cells primarily enriched genes involved in steroid biosynthesis, suggesting a more limited or distinct response. These findings underscore U937 cells as a more responsive and appropriate bioassay for modeling inflammatory macrophage polarization in response to PRF. Moreover, the identified gene signatures recapitulate key aspects of early wound healing, providing a relevant platform for studying macrophage reactivation in chronic wound environments. - Source: PubMed
Publication date: 2026/04/22
Panahipour LaylaHuang XiaoyuZampino FrancescaMiron Richard JGruber Reinhard - N-glycans are essential components of glycoproteins, influencing their properties and functions. While biochemical pathways of glycosylation are well-characterized, their genetic regulation remains poorly understood. This study utilizes matrix-assisted laser desorption/ionization-mass spectrometry (MALDI-MS) and ultra-high performance liquid chromatography-fluorescence detection (UHPLC-FD) to strengthen replication and further characterize previously identified genome-wide association signals for the total human plasma N-glycome (TPNG). Univariate and multivariate genetic association meta-analyses involved 3385 samples across 143 N-glycome traits from the Hoorn Diabetes Care System and DiaGene cohorts as well as 3224 samples across 117 N-glycome traits from TwinsUK, CEDAR, QMDiab and SABRE cohorts. We successfully replicated ten previously identified but not replicated glycosylation quantitative trait loci (glyQTLs) and prioritized five high-confidence putative causal genes, including the glycosyltransferase MGAT4B and inflammation-related genes - C3 and FCGR2B. The linkage-specific sialic acid derivatization in MALDI-MS enabled delineation of genetic effects on α2,3- and α2,6-sialylation. Mass spectrometry analysis, triggered and guided by association to a locus containing B3GAT1 glucuronosyltransferase, provided evidence for hexuronic acid-containing glycans in human blood plasma. These findings advance our understanding of the genetic regulation of protein N-glycosylation and highlight the complementarity of different analytical approaches in glycomics research. - Source: PubMed
Timoshchuk AnnaNaber AnnemiekeSlieker RoderickSoplenkova AnnaMaslov Denis EPotapova Nadezhda ANicolardi SimoneElders P J MSijbrands Eric J GSharapov Sodbo't Hart Leen Mvan Hoek MandyWuhrer ManfredAulchenko Yurii S - High-grade serous ovarian cancer (HGSOC) is characterized by a complex tumor microenvironment and poor prognosis, yet the roles of specific tumor-associated macrophages (TAMs) subpopulations in driving disease progression remain elusive. - Source: PubMed
Publication date: 2026/04/06
Zhou JialuZeng TaoLiu YiYe MingxiaLi MingxiaZhang ZheMeng Yuanguang - Epithelial ovarian cancer (EOC) encompasses five major histological subtypes with marked genetic, immunological, and clinical heterogeneity. While genome-wide association studies (GWAS) have identified subtype-specific risk loci, a critical gap remains in understanding how plasma proteins influence immune-cell traits and contribute to EOC pathogenesis. - Source: PubMed
Publication date: 2026/04/03
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