Human FcGR2A / CD32a (H131) Protein
- Known as:
- Human FcGR2A / CD32a (H131) Protein
- Catalog number:
- CD1-H5223
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human FcGR2A / CD32a (H131) Protein
Related genes to: Human FcGR2A / CD32a (H131) Protein
- Gene:
- CEP41 NIH gene
- Name:
- centrosomal protein 41
- Previous symbol:
- TSGA14
- Synonyms:
- DKFZp762H1311, FLJ22445, JBTS15
- Chromosome:
- 7q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-08-24
- Date modifiied:
- 2016-10-05
- Gene:
- FCGR2A NIH gene
- Name:
- Fc fragment of IgG receptor IIa
- Previous symbol:
- FCG2, FCGR2A1, FCGR2
- Synonyms:
- CD32, CD32A, IGFR2, CDw32
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-11-30
- Date modifiied:
- 2019-04-23
Related products to: Human FcGR2A / CD32a (H131) Protein
Related articles to: Human FcGR2A / CD32a (H131) Protein
- Progression to end-stage lung diseases is influenced by both environmental and genetic factors, yet predictive markers remain limited. The CD32-131H>R polymorphism in the FCGR2A gene alters the affinity of the FcγRIIa receptor for IgG and may impair immune clearance, potentially influencing immune responses involved in chronic lung disease. In our study, we investigated the association between the CD32-131H>R polymorphism and end-stage pulmonary diseases requiring LTX. - Source: PubMed
Publication date: 2026/05/25
Berger Sarah MKühner Laura MSchwarzinger Ines MHeiss Spornberger VerenaJaksch PeterPuchhammer-Stöckl ElisabethVietzen Hannes - Rituximab is an anti-CD20 monoclonal antibody used in autoimmune diseases, including glomerular diseases. The FCGR2A (rs1801274) and FCGR3A (rs396991) variants have been suggested to affect rituximab efficacy; this study evaluates their impact on rituximab efficacy in glomerular diseases. A clinical trial was performed including adults with glomerular diseases who required rituximab (NEFRTX; EudraCT: 2020-000484-23). Patients received 1.0 g or 0.5 g of rituximab on day 1 (± day 14); biochemical parameters and rituximab concentration were measured, and FCGR2A and FCGR3A variants were characterized. Clinical outcome was evaluated at 6 and 12 months. 30 patients were included. FCGR2A (rs1801274) and FCGR3A (rs396991) variants did not show an effect on clinical response to rituximab. When the effect of the variant was corrected by rituximab exposure, the expression of the FCGR2A rs1801274-A allele vs. no expression was related to a poorer response at month 6 (odds ratio 0.034; 95% confidence interval 0.002-0.725; p = 0.030); this effect was not seen for FCGR3A. Additional studies involving larger cohorts are warranted to validate these findings. - Source: PubMed
Larrosa-García MaríaPamplona Irene AgrazTolosa Susana RojoMorales Alberto JiménezMartínez María Teresa SanzGallo Mónica MartínezColobran RogerVicente Helena GenestalPena Nerea MorenoMacías Roxana Paola BuryRonsano José Bruno Montoro - Rheumatoid arthritis (RA) is a chronic inflammatory disease of immune-mediated origin. Janus kinase inhibitors (JAK inhibitors) have expanded therapeutic options in recent years; however, clinical response varies among patients, and no biomarkers are currently available to predict their efficacy. The aim of this study was to analyze the association between pharmacogenetic variants and clinical response to JAK inhibitors in patients with RA. - Source: PubMed
Publication date: 2026/04/23
Plasencia-Rodríguez ChamaidaNovella-Navarro MartaValdivieso Shephard Juan LuisMartínez-Feito AnaReche-Yebra KerenJuárez-García ManuelVillalba-Yllán AlejandroRubio-Lepe Tania SArias PedroCollada Sánchez Victoria LuciaMartin-López SusanaLosantos-García ItsasoBorobia Alberto MRosas-Alonso Rocío - 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 - Crohn's disease (CD) is a chronic, idiopathic inflammatory bowel disease. Understanding the genetic and immunological basis of CD can lead to better therapeutic strategies. - Source: PubMed
Publication date: 2026/04/21
Zhang XinweiLiu LinXu WenyuLi GuangxinQin QiuZhang Jinan