Ask about this productRelated genes to: FCGR2A antibody
- 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: FCGR2A antibody
Related articles to: FCGR2A antibody
- Numerous studies have demonstrated a pathogenic association between rheumatoid arthritis (RA) and type 2 diabetes mellitus (T2DM), 2 chronic inflammatory diseases. This study integrates transcriptomic and bioinformatic analyses to elucidate the shared molecular mechanisms underlying RA-associated T2DM, aiming to identify effective therapeutic strategies. RNA expression profile datasets for RA and T2DM were downloaded from the gene. Expression Omnibus and Gene Network (Grein) databases. Common differentially expressed genes shared between RA and T2DM were identified and subsequently subjected to gene enrichment analysis, protein-protein interaction network construction, GeneMANIA analysis, immune microenvironment evaluation, and drug prediction. Additionally, the diagnostic performance of hub genes was assessed using receiver operating characteristic curve analysis. Finally, molecular docking was employed to facilitate computer-aided drug design and to investigate drug-gene interactions. We identified 352 common differentially expressed genes, and functional analyses showed that they were mainly involved in the immune regulation of RA-associated T2DM. Thirteen key genes were confirmed through the protein-protein interaction network analysis and validation cohort. Receiver operating characteristic curves confirmed the reliability of their diagnostic value. GeneMANIA analyses suggested these genes were mainly associated with leukocytes, particularly neutrophils. Results from the immune microenvironment revealed abnormal levels of neutrophils in RA and T2DM. Among them, 10 key genes (LYN, TLR1, TLR2, TLR8, FCGR1A, FCGR2A, CCR1, CXCL1, FPR1, and SELL) were considered as neutrophil-related genes. Mechanistically, these genes activate pro-inflammatory signaling pathways, exacerbating tissue inflammation and promoting insulin resistance, ultimately leading to the onset of T2DM, neutrophils play a pivotal role in this process. Drug prediction and molecular docking results indicated that PD-169316 is a potential immunotherapeutic for patients with RA in combination with T2DM. This study concludes that neutrophil-driven inflammatory responses and their associated genes may accelerate the progression of type 2 diabetes caused by RA. - Source: PubMed
Qu XiaochaoZuo XuemeiDu HongChen YixuanZhang QingPeng HuiminMa KeqiangZhang FurongCai YishengTan LijunDeng HongwenChen Xiangding - Immunogenic cell death (ICD) influences tumor immune microenvironment remodeling and immunotherapy response. However, the prognostic value of ICD-related genes in colon cancer has not been systematically clarified. This study aimed to develop an ICD-based prognostic model and explore its association with the immune microenvironment and treatment sensitivity. - Source: PubMed
Publication date: 2026/01/22
Wang HaipengChen NingningWang Weijia - Chimeric antigen receptor macrophages (CAR-Ms) represent a novel approach in cellular immunotherapy. Human pluripotent stem cells (hPSCs) provide an unlimited and renewable cell source, enabling scalable and standardized production of CAR-Ms with consistent quality. - Source: PubMed
Publication date: 2026/01/12
Yang XinzhiLi LuZhu SijingLi ShengtaoWang XinluHan YulingYang Liuliu - Thyroid cancer comprises a heterogeneous group of malignancies with distinct clinical outcomes and molecular features, including papillary thyroid carcinoma (PTC), poorly differentiated thyroid carcinoma (PDTC), and anaplastic thyroid carcinoma (ATC). This study aimed to delineate the molecular and immune landscapes of these subtypes and identify potential biomarkers for the aggressive forms, ATC and PDTC. We assembled a well-annotated cohort of 120 formalin-fixed paraffin-embedded samples, including 35 ATC, 18 PDTC, 37 PTC cases, and 30 adjacent normal tissues (N) paired with PTC, collected over the past decade from multiple hospitals. To our knowledge, this represents the largest clinical ATC/PDTC cohort subjected to multiomics profiling and the first comprehensive proteomic analysis of these aggressive thyroid cancers. Using 4D-data-independent acquisition proteomics on 118 tumors (ATC 34, PDTC 18, PTC 36, and N 30), integrated with total RNA-seq on 69 samples (ATC 10, PDTC 5, PTC 31, and N 23), we revealed substantial molecular similarities between ATC and PDTC, both markedly distinct from PTC and adjacent normal tissues. ATC and PDTC exhibited significant enrichment in immune-related and metabolic pathways, with transcriptomic data indicating aggressive phenotypes and pronounced immunosuppression. Distinct immune landscapes of ATC and PDTC were revealed with neutrophil extracellular trap formation and M0 macrophage accumulation as key immunosuppressive mechanisms. Notably, Fc fragment of IgG receptor IIa (CD32) was identified as a promising biomarker for ATC, implicating a functional link between immune evasion and tumor aggressiveness. Our findings provide a comprehensive molecular and immunological characterization of thyroid cancer subtypes, offering novel insights into the pathogenesis of ATC and PDTC, and identifying potential targets for diagnosis and precision therapy. - Source: PubMed
Publication date: 2026/01/19
Gui ShanyingHuang KateQiang JianlingChen YunzhaoGan MeifuJiang ZhaochangQian JiaziYi ChenchenDing YiJiang HuihuiZheng FulongLei WanlinJin LuluZhang XiaoweiFang HezhiWang Maofeng - Sex differences, in terms of prevalence, symptoms and disease progression, are established in the etiology of complex neurodegenerative diseases, including amyotrophic lateral sclerosis, Parkinson's disease and Alzheimer's disease, but the underlying biology driving these differences remains poorly understood. There is emerging evidence, through genetic and functional analyses, affirming the role of the immune system in such diseases, but a thorough assessment of sex differences linking the immune system and neurodegenerative diseases is understudied. Here, we applied a robust causal inference approach, two-sample Mendelian randomization, to evaluate the causal effect of immune-related protein levels on three neurodegenerative diseases with large-scale sex-stratified genome-wide association data available: amyotrophic lateral sclerosis (females = 10,895 cases, 57,062 controls; males = 15,547 cases, 50,145 controls), Parkinson's disease (females = 7,947 cases, 90,662 controls; males = 13,020 cases, 89,660 controls) and Alzheimer's disease (females = 18,822 cases, 281,415 controls; males = 17,293 cases, 213,339 controls). As exposures, we focused on 932 immune system-related proteins with significant protein cis-quantitative trait loci (FDR cutoff < 0.01) from a large sex-combined plasma protein dataset (N = 33,477), for which corresponding genes were included in the Immunology Database and Analysis Portal gene list. We tested for a causal relationship between genetically predicted levels of each of these proteins and each neurodegenerative disease in sex-stratified and sex-combined data, followed by colocalization and estimation of sex-differential effects. We additionally performed exploratory analyses using sex-combined CSF protein cis-quantitative trait loci (N = 971) as exposures. We observed evidence for a sex-differential causal relationship between FCGR2A and Parkinson's disease, and between CD2AP, MAMDC2, PCDH17 or CSF3 and Alzheimer's disease. We validated significant results using two independent protein cis-quantitative trait loci datasets for those plasma proteins available. After performing sensitivity analyses, we validated the potential causal relationships of OMG on Parkinson's disease and of GRN, SERPINF2 and TREM2 on Alzheimer's disease. Mendelian randomization with CSF protein cis-quantitative trait loci showed a potential causal effect of ADGRE2, GPNMB and COLEC11 on Parkinson's disease and of CD33 on Alzheimer's disease, without evidence of sex-differential effects. Finally, we substantiated our findings of protein-disease pairs using triangulation, specifically reporting independent supporting evidence from the literature and drug-related databases. Overall, our results point to potential causal effects of genetically predicted levels of immune system-related plasma and CSF proteins in Alzheimer's disease and Parkinson's disease, some of which may be considered as potential candidates for drug development. - Source: PubMed
Publication date: 2025/12/24
Lona-Durazo FridaByrne Ross PPilon Marc-OlivierGreicius Michael DDubé Marie-PierreBelloy Michael EMcLaughlin Russell LGagliano Taliun Sarah A