Ask about this productRelated genes to: FCER1A antibody
- Gene:
- FCER1A NIH gene
- Name:
- Fc fragment of IgE receptor Ia
- Previous symbol:
- FCE1A
- Synonyms:
- -
- Chromosome:
- 1q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2016-10-05
Related products to: FCER1A antibody
Related articles to: FCER1A antibody
- B cells are integral components of the tumor microenvironment (TME) and influence the progression, prognosis, and immunotherapy response of gastric cancer (GC). However, the prognostic relevance of germline variants in B cell-related immune genes remains undefined. We performed a two-stage genome-wide association analysis to identify single-nucleotide polymorphisms (SNPs) in B cell-related immune genes associated with overall survival (OS) in patients with pathologic tumor-node-metastasis (pTNM) stage I-III GC. Clinical, follow-up, and genome-wide association study (GWAS) genotyping data were analyzed from two independent Eastern Chinese cohorts (Shanghai, N = 2211; Jiangsu, N = 1049). Functional annotation, quantitative trait loci (QTL), and immune infiltration analyses were conducted. Among 15,857 SNPs across 223 genes, 210 were associated with OS in the discovery cohort, nine of which were validated. Two independent functional variants-FCER1A rs539959920 C > T and PLCG2 rs72832034 C > T-were consistently associated with poorer OS (adjusted HR = 1.19, 95% CI = 1.04-1.37, p = 0.014; HR = 1.34, 95% CI = 1.09-1.64, p = 0.005). Patients carrying multiple unfavorable genotypes exhibited a dose-dependent decline in survival (P = 0.002). Incorporation of these SNPs modestly improved time-dependent AUCs for OS prediction at 36 months. Single-cell expression and splicing QTL analyses demonstrated allele-specific modulation of FCER1A and PLCG2 expression across immune cell subsets, consistent with altered immune infiltration patterns in the GC TME. These findings suggest that two germline variants in FCER1A and PLCG2 independently predict GC survival, likely through transcriptional and immunologic modulation, thereby nominating these variants as potential immune-genetic biomarkers for GC prognosis and therapeutic stratification. - Source: PubMed
Publication date: 2026/05/15
Zeng GuangLu GuoqiangHu BeipingXu MidieLi GuanlinWang MengyunQiu LixinCheng LeiZhang RuoxinXu WanghongLiu XiaowenJin GuangfuLiu HongliangWei Qingyi - Asthma constitutes a widespread chronic respiratory disease with multifactorial origins, in which definitive genetic components remain incompletely understood. This investigation synthesized transcriptomic data and Mendelian randomization (MR) to delineate causative genes contributing to asthma predisposition. Evaluation of the GSE43696 cohort disclosed 267 genes displaying expression alterations between healthy controls (n = 20) and asthmatic cases (n = 88). MR methods discerned seven causal genes, consisting of six protective determinants (GPRIN3, SHISA2, DUSP5, FCER1A, USP36, and LGALS2; OR < 1) and one risk-associated determinant (CXCL6; OR > 1). Independent validation with the GSE63142 series verified pronounced suppression of five genes in asthma specimens. Functional enrichment studies connected these genes to immune-related cascades, including IL-17/NF-κB signal transduction and Th17 cell differentiation, alongside metabolic activities. Single-cell transcriptomic assessment of 32,809 cells exposed compartmentalized expression profiles: FCER1A and LGALS2 predominated in dendritic cells, DUSP5 in goblet cells, SHISA2 in ionocytes, and USP36 in T cells. Immune cell infiltration evaluation demonstrated shifted distributions of mast cells, eosinophils, and monocytes, exhibiting substantial linkages with immune mediators such as CCR5 and CXCL10. Transcription factor exploration recognized cisbp__M0561 as the predominant regulatory element. Connectivity Map-based interrogation nominated KI-8751, verrucarin-A, and homoharringtonine as plausible therapeutic candidates. This consolidated multiomics framework elucidates previously uncharacterized pathological processes and prospective treatment avenues for asthma. - Source: PubMed
Liu FangCui HongtaoMei YanLi KeyuXu YanLi ShumanYuan Chao - Chronic Spontaneous Urticaria (CSU) is a debilitating skin condition characterized by recurrent wheals and pruritus, significantly impacting quality of life. Molecular mechanisms underlying different severity phenotypes are not fully understood. This study aimed to investigate the expression of FCER1A and PTAFR genes in basophils implicated in CSU pathogenesis from CSU patients with varying disease severities. - Source: PubMed
Soetanto Kevin MuliawanSripatumtong ChattipParingkarn TeerapatAngkoolpakdeekul NatthaKulthanan KanokvalaiSrinoulprasert Yuttana - Sepsis, involving systemic inflammation and organ failure, presents significant challenges due to its complex and heterogeneous immunological reactions. T-helper 17 (Th17) cells contribute significantly to immune regulation, and their dysregulation is implicated in sepsis pathogenesis. Understanding how Th17 cell differentiation-related genes contribute to sepsis heterogeneity and prognosis is crucial for improving patient prognosis. - Source: PubMed
Publication date: 2026/02/27
Li XiuhuaTan LifeiDing YingweiZhang Bingwen - Colorectal cancer (CRC) and Coronavirus Disease 2019 (COVID-19) are distinct diseases that may share overlapping molecular mechanisms, particularly in immune dysregulation. However, the specific regulatory pathways driving this shared pathophysiology have remained elusive, as prior studies have been limited by single-level data. To dissect this common pathobiology, we implemented a synergistic computational framework, integrating bulk transcriptomics with single-cell data. Through a multi-tiered analysis pipeline employing differential expression, weighted gene co-expression networks, and machine learning-based feature selection, we pinpointed a core molecular signature of 31 shared hub genes. Among these, four core candidates-GPR15, PTGDR2, FCER1A, and MAL-were significantly downregulated, a finding robustly associated with impaired CD8+ T cell infiltration. Delving deeper into the regulatory architecture using a modified weighted out-degree centrality algorithm, we constructed an integrated transcription factor-microRNA-target network. Network analysis revealed upregulation of p53 and downregulation of miR-3619-5p as possible drivers of immune dysfunction. Finally, E-4031 was identified through molecular simulation as a potential therapeutic agent targeting all four core genes. These findings uncover a shared regulatory axis involving immune suppression and transcriptional disruption, and provide promising diagnostic and therapeutic targets for CRC and COVID-19. - Source: PubMed
Wang HairuiYao HaodongNiu WenchaoXing RongchangCai LuXi ZuoxinGao ShichenZhao Lina