FCGR1A Antibody
- Known as:
- FCGR1A Antibody
- Catalog number:
- 32221
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- FCGR1A Antibody
Related genes to: FCGR1A Antibody
- Gene:
- FCGR1A NIH gene
- Name:
- Fc fragment of IgG receptor Ia
- Previous symbol:
- -
- Synonyms:
- CD64, CD64A
- Chromosome:
- 1q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-12-03
- Date modifiied:
- 2019-04-23
Related products to: FCGR1A Antibody
Related articles to: FCGR1A Antibody
- The red-spotted grouper nervous necrosis virus (RGNNV) exhibits high pathogenicity in larval , yet the immune molecular mechanism remains unclear. Non-coding RNAs (ncRNAs) are vital in the host's immune responses during viral infection. However, there has been no study on ncRNA research for this species to date. We systematically identified 105 DE microRNAs (miRNAs), 157 DE long non-coding RNAs (lncRNAs) and 31 DE circular RNAs between the infection group and control group. Functional enrichment analysis revealed that these differentially expressed genes were significantly enriched in pathways associated with innate immune defense, inflammatory, and cell death, such as JAK-STAT signaling pathway, NF-κB signaling pathway, apoptosis, and necroptosis. Furthermore, the lncRNA-miRNA-mRNA interaction network involving miR-93 was constructed, which may represent a promising candidate therapy target for future investigations. This study presents the first comprehensive ncRNA transcriptome dataset of infected with RGNNV, identifies key antiviral defense and cell death-related genes and hub pathways, and thereby identifies miR-93-involved lncRNA-miRNA-mRNA network and key targeted genes () as hub molecular regulators in immune response of this species. - Source: PubMed
Publication date: 2026/08/12
Guo XiaoliGao ChengbinChen ZhangfanLu ShengWang LeiLi WenshengHe XinleiYang ChuanjunLi JianweiChen Songlin - Behçet's disease (BD) is a rare chronic systemic vasculitis of unknown etiology. The heterogeneity of peripheral blood immune cells and the dysregulation of intercellular communication in BD remain insufficiently characterized. The present study employs single-cell transcriptomics to comprehensively delineate the peripheral blood immune cell atlas of BD, identify candidate diagnostic biomarkers, and dissect the remodeling patterns of intercellular communication networks. - Source: PubMed
Publication date: 2026/08/04
Yang YanfeiChen Yuexin - Kawasaki disease (KD) is a multisystemic vasculitis of unknown aetiology in children. KD with coronary artery lesion (CAL) is now the leading acquired heart disease in children. Peripheral blood mononuclear cells (PBMCs) play roles in KD. We identified hub genes based on RNA sequencing data and validated them in PBMCs and human umbilical vein endothelial cells (HUVECs) co-culture with PBMCs. Expression profiling by high throughput sequencing (RNA-seq data) PBMCs from 12 acute KD patients and 12 healthy controls was performed to screen differentially expressed mRNAs (DE-mRNAs). We selected 20 KD with CAL, 20 KD patients without CAL and 40 healthy controls for validation, and established HUVECs co-culture with PBMCs. Real time-PCR was finally conducted to confirm the reliability and validity of the expression level of DE-mRNAs from PBMC-HUVECs co-cultures. A total of 6039 DE-mRNAs were found (2267 upregulated, 3772 downregulated). Thirty hub genes were selected. KD PBMCs significantly impaired HUVECs viability and migration. IL1R2 was downregulated, FCGR1A, and CD177 mRNAs were upregulated in acute KD and KD with CAL. IL1R2 was elevated, FCGR1A and CD177 mRNAs were downregulated in convalescence and KD without CAL. And the real-time PCR and ELISA results showed IL1R2 was downregulated in acute KD PBMC-HUVECs co-cultures and elevated in convalescence. These findings may improve our understanding of PBMCs and PBMC-HUVECs co-cultures with PBMCs in KD. - Source: PubMed
Publication date: 2026/06/30
Hong XiaofengWang QianwenLan TianXu JianxinZhan YiShi Jiandong - Orofacial clefts are among the most common congenital craniofacial anomalies in the world. Immunity factors modulate response, inflammation, and healing in clefted tissue. This study aims to evaluate the levels of the pro-inflammatory biomarkers Granulysin, Resistin, FCGR1A, NF-kßp65, and CD68 to describe and understand the morphopathological basis of inflammation. The comparison was done between patient and control samples across milk and mixed dentition age groups. In total, 14 patient samples were analyzed with a total of 10 control samples to form two distinct control groups with milk dentition age and mixed dentition age. Samples were analyzed using light microscopy, and a semi-quantitative method of evaluation and comparison was used to determine the number of immunohistochemically positive structures of patient and control samples. Statistics included Spearman's correlation and Fisher's exact test to compare groups and detect significant differences. NF-kßp65 in the milk dentition age group ( = 0.043 for NF-kßp65 in connective tissue, = 0.017 for NF-kßp65 in salivary glands), and FCGR1A and CD68 in the mixed dentition age group showed statistically significant differences in the expression of palatal tissues compared to the controls ( = 0.016 for FCGR1A in connective tissue, = 0.048 for CD68 in epithelium). Spearman's rank correlation revealed eight very strong correlations among several factors and one strong correlation between factors. The presence of many very strong and strong Spearman's correlations among inflammatory factors in cleft-affected individuals suggests heightened signaling in these pathways. Furthermore, the difference in the inflammatory factor expression at different dentition ages suggests variation in the inflammation character with age. - Source: PubMed
Publication date: 2026/06/12
Kuļibaba GeorgijsPilmane Māra - Protollin, a nasal adjuvant, was evaluated in a randomized double-blind phase 1 study of 16 early Alzheimer's disease (AD) patients to determine safety and to assess its immunomodulatory effects. In a double-blind dose escalation study, subjects received nasal Protollin at doses of 0.1 mg, 0.5 mg, 1.0 mg, and 1.5 mg or placebo twice over a two-week period. Treatment was well-tolerated with minimal side effects. Transcriptomic and single-cell analyses demonstrated that prior to treatment, AD blood monocytes had downregulation of phagocytosis-related genes and an increased pro-inflammatory signature. These AD monocyte abnormalities were reversed by nasal Protollin beginning at a dose of 1.0 mg. Protollin induced a robust phagocytic gene signature, including upregulation of CD36, ITGAL, LYST, and FCGR1A. A similar phagocytic signature was observed in brain-infiltrating amyloid-clearing monocytes in an APP Tg mouse model treated with nasal Protollin. Protollin treatment decreased the expression of costimulatory molecules on monocytes and decreased CD8 T cell activation and cytotoxicity. Our results provide the basis for a phase 2 study of nasal Protollin in subjects with AD in which nasal Protollin at a dose of 1.0 mg will be administered weekly over 6 months to modulate peripheral immunity and clear amyloid from the brain. ClinicalTrials.gov registration no NCT07187141. - Source: PubMed
Publication date: 2026/06/05
Kolypetri Panayotada Silva PatrickFrancisco Ronaldo SFrenkel DanCecere Rachael RKiliaan Pien C JMontini FedericoSaxena ShrishtiClementi William ALiu XuejunSun ChengBergmark Regan WSinghal TarunSaraceno Taylor JZimmermann JosephGale Seth ASelkoe Dennis JChitnis TanujaWeiner Howard L