Ask about this productRelated genes to: A4GNT Blocking Peptide
- Gene:
- A4GNT NIH gene
- Name:
- alpha-1,4-N-acetylglucosaminyltransferase
- Previous symbol:
- -
- Synonyms:
- alpha4GnT
- Chromosome:
- 3q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-12
- Date modifiied:
- 2016-10-05
Related products to: A4GNT Blocking Peptide
Related articles to: A4GNT Blocking Peptide
- Trefoil factor 2 (TFF2) has been shown to reduce inflammation and promote mucosal repair in models of gastric and colonic injury. However, the role of TFF2 in acute respiratory tract infection remains elusive. Here, we demonstrate that TFF2 protects mice against pneumonia in influenza virus infections. studies have revealed that TFF2 does not directly bind to the previously reported potential receptors but recognizes the terminal GlcNAc-α-1,4-Gal disaccharide of cell surface proteins mediated by the glycosyltransferase activity of α1,4-N-acetylglucosaminyltransferase (A4GNT). Functionally, TFF2 organized membranous TFF2-A4GNT-glycan protein complex serves to restrain cellular inflammation pathways by augmenting inhibitory Tyr527 phosphorylation at the C-terminus of Src-family kinases (SFKs), thereby effectively preventing the phosphorylation of stimulatory SFKs Tyr416. Finally, we have conclusively verified that the protective effect of TFF2 relies on the TFF2-A4GNT-glycan axis during influenza virus infection. In the future, TFF2 may offer a potential intervention strategy for acute respiratory inflammatory diseases. - Source: PubMed
Publication date: 2025/08/14
Fu WeihuiFan JunPeng TianyunSun PengYuan SonghuaZhu CuisongDing LongfeiZhang LinxiaZhao ChenZhang ShuyeZhang XiaoyanXu Jianqing - [This corrects the article DOI: 10.3389/fmicb.2025.1541800.]. - Source: PubMed
Publication date: 2025/04/22
Gong DaweiGao YuqiangShi RuiXu XiaonaYu MengchaoZhang ShuminWang LiliDong Quanjiang - Cardiovascular diseases (CVDs) encompass a group of diseases that affect the heart and/or blood vessels, making them the leading cause of global mortality. In our study, we performed proteome-wide Mendelian randomization (MR) and colocalization analyses to identify novel therapeutic protein targets for CVDs and evaluate the potential drug-related protein side effects. We conducted a comprehensive proteome-wide MR study to assess the causal relationship between plasma proteins and the risk of CVDs. Summary-level data for 4907 circulating protein levels were extracted from a large-scale protein quantitative trait loci (pQTL) study involving 35,559 individuals. Additionally, genome-wide association study (GWAS) data for CVDs were extracted from the UK Biobank and the Finnish database. Colocalization analysis was utilized to identify causal variants shared between plasma proteins and CVDs. Finally, we conducted a comprehensive phenome-wide association study (PheWAS) using the R10 version of the Finnish database. This study was aimed at examining the potential drug-related protein side effects in the treatment of CVDs. A total of 2408 phenotypes were included in the analysis, categorized into 44 groups. The research findings indicate the following associations: (1) In coronary artery disease (CAD), the plasma proteins A4GNT, COL6A3, KLC1, CALB2, KPNA2, MSMP, and ADH1B showed a positive causal relationship (-fdr < 0.05). LAYN and GCKR exhibited a negative causal relationship (-fdr < 0.05). (2) In chronic heart failure (CHF), PLG demonstrated a positive causal relationship (-fdr < 0.05), while AZGP1 displayed a negative causal relationship (-fdr < 0.05). (3) In ischemic stroke (IS), ALDH2 exhibited a positive causal relationship (-fdr < 0.05), while PELO showed a negative causal relationship (-fdr < 0.05). (4) In Type 2 diabetes (T2DM), the plasma proteins MCL1, SVEP1, PIP4K2A, RFK, HEXIM2, ALDH2, RAB1A, APOE, ANGPTL4, JAG1, FGFR1, and MLN demonstrated a positive causal relationship (-fdr < 0.05). PTPN9, SNUPN, VAT1, COMT, CCL27, BMP7, and MSMP displayed a negative causal relationship (-fdr < 0.05). Colocalization analysis conclusively identified that AZGP1, ALDH2, APOE, JAG1, MCL1, PTPN9, PIP4K2A, SNUPN, and RAB1A share a single causal variant with CVDs (PPH3 + PPH4 > 0.8). Further phenotype-wide association studies have shown some potential side effects of these nine targets (-fdr < 0.05). This study identifies plasma proteins with significant causal associations with CVDs, providing a more comprehensive understanding of potential therapeutic targets. These findings contribute to our knowledge of the underlying mechanisms and offer insights into potential avenues for treatment. - Source: PubMed
Publication date: 2025/02/21
Fan MaoxiaLi NaHuang LibinChen ChenDong XueyanGao Wulin - Selective antimicrobial effects have been found for α1,4-linked N-acetylglucosamine residues at the terminus of O-glycans attached to a core protein of gastric gland mucin. encodes α1,4-N-acetylglucosaminyl transferase, which is responsible for the biosynthesis of α1,4-linked N-acetylglucosamine. The impact of A4GNT on the establishment and homeostasis of the gastric microbiome remains to be clarified. The aim of this study was to characterize the gastric microbiome in mice deficient for the production of α1,4-linked N-acetylglucosamine. - Source: PubMed
Publication date: 2025/02/12
Gong DaweiGao YuqiangShi RuiXu XiaonaYu MengchaoZhang ShuminWang LiliDong Quanjiang - Gastric cancer is often accompanied by a loss of mucin 6 (MUC6), but its pathogenic role in gastric carcinogenesis remains unclear. - Source: PubMed
Publication date: 2024/04/06
Arai JunyaHayakawa YokuTateno HiroakiMurakami KeitaHayashi TakeruHata MasahiroMatsushita YukiKinoshita HirotoAbe SoheiKurokawa KenOya YukikoTsuboi MayoIhara SozaburoNiikura RyotaSuzuki NobumiIwata YusukeShiokawa ToshiroShiomi ChihiroUekura ChieYamamoto KeisukeFujiwara HiroakiKawamura SatoshiNakagawa HayatoMizuno SeiyaKudo TakashiTakahashi SatoruUshiku TetsuoHirata YoshihiroFujii ChifumiNakayama JunShibata ShinsukeWoods SusanWorthley Daniel LHatakeyama MasanoriWang Timothy CFujishiro Mitsuhiro