Ask about this productRelated genes to: GALNT4 antibody
- Gene:
- GALNT4 NIH gene
- Name:
- polypeptide N-acetylgalactosaminyltransferase 4
- Previous symbol:
- -
- Synonyms:
- GalNAc-T4
- Chromosome:
- 12q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-13
- Date modifiied:
- 2015-08-27
Related products to: GALNT4 antibody
Related articles to: GALNT4 antibody
- Vascular smooth muscle cells (VSMCs) are essential for maintaining vascular tone and participate in all stages of atherosclerosis. The transition of VSMCs into macrophage-like cells is a major source of plaque foam cells. Nevertheless, the mechanisms regulating this phenotypic transition remain elusive. RNA Binding Motif Protein 47 (RBM47) expression was increased by more than twofold in aortas of ApoE/ mice and was markedly elevated in RBM47α-SMA double-positive cells within atherosclerotic plaques. RBM47 knockdown significantly reduced plaque burden and vascular inflammation, and suppressed VSMC-to-macrophage-like transition. In POV-PC-treated VSMCs, RBM47 knockdown inhibited VSMC proliferation, migration, inflammation, and macrophage-like transition. Mechanistically, RBM47 was found to directly bind to two specific sequences within the 3'UTR of GALNT4 mRNA and enhance its stability. Functional rescue experiments confirmed that GALNT4 mediated the effects of RBM47 on VSMC-to-macrophage-like transition. These findings suggest that RBM47 contributes to atherosclerosis by stabilizing GALNT4 mRNA and promoting VSMC-to-macrophage-like transition. - Source: PubMed
Publication date: 2026/08/06
Wang HaijunJing BaoDong XinyuWang MuningXuan YanChang SiyaoQin YuxinZhang BojianZhou WeizhongWang ShengLin YufengHan Zhiyang - Extramammary Paget's disease is a rare cutaneous adenocarcinoma characterized by mucin-rich Paget cells and chronic inflammation, yet its molecular basis remains unclear. - Source: PubMed
Publication date: 2026/06/29
Du XinyuZhao ChunxiaTian JieYu HonghaoKuang QiqiSu MiaotongZhang GuohongLi Hang - Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation and joint destruction. Metabolic reprogramming and immune dysregulation are increasingly recognized as pivotal contributors to RA pathogenesis. However, a comprehensive understanding of metabolism-related genes that act as key regulators of RA progression and their impact on the immune microenvironment is lacking. We obtained RA mRNA expression profiles and single-cell RNA sequencing (scRNA-seq) data from the Gene Expression Omnibus. Weighted Gene Co-expression Network Analysis identified RA-associated gene modules, followed by functional enrichment (Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and Gene Set Enrichment Analysis) and Gene Set Variation Analysis. Four machine learning algorithms (Least Absolute Shrinkage and Selection Operator, Random Forest, Support Vector Machine-Recursive Feature Elimination, and Boruta) were applied to select diagnostic biomarkers. Model performance was validated using Receiver Operating Characteristic curves. Immune infiltration was assessed via CIBERSORT and Single-sample Gene Set Enrichment Analysis. Consensus clustering identified RA subtypes, and scRNA-seq data were analyzed using CellChat to characterize cellular profiles and intercellular interactions. Four robust metabolism-related biomarkers, ACSL4, ARG1, GALNT4, and ST3GAL6, were identified and validated across datasets, demonstrating strong diagnostic performance. The model stratified RA patients into two subtypes with distinct immune infiltration patterns. Single-cell analysis revealed increased CD4 T cells and B cells proportions in RA, with enhanced migration inhibitory factor (MIF) signaling and upregulated metabolic pathways. Regulatory networks (Competing Endogenous RNA, Transcription Factor) and single-gene GSEA highlighted the roles of hub genes in immune and metabolic processes. This study provides a comprehensive analysis of metabolism-related genes in RA, identifying four diagnostic biomarkers. The integration of single-cell transcriptomics offers novel insights into RA pathogenesis and suggests potential biomarkers and therapeutic targets for precision medicine. - Source: PubMed
Publication date: 2026/06/24
Fang ChangfengXu HengwuWu YifanZeng PingkaiLu YuqiYe Zhijian - Endothelial inflammation is a critical driver of atherosclerosis (AS). Although N-acetylgalactosaminyltransferase 4 (GALNT4) has been genetically linked to coronary artery disease, its specific function and mechanism within endothelial cells (ECs) during AS progression remain poorly understood, presenting a significant knowledge gap. This study aimed to elucidate the precise role of GALNT4 in endothelial inflammation and AS development. GALNT4 expression was assessed in human and mouse atherosclerotic plaques. ApoE/ mice fed on a high-fat diet (HFD) received AAV-shRNA-mediated GALNT4 knockdown to evaluate atherosclerotic lesions and vascular inflammation. In vitro, gain and loss-of-function studies were conducted in TNF-α-treated human umbilical vein endothelial cells (HUVECs) to investigate monocyte adhesion and NF-κB activation. Mechanistic insights were gained through lectin blot, co-immunoprecipitation, and chromatin immunoprecipitation (ChIP) assays. Results showed that GALNT4 expression was significantly upregulated in human and mouse atherosclerotic plaques. In ApoE/ mice, GALNT4 knockdown markedly attenuated atherosclerotic lesion area (45.1 % reduction) and reduced ICAM-1/VCAM-1 expression without altering plasma lipids. In HUVECs, TNF-α induced GALNT4 expression in a dose and time-dependent manner. Functionally, GALNT4 knockdown suppressed TNF-α-induced monocyte adhesion, while its overexpression exacerbated these effects. Mechanistically, GALNT4 knockdown reduced O-GalNAcylation of TNFR1, diminished TNF-α-triggered phosphorylation and nuclear translocation of NF-κB p65, and inhibited NF-κB binding to the ICAM-1 and VCAM-1 promoters. Our findings demonstrate that GALNT4, upregulated in AS, promotes endothelial inflammation by enhancing the O-GalNAcylation of TNFR1 and subsequent activation of the NF-κB pathway. Targeting GALNT4 represents a promising therapeutic strategy for attenuating AS. - Source: PubMed
Publication date: 2025/11/01
Wei PengchengLi DuanChen WenxuanZhang XiaoxuanXinru WangHan ZhaoWang YikaiGuo Liwei - The beak bean, found only in waterfowl and Galliformes, aids in foraging, self-defense and pecking hard objects. Its rich coloration results from prolonged evolutionary adaptation. This study analyzed beak bean phenotypes of duck at 10, 20, 30 and 40 days of age, revealing that the most common type is the black beak bean, characterized by melanin deposition on the beak surface. This study performed single nucleotide polymorphism (SNP)-based genome-wide association studies (GWASs) to investigate the genetic basis of beak bean color, identifying signals on chromosome 1. The copy number variation region-based GWAS revealed a consistent candidate region overlapping with the SNP-based GWAS signals, further supporting the importance of this genomic region. Locus zoom analysis further refined the candidate regions to 48.5-50.5 and 50.8-52.8 Mb. Functional enrichment analysis highlighted six candidate genes within these regions: KITLG, DUSP6, GALNT4, MGAT4C, ATP2B1 and NTS. Notably, KITLG and DUSP6, which are linked to melanin production, were identified as key candidate genes for beak bean color. Our finding revealed the genetic basis of the bean color traits for the first time in ducks, providing a theoretical foundation and technological framework for enhancing duck beak coloration. - Source: PubMed
Qi JingjingHu QianXi YangYang ZhaoXu MengruLi LiangBai LiliLiu Hehe