Ask about this productRelated genes to: GALNT4 Blocking Peptide
- 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 Blocking Peptide
Related articles to: GALNT4 Blocking Peptide
- 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 - Pancreatic ductal adenocarcinoma (PDAC), the predominant form of pancreatic cancer, remains a therapeutic challenge. While GALNT4 (a member of the N-acetylgalactosaminyltransferases family) shows significant upregulation in PDAC cells, its precise oncogenic mechanisms remain poorly understood. - Source: PubMed
Publication date: 2025/08/12
Gao DekangZhu ZhaobiYu JingjingWei ShaohuaXing Chungen - Atherosclerosis, a chronic lipid metabolism disorder, remains a leading cause of morbidity and mortality. While Galnt4, an O-glycosyltransferase, has been implicated in several diseases, its role in atherosclerosis remains poorly understood. This study aimed to elucidate the effects of Galnt4 dysregulation on atherosclerotic lesion formation and its involvement in macrophage lipid metabolism. In this study, we analyzed Galnt4 expression in atherosclerotic plaque tissues and foam cells. In vivo and in vitro experiments were conducted to assess the effects of Galnt4 deficiency on macrophage foam cell formation and plaque development. O-glycoproteomic analysis was performed to explore the mechanistic role of Galnt4 in foam cell formation. Our results revealed that Galnt4 expression was significantly elevated in plaque tissues and foam cells, predominantly localized in macrophages. Galnt4 knockdown reduced macrophage foam cell formation and attenuated plaque development. Mechanistic studies reflected that Galnt4 regulates foam cell formation by modulating lysosomal function, specifically through Lamp-1 glycosylation, leading to decreased lysosomal free cholesterol and reduced foam cell formation. In conclusion, our findings highlighted that Galnt4 in macrophages plays a crucial role in modulating Lamp-1 glycosylation and lysosomal function, thereby impacting foam cell formation and atherosclerosis progression. These findings identify Galnt4 as a potential therapeutic target for atherosclerosis. - Source: PubMed
Teng DaJia WenjuanChe HaijieChen HongpingHe XingqiangGong LeiDong HaibinSong JikaiPan YangWang HuaYang JunZhong Lin