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
- 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 - Aortic dissection (AD) is a life-threatening vascular disorder whose underlying molecular mechanisms remain poorly understood. Polypeptide N-acetylgalactosaminyltransferase 4 (GALNT4), an enzyme that transfers N-acetylgalactosamine (GalNAc) to serine and threonine residues on target proteins, has been implicated in the development of cardiovascular diseases. However, its specific role in AD remains unclear. This study analyzed GALNT4 expression in human AD tissues and murine AD models induced by β-aminopropionitrile (BAPN) and angiotensin II (Ang II). Results revealed significantly elevated GALNT4 expression in the arteries of both human AD patients and AD mice (P < 0.01). Specifically, GALNT4 levels in vascular smooth muscle cells (VSMCs) from human and mouse AD arteries were markedly higher than in normal arteries. Smooth muscle cell (SMC)-specific knockdown of GALNT4 reduced AD incidence (53.8 % vs. 76.9 %) and rupture rates (28.6 % vs. 70.0 %), while improving AD pathology. This improvement was characterized by preserved contractile markers (α-SMA, SM22α) and suppressed synthetic markers (OPN, MMP2/9) in mice. In vitro, GALNT4 knockdown inhibited Ang II-induced phenotypic switching and migration of human aortic SMCs (29 % vs. 41 %, P < 0.01), whereas GALNT4 overexpression reversed these effects. Mechanistically, GALNT4 knockdown reduced O-GalNAcylation of TGF-βR2, inhibiting Smad2/3 phosphorylation and consequently blocking downstream Smad signaling pathway activation. In conclusion, GALNT4 regulates VSMC phenotypic switching and dysfunction through glycosylation-dependent activation of the TGF-β/Smad signaling pathway, positioning it as a potential therapeutic target for AD intervention. - Source: PubMed
Publication date: 2025/07/02
Guo LiweiWei PengchengZhou LuluHan ZhaoWang XinruLi Duan