Ask about this productRelated genes to: GAL3ST3 antibody
- Gene:
- GAL3ST3 NIH gene
- Name:
- galactose-3-O-sulfotransferase 3
- Previous symbol:
- -
- Synonyms:
- GAL3ST2
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-01
- Date modifiied:
- 2014-11-19
Related products to: GAL3ST3 antibody
Related articles to: GAL3ST3 antibody
- Deoxynivalenol (DON), a prevalent trichothecene mycotoxin, poses a global threat to the gut health of both humans and livestock. This study investigates the protective effects and underlying mechanisms of glucuronolactone (GLU) against DON-induced intestinal injury. In a piglet model, GLU effectively alleviated DON-induced intestinal injury and inflammation. Transcriptomic analysis revealed that GLU promotes mucin sulfation, a critical process for fortifying the intestinal mucus barrier. On the one hand, integrated microbiome and metabolomics analyses uncovered that GLU increased probiotic Lactobacillus amylovorus abundance and luminal indole-3-acetic acid level, thereby facilitating mucin sulfation. On the other hand, GLU itself directly boosted mucin sulfation in a microbiota-independent manner. Mechanistically, both the microbiota-dependent and -independent pathways through which GLU promoted mucin sulfation converged on the activation of aryl hydrocarbon receptor (AHR). Activated AHR transcriptionally up-regulated the expression of the sulfotransferase GAL3ST3, which drove mucin sulfation. This study identifies GLU as a promising nutritional intervention against DON-induced intestinal injury and reveals AHR-mediated mucin sulfation as a vital mechanism for maintaining intestinal barrier homeostasis. - Source: PubMed
Publication date: 2026/02/23
Cui ChenbinZhang BeibeiTang JiaxiHou JingQiu YueqinGao KaiguoWang LiJiang ZongyongYang Xuefen - Clozapine is an effective antipsychotic medication for the management of treatment-resistant schizophrenia. However, the use of clozapine is limited due to severe and sometimes fatal adverse events, including cardiac inflammation (myocarditis). To date, studies of clozapine dosing and genetic studies have not identified robust risk markers. Our study aimed to identify potential epigenetic markers for clozapine-induced myocarditis using genome-wide profiling of DNA methylation and RNA sequencing in a novel in vitro model using patient-derived cells. Induced pluripotent stem cells (iPSCs) from treatment-resistant schizophrenia patients with (case) and without (control) a history of clozapine-induced myocarditis were differentiated into beating cardiomyocytes (iPSC-CMs). These cells were exposed to clozapine at a physiologically relevant concentration (2.8 µmol/L) for 24 h. Before and after clozapine treatment, RNA from the iPSC-CMs was sequenced (RNA-seq), and DNA was assessed for methylation using the EPIC array. Our analysis revealed that hypermethylation at the promoter regions of and is associated with reduced gene expression in cases relative to controls, regardless of clozapine exposure. Additionally, hypermethylation in the gene bodies of and was associated with increased expression in cases relative to controls. Conversely, hypomethylation in the gene bodies of and correlated with lowered gene expression in cases relative to controls. These findings highlight a potential involvement of DNA methylation in gene expression regulation and its putative impact on clozapine-induced myocarditis. Additional studies are warranted to validate our findings and further elucidate a potential mechanism. - Source: PubMed
Publication date: 2025/10/24
Marques Diogo FSpindola Leticia MNarang AnkitaVaziri NazaninStavrum Anne-KristinJayaram MaheshThomas NaveenPantelis ChristosLe Hellard StephanieHemberger MyriamDean WendyGreenway Steven CBousman Chad - Decision regarding local treatment of colorectal liver metastases (CRLM) is a multidisciplinary assessment, and liver intervention should be performed when the metastases are deemed resectable. There is no standard biomarker to aid neither this decision nor the postoperative treatment decisions. The present prospective, observational study aimed to investigate the potential clinical utility of a combined tumor-specific and organ-specific methylated circulating DNA assay in the perioperative setting of CRLM. - Source: PubMed
Publication date: 2025/01/06
Raunkilde LouiseAndersen Rikke FredslundThomsen Caroline BrennerHansen Torben FrøstrupJensen Lars Henrik - Exposure to heavy metals has been reported to be associated with impaired cognitive function, but the underlying mechanisms remain unclear. This pilot study aimed to identify key heavy metal elements associated with cognitive function and further explore the potential mediating role of metal-related DNA methylation. - Source: PubMed
Publication date: 2024/04/25
Wei YueZhou Yan-FengXiao LiliQin JianCheng HongCai HaiqingChen XingZou YunfengYang LiZhang HaiyingZhang ZhiyongYang Xiaobo - The immunomodulatory family of Siglecs recognizes sialic acid-containing glycans as "", which is exploited in cancer for immune evasion. The biochemical nature of Siglec ligands remains incompletely understood, with emerging evidence suggesting the importance of carbohydrate sulfation. Here, we investigate how specific sulfate modifications affect Siglec ligands by overexpressing eight carbohydrate sulfotransferases (CHSTs) in five cell lines. Overexpression of three CHSTs─CHST1, CHST2, or CHST4─significantly enhance the binding of numerous Siglecs. Unexpectedly, two other CHSTs (Gal3ST2 and Gal3ST3) diminish Siglec binding, suggesting a new mode to modulate Siglec ligands via sulfation. Results are cell type dependent, indicating that the context in which sulfated glycans are presented is important. Moreover, a pharmacological blockade of - and -glycan maturation reveals a cell-type-specific pattern of importance for either class of glycan. Production of a highly homogeneous Siglec-3 (CD33) fragment enabled a mass-spectrometry-based binding assay to determine ≥8-fold and ≥2-fold enhanced affinity for Neu5Acα2-3(6--sulfo)Galβ1-4GlcNAc and Neu5Acα2-3Galβ1-4(6--sulfo)GlcNAc, respectively, over Neu5Acα2-3Galβ1-4GlcNAc. CD33 shows significant additivity in affinity (≥28-fold) for the disulfated ligand, Neu5Acα2-3(6--sulfo)Galβ1-4(6--sulfo)GlcNAc. Moreover, joint overexpression of CHST1 with CHST2 in cells greatly enhanced the binding of CD33 and several other Siglecs. Finally, we reveal that CHST1 is upregulated in numerous cancers, correlating with poorer survival rates and sodium chlorate sensitivity for the binding of Siglecs to cancer cell lines. These results provide new insights into carbohydrate sulfation as a general mechanism for tuning Siglec ligands on cells, including in cancer. - Source: PubMed
Publication date: 2021/10/18
Jung JaesooEnterina Jhon RBui Duong TMozaneh FahimaLin Po-HanNitin Kuo Chu-WeiRodrigues EmilyBhattacherjee AbhishekRaeisimakiani ParisaDaskhan Gour CSt Laurent Chris DKhoo Kay-HooiMahal Lara KZandberg Wesley FHuang XuefeiKlassen John SMacauley Matthew S