Ask about this productRelated genes to: B4GALT3 Blocking Peptide
- Gene:
- B4GALT3 NIH gene
- Name:
- beta-1,4-galactosyltransferase 3
- Previous symbol:
- -
- Synonyms:
- beta4Gal-T3
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-02
- Date modifiied:
- 2016-03-15
Related products to: B4GALT3 Blocking Peptide
Related articles to: B4GALT3 Blocking Peptide
- Aberrant protein glycosylation contributes significantly to hepatocellular carcinoma (HCC) progression. β-1,4-Galactosyltransferase 3 (B4GALT3), an enzyme involved in glycosylation, is overexpressed in HCC and promotes tumour growth by stabilizing integrin β1 (ITGB1). This study aimed to evaluate B4GALT3 as a therapeutic target and develop a precision nanotherapeutic approach for HCC. - Source: PubMed
Publication date: 2026/05/19
Yu XiaohuiChen XiaoyanGuo HuiJin XiaTan PingpingZeng LongwuHe YanLi Junjun - Genome-wide studies in late-onset Alzheimer's disease (LOAD) have uncovered many risk loci, yet identifying the causal genes and clarifying how these genetic signals connect to molecular and cellular mechanisms relevant to AD pathogenesis remains challenging. - Source: PubMed
Publication date: 2026/03/30
Waghmare Swapnil GKrishna Meera MMaccoux Emily CFranitza Ariel LLink Brian ALezi E - Bladder cancer (BLCA) poses a significant clinical challenge due to its high mortality rates and the inadequacy of current prognostic biomarkers. Programmed cell death (PCD) is crucial in BLCA initiation, progression, and treatment, yet the interplay and specific roles of different PCD pathways in BLCA prognosis remain elusive. This study aimed to develop and validate predictive models by integrating 14 PCD patterns using comprehensive analyses of bulk RNA and single-cell RNA transcriptomic data from TCGA-BLCA and six GEO datasets. Through weighted gene co-expression network (WGCNA) analyses, 24 hub PCD-related genes (PCDGs) were identified in BLCA. Subsequently, we implemented a computational framework that integrated 10 machine learning algorithms along with 101 of their combined permutations. This framework was used to develop a programmed cell death-related signature (PCDRS). The final PCDRS consisted of 12 prognostic genes: P4HB, CHEK2, PTPN2, ATP13A2, CCT6A, TFRC, RRP12, TRAF7, POLR1B, B4GALT3, SIVA1, and TP73.The PCDRS was validated in training and external validation sets, with multivariate analysis confirming its independent prognostic value in BLCA. The PCDRS-integrated nomogram was also developed as a quantitative clinical tool. Furthermore, differences in reactive oxygen species (ROS) levels were observed in the tumor microenvironment between high- and low-risk groups based on PCDRS risk scores. Additionally, the elevated expression and tumorigenic role of P4HB in BLCA were validated through in vitro assays. In summary, P4HB may serve as a candidate gene with potential relevance to BLCA prognosis that could enhance personalized treatment strategies for patients with BLCA. - Source: PubMed
Publication date: 2026/04/02
Cao YangLi CanHua YiboWu TingtingShen QiuyuLin ZeyuHuang Yuhua - Retinoblastoma (RB) is the most common primary intraocular malignancy in children, and its extraocular extension is closely linked to poor prognosis. However, the molecular drivers underlying local invasion remain incompletely defined. Here, we identify β‑1,4‑galactosyltransferase III (B4GALT3) as a glycosyltransferase selectively upregulated in highly proliferative MKI67⁺ RB subpopulations. B4GALT3 promotes RB cell proliferation, fibronectin adhesion, and invasion by enhancing β1-integrin glycosylation, thereby activating FAK signaling and inducing MMP2 expression to disrupt retinal epithelial barriers. Genetic modulation of B4GALT3 significantly altered both tumor burden and invasive behavior in orthotopic xenograft models. Structure-based virtual screening identified myricoside as a B4GALT3 inhibitor, which suppressed RB malignancy in vitro and in vivo. Overall, our findings uncover a B4GALT3-integrin-FAK axis as a key regulator of RB progression and highlight B4GALT3 inhibition as a promising therapeutic strategy for advanced RB. - Source: PubMed
Publication date: 2026/03/23
Tang JunjieLi JinmiaoWang MengLiu YaomingSun HetianZhang ZhihuiGao YangCheng ChaoChen ShuxiaZhang PingAi SimingSu ShicaiHu YoujinLu Rong - Glycosylation abnormalities are critical in the progression of various cancers. However, their role in the onset and prognosis of multiple myeloma (MM) remains underexplored. This study aims to identify glycosyltransferase (GT)-related biomarkers and investigate their underlying mechanisms in MM. GT-related genes were extracted from the MMRF-CoMMpass and GSE57317 data sets. Potential biomarkers were identified using Cox regression and Lasso analyses. A glycosyltransferase-related prognostic model (GTPM) was developed by evaluating 113 machine learning algorithm combinations. The expression of B4GALT3, a key gene identified through this model, was analyzed in MM bone marrow samples using immunohistochemistry, quantitative PCR, and Western blot. Functional roles of B4GALT3 in MM cell behavior were assessed through knockdown experiments, and its mechanism of action was investigated. The GTPM stratified MM patients into high- and low-risk groups, with significantly better survival in the low-risk group (HR = 55.94, 95% CI = 40.48-77.31, p < 0.001). The model achieved AUC values of 0.98 and 0.99 for 1- and 3-year overall survival, outperforming existing gene signatures (including EMC92, UAMS70, and UAMS17). B4GALT3 expression was significantly elevated in advanced MM stages (p < 0.001) and correlated with poorer survival. Knockdown of B4GALT3 reduced MM cell proliferation, invasion, and increased apoptosis. Mechanistic analyses revealed that B4GALT3 modulates MM cell behavior via the Wnt/β-catenin/GRP78 pathway, primarily by regulating endoplasmic reticulum (ER) stress. This study developed a novel GTPM for predicting survival in MM and identified B4GALT3 as a key gene influencing disease progression. Experimental evidence highlights B4GALT3's role in modulating ER stress and Wnt/β-catenin pathways, positioning it as a potential prognostic biomarker and therapeutic target in MM. - Source: PubMed
Publication date: 2025/07/13
Yang ApengKe MengyingFeng LinYang YeChen JunminZeng Zhiyong