B3GALT2
- Known as:
- B3GALT2
- Catalog number:
- 002345A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- B3GALT2
Related genes to: B3GALT2
- Gene:
- B3GALT2 NIH gene
- Name:
- beta-1,3-galactosyltransferase 2
- Previous symbol:
- -
- Synonyms:
- beta3Gal-T2
- Chromosome:
- 1q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-01
- Date modifiied:
- 2016-10-05
Related products to: B3GALT2
Related articles to: B3GALT2
- Gouty arthritis (GA) is an inflammatory joint disease driven by monosodium urate (MSU) crystal deposition. The NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome-mediated pyroptosis is central to GA pathogenesis, yet potential regulatory targets remain limited. The role of β-1,3-galactosyltransferase 2 (B3GALT2), a glycosyltransferase, is entirely unknown in GA. This study aims to identify novel biomarkers for GA and investigate the role and regulatory mechanism of B3GALT2. - Source: PubMed
Publication date: 2026/02/08
Han Hui-LiCheng Zeng-YuMeng Qing-LiangDu Xu-Zhao - β-1,3-galactosyltransferase 2 (B3galt2) has been increasingly recognized as an essential mediator in the pathogenesis of ischemic stroke (IS); nonetheless, its exact functional role has not been fully elucidated. This research aimed to clarify the regulatory mechanisms by which B3galt2 influences cerebral angiogenesis during the repair phase following ischemic injury. A mouse model of cerebral ischemia/reperfusion (I/R) injury was generated by subjecting animals to 1-h middle cerebral artery occlusion (MCAO), succeeded by reperfusion for varying time intervals. Recombinant human B3galt2 (rh-B3galt2) was administered intranasally beginning on day one post-injury and continued until tissue collection. Experimental outcomes revealed that rh-B3galt2 substantially diminished brain atrophy and enhanced neurological recovery during the repair phase of ischemia. Furthermore, rh-B3galt2 facilitated angiogenesis through increased expression of vascular endothelial growth factor A (VEGFA) and the tight junction proteins, occludin and claudin 5. Moreover, rh-B3galt2 activated the TGF-βR(II)/ALK1/Smad1/5 pathway. The galactosylation levels of TGF-βR(II) and ALK1 were increased after rh-B3galt2 treatment, suggesting that B3galt2 may regulate TGF-βR(II) and ALK1 through glycosylation modification. Moreover, the advantageous impacts of rh-B3galt2 on reducing brain atrophy and alleviating neurological deficits were reversed upon treatment with the ALK1 inhibitor, ML347. ML347 also counteracted the angiogenic promotion induced by rh-B3galt2, demonstrating that inhibition of ALK1 abolishes the protective benefits mediated by rh-B3galt2. Collectively, the results indicated that rh-B3galt2 significantly promotes angiogenesis and neurological function recovery during the cerebral ischemic repair stage, likely by regulating TGF-βR(II)/ALK1/Smad1/5 signaling pathway through glycosylation modification. - Source: PubMed
Publication date: 2026/01/19
Liu ChangMa YaoLi JiachenXu YunhaoLi MeixuanLi HongLi ZongzeWang ZhanyouLiang JiaWang Peng - Antisense oligonucleotides (ASOs) are a promising class of therapeutics made of chemically modified synthetic single-stranded nucleic acid molecules, yet their clinical translation is often hindered by challenges in cellular uptake and delivery. Identifying cellular factors that modulate ASO activity is crucial for overcoming these limitations. Utilizing a whole-genome open reading frame (ORF) overexpression screen with a genetic splice reporter system to identify genes that can increase or decrease ASO activity, we identified B3GALT2 as the most significant hit for increasing ASO activity. Subsequent validation in HEK293 and U2OS cell lines demonstrated that B3GALT2 overexpression consistently and significantly enhances the activity of both splice-switching and mRNA-degrading ASOs across different targets (CD81, MALAT1, and CERS2). Transcriptomic analysis of B3GALT2-overexpressing cells showed upregulation of endocytic scavenger receptors CUBN and SCARA5, and gene set enrichment analysis indicated an enrichment of proteins involved in clathrin-mediated endocytosis. Mechanistic investigations revealed that B3GALT2 overexpression leads to a significant increase in ASO uptake. These findings highlight B3GALT2 as a modulator of ASO cellular entry and offer an avenue for potentially improving ASO-based therapeutic strategies. - Source: PubMed
Publication date: 2025/11/05
Hesselmann JuliaHager CarolinaMalong LizaFortin Jean-PhilippeSchmucki RolandLau TedMartin ScottCosta MikeModrusan ZoraHaley BenjaminRoudnicky Filip - This study aimed to identify and compare the microRNA (miRNA) profiles of exosomes derived from human induced pluripotent stem cells (iPSCs), bone marrow mesenchymal stem cells (BMSCs), and adipose tissue-derived stem cells (ADSCs) (hiPSC-Exos, hBMSC-Exos, and hADSC-Exos), and their functional effects on human articular chondrocytes (hACs). - Source: PubMed
Publication date: 2025/08/18
Chang Ling-HuaChuang Shu-ChunWu Shun-ChengFu Yin-ChihChen Jhen-WeiWu Che-WeiLin Yi-ShanLiu Cyong-YueChung Yu-HsuanChang Je-KenChen Chung-HwanHo Mei-Ling - Bladder urothelial carcinoma (BLCA) is a highly heterogeneous cancer with a wide range of prognoses, ranging from low-grade non-muscle-invasive bladder cancer (NMIBC), which has a good prognosis but a high recurrence rate, to high-grade muscle-invasive bladder cancer (MIBC), which has a poor prognosis. Glycosylation dysregulation plays a significant role in cancer development. Therefore, this study aimed to investigate the role of glycosyltransferases (GT)-related genes in the prognosis of BLCA and to develop a prognostic model based on these genes to predict overall survival (OS) and assess its clinical application. - Source: PubMed
Publication date: 2024/12/28
Li WeipingZuo KangweiZhao QiGuo ChenhaoLiu ZirongLiu ChengJing Suoshi