B3GNT2
- Known as:
- B3GNT2
- Catalog number:
- 002355A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- B3GNT2
Related genes to: B3GNT2
- Gene:
- B3GNT2 NIH gene
- Name:
- UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2
- Previous symbol:
- B3GNT1
- Synonyms:
- B3GNT-2, BETA3GNT, B3GN-T2, B3GN-T1
- Chromosome:
- 2p15
- Locus Type:
- gene with protein product
- Date approved:
- 2001-05-14
- Date modifiied:
- 2017-01-17
Related products to: B3GNT2
Related articles to: B3GNT2
- Placental dysfunction and immune dysregulation are central to disorders such as fetal growth restriction (FGR) and preeclampsia (PE). Although aberrant placental glycosylation has been implicated in various pregnancy complications, the specific expression patterns of glycosylation-related genes (GRGs) associated with placental pathology and their potential role in driving immune imbalance at the maternal-fetal interface remain poorly understood. - Source: PubMed
Publication date: 2026/07/23
Yin TingxuanHu XianyangYu HailinZhang TianqiYu QinHuang XixiXu ChunfangTang ChuanlingLiu LuDu Meirong - Kaposi sarcoma-associated herpesvirus (KSHV) reprograms host cellular pathways to promote viral persistence and tumor development by supporting the survival and expansion of infected and bystander cells. Among the signaling axes implicated in this process, oncogenic activation of receptor tyrosine kinases, particularly platelet-derived growth factor receptor alpha (PDGFRA), is a well-established hallmark of Kaposi sarcoma pathogenesis. However, the impact of virus-driven cell surface glycosylation changes in PDGFRA-associated signaling remains uncertain. Here, we identified a critical role for KSHV in reshaping the glycosylation landscape of mesenchymal stromal cells (MSCs), thereby reprogramming PDGFRA signaling. We show that KSHV infection enhances a unique glycan profile in human and mouse MSCs, enriched in branched complex N-glycans with limited α(2-6) sialylation, Transcriptomic analyses of KSHV-infected MSCs and Kaposi's Sarcoma patient samples revealed a coordinated dysregulation of pathways involved in carbohydrate metabolism, nucleotide-sugar transport, and sialic acid turnover, with a particular focus on sialic acid turnover (NPL/NEU3), the UDP-N-acetylglucosamine transporters SLC35A3/B4, and complex N-glycan elongation (MGAT5/B3GNT2/B4GALT1) as critical nodes underlying reduced α(2-6) sialylation and increased N-glycan branching. This remodeled glycan landscape contributes to create a permissive context for galectin-1 (Gal-1) binding, which in turn enhances PDGFRA activation and downstream signaling. These findings identify an integral component of KSHV-driven mesenchymal cell reprogramming, unveiling a lectin-dependent mechanism of RTK activation in Kaposi sarcoma pathogenesis. - Source: PubMed
Publication date: 2026/06/30
Tudela Julián GambarteGutiérrez Patricia NMontani M ANadia BannoudGarcía Pablo AMariño Karina VAbba MartinCerliani Juan PNaipauer JuliánLacunza EzequielMesri Enrique ARabinovich Gabirel ACroci Diego O - Gastric cancer (GC) is characterized by a high metastatic propensity, which constitutes the primary cause of poor patient prognosis. Receptor-like tyrosine kinase (RYK) is associated with GC metastasis, but its regulatory mechanism remains unclear. - Source: PubMed
Publication date: 2026/07/05
Fu YonganWang YangqiangCai ZongdaHuang ShurongChen JinpingYe Jianxin - Human milk oligosaccharides (HMOs) are complex sugars that play crucial roles in infant health by supporting the development of the gut microbiota and the immune system. HMOs are structurally based on lactose, which serves as the core disaccharide. These HMOs are synthesized in mammary epithelial cells through sequential glycosylation reactions catalyzed by specific glycosyltransferases, whereas little to no HMO production has been observed in other cell types and commonly used cultured mammalian cell lines. In this study, we reconstituted the biosynthesis of HMOs in cultured cells by applying targeted glycoengineering strategies. HEK293 cells expressing α-lactalbumin (LALBA) gene produced various HMOs including 3'-sialyllactose, 2'-fucosyllactose, sialyllacto-N-tetraose a/d, and disialyllacto-N-tetraose. We showed that different cell lines, such as HCT116 and CHO-K1 cells, can produce HMOs when engineered to express LALBA. By manipulating genes like B4GALT1, B3GNT2, and B3GALT5, we altered the complexity and composition of the HMOs produced. By supplementing the culture medium with N-azidoacetylmannosamine, we achieved efficient metabolic incorporation of azido groups into 3'-sialyllactose. Furthermore, HMOs produced by HEK293 cells promoted the growth of Bifidobacterium, demonstrating prebiotic effects. Our findings highlight the potential to tailor HMO production in vitro, offering a platform for generating these bioactive molecules. - Source: PubMed
Publication date: 2026/06/20
Noda FukiOhno AikaNakajima ArutoIchihashi HirokoNakajima KazukiKizuka YasuhikoKatayama TakaneKatoh ToshihikoFujita Morihisa - Psoriasis is a chronic, immune-mediated disorder with an unmet need for effective treatments. To systematically prioritize therapeutic targets, we integrated proteome-wide Mendelian randomization (MR) with expression validation in blood/skin, genetic susceptibility analysis, differential gene expression (DGE) from bulk and single-cell RNA sequencing (scRNA-seq), colocalization, pathway enrichment, and protein-protein interaction analyses. - Source: PubMed
Si ShuchengWang XiaoxiaoZhan Siyan