b4GALT1 ELISA kit
- Known as:
- b4GALT1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-b4GALT1-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- b4GALT1 ELISA kit
Related genes to: b4GALT1 ELISA kit
- Gene:
- B4GALT1 NIH gene
- Name:
- beta-1,4-galactosyltransferase 1
- Previous symbol:
- GGTB2
- Synonyms:
- beta4Gal-T1
- Chromosome:
- 9p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
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- Osteoarthritis (OA) is a prevalent degenerative joint disease with an unclear molecular pathogenesis. B4GALT1 has been implicated in various pathological processes, but its role and mechanism in OA remain largely unexplored. - Source: PubMed
Publication date: 2026/04/17
Ma WeibangOuYang DongXu ZheLuo WeiTian GuangJiang NingLiu ChenZhang RuguoYu Qiao - Cytotoxic CD8 T-cells play central roles in tumor immunotherapy. Understanding the mechanisms that regulate development, differentiation, and functions of cytotoxic CD8 T-cells leads to the development of better immunotherapies. By combining primary T-cell culture and a syngeneic mouse tumor model with both genome-wide and custom CRISPR/Cas9 screenings, we systematically identified genes and pathways that regulate PD-1 expression and functions of CD8 T-cells. Among them, inactivation of a key enzyme in glycoconjugate biosynthesis, beta 1,4-galactosyltransferase 1 (B4GALT1), leads to significantly enhanced T-cell receptor (TCR) activation and functions of CD8 T-cell. Interestingly, suppression of B4GALT1 enhances functions of TCR-T-cells, but has no effect on chimeric antigen receptor T (CAR-T) cells. We systematically identified the substrates of B4GALT1 on CD8 T-cell surface by affinity purification and mass spectrometry analysis, which include protein components in both TCR and its co-receptor complexes. The galactosylation of TCR and CD8 leads to reduced interaction between TCR and CD8 that is essential for TCR activation. Artificially tethering TCR and CD8 by a TCR-CD8 fusion protein could bypass the regulation of B4GALT1 in CD8 T-cells. Finally, the expression levels of B4GALT1 normalized to tumor-infiltrated CD8 T-cells in tumor microenvironment are significant and negatively associated with prognosis of human patients. Our results reveal the important roles of protein N-glycosylation in regulating functions of CD8 T-cells and prove that B4GALT1 is a potential target for tumor immunotherapy. - Source: PubMed
Publication date: 2026/03/20
Hong YuSi XiaofangLiu WenjingMai XueyingZhang Yu - Lipotoxicity, driven by dysregulated lipid metabolism, is a key initiator of hepatocyte injury in metabolic dysfunction-associated steatotic liver disease (MASLD). β-1,4-galactosyltransferase 1 (B4GALT1), which primarily mediates galactosylation of glycoproteins and glycolipids, is involved in the regulation of plasma lipid composition. Previous studies have implicated aberrant glycosylation in MASLD progression. However, the role and underlying molecular mechanisms of B4GALT1 in MASLD progression remain unclear. - Source: PubMed
Publication date: 2026/03/20
Chien YoujungXia RuiqiZhou DaAi YingjieWu LinfengZeng XiaoqingChen Shiyao - Convergent evolution offers a unique lens through which to explore the molecular underpinnings of significant phenotypic transformations. Similar selective pressures likely drove the evolution of analogous milk traits in sheep and goats. Consequently, the current study aimed to identify common selection signals for milk traits across dairy and non-dairy breeds of sheep and goats worldwide. - Source: PubMed
Publication date: 2026/02/06
Akhatayeva ZhanerkeShi YilongDossybayev KairatMalmakov NurlanCheng HairongBaatar NarantuyaYang JiLi MenghuaLin KejianXu Songsong - Lung cancer remains the leading cause of cancer-related mortality. Single-cell RNA sequencing (scRNA-seq) enables high-resolution mapping of tumor microenvironment, but how malignant cell states connect to patient outcomes and therapeutic vulnerabilities is not fully understood. - Source: PubMed
Publication date: 2026/01/06
Guo PengXiang MengqiChen JingZhang Huachuan