B4GALT4
- Known as:
- B4GALT4
- Catalog number:
- 002371A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- B4GALT4
Related genes to: B4GALT4
- Gene:
- B4GALT4 NIH gene
- Name:
- beta-1,4-galactosyltransferase 4
- Previous symbol:
- -
- Synonyms:
- beta4Gal-T4
- Chromosome:
- 3q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-02
- Date modifiied:
- 2016-10-05
Related products to: B4GALT4
Related articles to: B4GALT4
- Keratan sulfate (KS) is a glycosaminoglycan consisting of repeating -acetyllactosamine disaccharides, in which both galactose and -acetylglucosamine are often 6--sulfated. It has been reported that KS recognized by the monoclonal antibodies 5D4 and 373E1 is preferentially expressed in papillary thyroid carcinoma (PTC) and only minimally in other thyroid tumors/lesions or normal thyroid tissue. However, the precise epitopes recognized by these antibodies remain incompletely characterized, and the expression and extent of low-sulfated KS in PTC have not been systematically evaluated. To better understand the nature of KS expressed in PTC, we generated a novel anti-KS monoclonal antibody, 299-1C1, and performed immunohistochemical analyses using 299-1C1 together with two existing anti-KS monoclonal antibodies, 5D4 and R-10G, in combination with keratanase II and endo-β-galactosidase. The results showed that both highly sulfated and low-sulfated KS are preferentially expressed in PTC, including lymph node metastases, accompanied by upregulation of genes encoding key KS biosynthetic enzymes (, , , and ) in integrated TCGA/GTEx transcriptomic datasets. Expression of , , and , but not , was further increased in -mutant PTCs. These findings indicate that anti-KS monoclonal antibodies are useful for the pathological diagnosis of PTC, particularly for distinguishing lymph node metastases from intranodal thyroid inclusions. - Source: PubMed
Publication date: 2026/08/28
Kato EiichiAkama Tomoya OYonemoto NatsumiMuramoto AkifumiFujieda ShigeharuKobayashi Motohiro - Lenvatinib is the primary targeted drug for hepatocellular carcinoma(HCC). However, the development of drug resistance significantly hinders its therapeutic efficacy. The present study aimed to identify new target molecules of lenvatinib-resistant HCC, and improve the treatment of liver cancer. A lenvatinib-resistant HCC cell line, Bel7404(named Bel7404-R), was established, and the protein expression profile of the Bel7404-R cell line and changes in functional enrichment were analyzed. The expression of the identified lenvatinib-resistant critical protein B4GALT4 was validated, and its correlation with immune infiltration and drug resistance was analyzed. Apoptosis and ferroptosis of HCC cell were observe by Calcein-AM/PI staining and transmission electron microscopy. The results indicated that Bel7404-R cells significantly enhanced colony formation and decreased apoptosis ratio compared with parental Bel7404 cells. 111 upregulated and 170 downregulated proteins in the Bel7404-R cells. Notably, upregulated proteins included B4GALT4, CD55, RFTN1, and SHROOM3, whereas downregulated proteins included GRHPR, CLU, TPM2, TMEM185B and TRPM2. B4GALT4 was significantly overexpressed in Bel7404-R cells and identified as a central protein in the molecular regulatory network of these cells. Knockdown of B4GALT4 expression inhibited the levels of PKM2, LDHA and PI3K/AKT signaling, while stimulating the expression of cleaved-Caspase-3. B4GALT4 could protect the integrity of mitochondria and inhibit ferroptosis. The protein expression profile of Bel7404-R cells were significantly different from those of the parental HCC cells. B4GALT4 was identified as a critical molecule for HCC resisting to lenvatinib, and B4GALT4 can be used as a new therapeutic target for lenvatinib-resistant liver cancer. - Source: PubMed
Publication date: 2026/05/07
Wu XueqinPan YinglianPu JianghanFeng SirenLiu KunWu GangLin BoYin QiushiZhu MingyueLi Mengsen - O-Mannose (Man) glycans are branched specifically in the brain by a dedicated glycosyltransferase, N-acetylglucosaminyltransferase IX (GnT-IX, also known as MGAT5B). Such branching of O-Man glycans was reported to be involved in diseases, including demyelination and glioma, but the enzymatic mechanisms by which O-Man glycan is specifically recognized by GnT-IX and how branched O-Man glycans are subsequently elongated by other enzymes in the brain have remained unclear. To shed light on these issues, we here first compared the structural model of GnT-IX complexed with its O-Man substrate with the crystal structure of the homologous N-glycan branching enzyme GnT-V (also known as MGAT5). Several residues in GnT-IX were predicted to be critical to recognition of the O-Man substrate, and an enzyme assay revealed that R304 in GnT-IX is crucial for the specificity toward O-Man glycans. We further investigated the role of O-Man branching for subsequent elongation in the brain and found that the level of keratan sulfate (KS) in O-Man glycans was significantly reduced in GnT-IX-knockout (KO) mouse brain, suggesting that O-Man branching promotes KS biosynthesis. Mechanistically, our enzymatic assays of the KS biosynthetic enzymes demonstrated that B4GALT1, B4GALT4, and CHST1 exhibited significantly higher activity toward branched O-Man glycans than toward their linear counterparts. These results imply that branching of O-Man glycans by GnT-IX provides the scaffold for efficient subsequent glycan elongation. Our findings deepen our understanding of the complex biosynthetic pathway of O-Man glycans in the brain. - Source: PubMed
Publication date: 2026/01/07
Itoh TomoyaTanaka Hide-NoriPareek MohitNagae MasamichiManya HiroshiIdo AkemiMishra Sushil KKizuka Yasuhiko - Lung adenocarcinoma (LUAD) shows high recurrence rate and poor prognosis. Genes associated with ubiquitin play a role in the onset and advancement of cancers; however, they have yet to be employed for the diagnosis and prognosis of LUAD. - Source: PubMed
Publication date: 2025/08/15
Li YueTian WeiChen ChenLiu HailinZhang ZhenfaWang Changli - Chronic obstructive pulmonary disease (COPD) causes significant morbidity and mortality, ranking as the third leading cause of death globally. Cordyceps sinensis (C. sinensis), has long been used in Asia as a tonic of traditional Chinese medicine, to alleviate lung ailments, and exhibits a potential therapeutic effect on COPD. This study aimed to explore the protective effects of C. sinensis on COPD and elucidate the underlying molecular mechanism. In this study, COPD was induced in rats via cigarette smoke exposure combined with intratracheal lipopolysaccharide (LPS) administration, followed by C. sinensis treatment. Pathological alterations in lung tissue and inflammatory cytokines in serum and lung tissue were assessed, and an integrated analysis combining proteomics, metabolomics, serum pharmacochemistry, network pharmacology, and molecular biology was conducted. The result showed that C. sinensis treatment significantly alleviated lung tissue injury in COPD rats, with the medium dose exhibiting particularly notable efficacy. Furthermore, C. sinensis administration reduced the levels of inflammatory factors (TNF-α, IL-8, MMP-9) in serum and lung tissue, suggesting a potential anti-inflammatory role in COPD. Integrated metabolomics and proteomics analysis revealed that the protective effect of C. sinensis against COPD critically depended on regulating glycerophospholipid and sphingolipid metabolism by targeting PLA2G4E and B4GALT4 proteins, which confirmed by WB and qRT-PCR. The analysis of serum samples identified 20 blood-entering compounds from C. sinensis. Network pharmacology analysis revealed that sphingolipid components in C. sinensis exert therapeutic effects against COPD through multi-target interactions, primarily involving AKT1, ESR1, TLR4, and MMP9. The findings further revealed that C. sinensis mainly modulated COPD through the PI3K-AKT signaling pathway. Additionally, WB experiments verified that C. sinensis reversed p-AKT in the lung tissue of COPD rats. In conclusion, C. sinensis may influence the PI3K-AKT signaling pathway in COPD rats, potentially affecting glycerophospholipid metabolism and sphingolipid metabolism by targeting PLA2G4E and B4GALT4 proteins, thereby alleviating the inflammatory response and mitigating lung tissue damage caused by COPD. - Source: PubMed
Publication date: 2025/07/22
Zhou WenbinLiu YingyingGao YaqiSuonanlamao Ma YuananXiao YuancanWei Lixin