B4GALT5
- Known as:
- B4GALT5
- Catalog number:
- 002372A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- B4GALT5
Related genes to: B4GALT5
- Gene:
- B4GALT5 NIH gene
- Name:
- beta-1,4-galactosyltransferase 5
- Previous symbol:
- -
- Synonyms:
- beta4GalT-V
- Chromosome:
- 20q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1999-03-15
- Date modifiied:
- 2016-10-05
Related products to: B4GALT5
Related articles to: B4GALT5
- Mitochondrial metabolism and oxidative stress (OS) play critical roles in the progression of hepatocellular carcinoma (HCC). However, reliable prognostic biomarkers for these processes remain unidentified. This study integrated bulk RNA sequencing and single-cell RNA sequencing (scRNA-seq) to identify OS&mitochondrial metabolism-related genes (OMRGs). A prognostic model was constructed using LASSO regression, followed by external validation. Associations of the model with clinicopathological features, tumor microenvironment (TME), immune functions, therapeutic response, and drug sensitivity were systematically explored. Finally, the relationships between key OMRGs and mitochondrial metabolism as well as OS were validated. A risk score based on five key OMRGs (LPCAT1, IMPDH1, RAMP3, FZD7, and B4GALT5) was established. Low OMRS was significantly associated with improved overall survival and identified as an independent prognostic factor. Two subtypes (C1/C2) were characterized based on the OMRGs: the C1 subtype exhibited poorer survival and epithelial-mesenchymal transition (EMT) enrichment, whereas the C2 subtype showed greater immune infiltration and sensitivity to immunotherapy. High OMRS was associated with higher predicted IC values to oxaliplatin and cisplatin, while low OMRS indicated favorable responses to TACE, sorafenib, and immunotherapy. FZD7 knockdown increased reactive oxygen species (ROS) levels and reduced mitochondrial membrane potential in HCC cells. FZD7, a key gene among OMRGs, represent promising prognostic biomarkers and therapeutic targets in HCC. - Source: PubMed
Huang PeishuWei FuqunChen YipingYang Yuanmeng - Tumor metabolic dysregulation is a critical determinant of tumor progression and response to immunotherapy. Aberrant glutamine metabolism is a hallmark of gastric cancer (GC). However, beyond fueling GC cell anabolism, its role in remodeling the immunosuppressive tumor microenvironment remains poorly understood. Here, we show that GC cells overexpress solute carrier family 1 member 5 (SLC1A5) to drive glutamine accumulation, which not only promotes their own proliferation but also reduces glutamine availability to CD8 T cells, thereby suppressing antitumor immunity. These dual effects cooperatively drive GC progression. Mechanistically, loss of methyltransferase-like protein 7A (METTL7A) stabilizes SLC1A5 mRNA by reducing its m6A modification. Concurrently, METTL7A deficiency increased N-glycosyltransferase β-1,4-galactosyltransferase 5 (B4GALT5) expression. B4GALT5 stabilizes SLC1A5 via N-glycosylation at the N212 site, which blocks K48-linked polyubiquitination and proteasomal degradation. We identify the natural flavonoid luteolin as an agent that upregulates METTL7A expression, which subsequently downregulates SLC1A5 expression and inhibits GC progression. Furthermore, luteolin significantly enhances the efficacy of anti-PD-1 therapy in GC. Collectively, our findings reveal that SLC1A5-mediated glutamine competition drives both tumor cell proliferation and immune evasion in GC, and suggest that targeting the METTL7A/SLC1A5 axis may represent a promising therapeutic strategy. - Source: PubMed
Publication date: 2026/08/03
Sun MingjunDang ShuweiZhou DazhiDing LixianSun XunSuo WeiNiu JiruiYang QingzhuZhang ZhichengSun YanyanLi JinxingChen ZhongshengBan TaoWang YingjiLi TianzhuLiu MingLi Guodong - Glycosphingolipids (GSLs) are glycoconjugates in which a short and heterogeneous saccharide chain is attached to a lipid moiety called ceramide. Based on their sugar backbone, mammalian GSLs are primarily grouped into the ganglio-, lacto-/neolacto-, and globo-series. Sialic acid-containing GSLs are known as gangliosides. Complex ganglio-series gangliosides are particularly abundant in the brain, whereas simple ganglio-series gangliosides, as well as those belonging to other series or neutral GSLs, are less abundant and typical of non-neural tissues. Congenital disorders in the biosynthesis of the lipid moiety of sphingolipids (SLs) result from defects in enzymes and proteins involved in ceramide biosynthesis and transport. Congenital disorders in the biosynthesis of the sugar chain of GSLs specifically affect ganglio-series ganglioside biosynthesis and are caused by pathogenic variants in GM3 synthase (ST3GAL5) or GM2/GD2/asialo-GM2 synthase (B4GALNT1). Defective variants of the sialyltransferase ST3GAL3 and the galactosyltransferase B4GALT5 have been reported and proposed to impair GSL biosynthesis. The occurrence of these syndromes has provided new insights into the physiological and pathological roles of GSLs. Most of these disorders are associated with completely inactive enzyme variants, leading to severe neurological syndromes. Only a few cases highlighted variants that retained partial activity, resulting in milder phenotypes, which included non-syndromic intellectual disability. It is therefore conceivable that many undiagnosed patients, with mild neurological symptoms, may carry variants retaining residual enzyme activity, insufficient to ensure normal levels of brain GSLs. The purpose of this article is to encourage clinicians to look for additional GLS hereditary disorders associated with a milder phenotype. We also hope to boost future investigations by highlighting the most critical issues emerging from recent literature on SL and GSL biosynthesis and their related defects. - Source: PubMed
Publication date: 2026/07/03
Montavoci LindaDei Cas MichelePenati SaraTrinchera Marco - Lactosylceramide is a glycosphingolipid precursor synthesized by two dedicated galactosyltransferases, B4GALT5 and B4GALT6. The specific roles of B4GALT5 and B4GALT6 in humans have not yet been clearly defined. Here, we report the first human case with bi-allelic loss-of-function variants in B4GALT5, suggesting that intact B4GALT5 activity is indispensable for normal glycosphingolipid biosynthesis and human development. We identified bi-allelic variants in the B4GALT5 gene in a child presenting with microcephaly, mild cognitive impairment, and bilateral cataracts. B4GALT5/6 double KO cells transfected with B4GALT5 carrying either of the variants identified in the patient lacked lactosylceramide synthase activity and failed to produce glycosphingolipids. In silico analyses predicted decreased protein stability and impaired UDP-Gal binding for both B4GALT5 variants. Together, these findings indicate that both variants result in deficient B4GALT5 activity, leaving B4GALT6 as the sole source of lactosylceramide synthase activity. Consistent with this, patient plasma and fibroblasts exhibited an approximately 80% reduction in glycosphingolipid levels compared with healthy controls. Unexpectedly, when expressed in model cells human B4GALT6 displayed lower expression and lower catalytic activity, than human B4GALT5, raising questions about its capacity to compensate for B4GALT5 deficiency. In conclusion, we identified a potential new congenital disorder of glycosylation caused by deficient lactosylceramide synthase activity that may be insufficient to support glycosphingolipids synthesis at levels required for normal brain function. - Source: PubMed
Publication date: 2026/07/09
Montavoci LindaDei Cas MicheleCaretti AnnaBen Mariem OmarEberini IvanoGiaquinto LauraDe Falco AlessandroAntonietta de Matteis MariaBrunetti-Pierri NicolaTrinchera Marco - Glycosphingolipids (GSLs) represent an important group of bioactive lipids that serve both as structural components of membranes, and as signaling molecules involved in the regulation of numerous biological processes, such as control of cell growth and cell death. Their significant deregulation in colon cancer cells suggests their potential role in the disease progression. Lactosylceramide (LacCer) is a key intermediate in GSL metabolism and an important precursor of more complex GSLs. Here, we studied the impact of inhibition of LacCer synthesis (using selective targeting of specific LacCer synthases (LCS), B4GALT5 or B4GALT6, via CRISPR/Cas9-mediated gene knockdown) on control of the human DLD-1 colon adenocarcinoma cell proliferation, death and chemosensitivity. The downregulation of the selected enzymes, as verified by a decrease in respective mRNA and protein levels, significantly reduced levels of LacCers and several more complex GSLs (in particular, GM3 and GM1a gangliosides) in LCS-knockdown cells. Importantly, it enhanced the sensitivity of DLD-1 cells to the cytotoxic effects of oxaliplatin, a chemotherapy drug commonly used in colorectal cancer treatment. This was demonstrated by a general decrease in cell viability, an enhanced apoptotic cell death, caspase-8, -9, -3 cleavage/activation and cleavage of caspase substrates. We also observed a modulation of endoplasmic reticulum stress response, in particular decreased levels of ATF6, in LCS-knockdown cells treated with oxaliplatin. The present findings support the functional role of LCS in regulating the chemosensitivity of colon cancer cells towards the action of chemotherapy drugs, such as oxaliplatin, with possible further implications for the mechanisms underlying toxic action of platinum-based drugs in cancer cells. - Source: PubMed
Publication date: 2026/06/06
Lujka BarboraŠošolíková TerezaVázquez-Gómez GerardoKováč OndrejMachala MiroslavVaculová Alena HyršlováVondráček Jan