Ask about this productRelated genes to: B4galt5 antibody
- 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 antibody
Related articles to: B4galt5 antibody
- Altered cell-surface glycans are established cancer biomarkers, yet no oncogenes have been identified within glycan biosynthesis machinery. This represents a critical gap, as defining a gene as a true oncogene, rather than merely a component of an oncogenic pathway, reveals targetable dependencies that can improve clinical decisions. To date, no gain-of-function mutations have been detected in glycogenes, and the search for such mutations is largely saturated. To address this gap, we developed a bioinformatic-experimental pipeline to identify copy number alteration (CNA)-based driver genes, overcoming noise from passenger genes. The approach recovered known oncogenes and tumor suppressors, while revealing novel candidates, including glyco-oncogenes. Focusing on the glycosphingolipid (GSL) biosynthetic pathway, we validated as a bona fide glyco-oncogene whose genomic amplification drives proliferation, oncogene addiction, and poor prognosis, effects that can be reversed by targeted pathway inhibition. Mechanistic studies show that B4GALT5 promotes cancer cell survival via integrin-Src signaling under anchorage-independent conditions. Collectively, these findings establish glycosylation enzymes as a druggable oncogene class and provide a resource of high-confidence CNA-based cancer regulatory genes. - Source: PubMed
Publication date: 2026/04/01
Sahu PranoyRusso FrancescoRusso DomenicoAgliarulo IleniaAmbrosio PasqualinaRizzo RiccardoLo Monte MatteoNormanno NicolaSoddu SilviaCarlomagno FrancescaLuini AlbertoParashuraman Seetharaman - Focal segmental glomerulosclerosis (FSGS) is a major cause of nephrotic syndrome and chronic kidney disease, characterized by podocyte injury and glomerular scarring. Its heterogeneity complicates early diagnosis and treatment. - Source: PubMed
Publication date: 2026/03/24
Zhang JingkeNing HanHou YunTang Ning - Sheep have diversified into distinct breeds worldwide through both natural adaptation and human-driven selection, with hybridization serving as an effective strategy for rapid trait improvement. The Tianhua mutton sheep (TMS) is a novel breed derived from crossing South African Mutton Merino (SAMM) with Gansu alpine fine-wool sheep (GAFS). After nearly two decades of selective breeding, TMS has developed great meat quality traits and impressive cold toleranceĀ at high altitudes. To study the genetic mechanism and provide new insights into phenotypic variation, we analyzed the genetic diversity, population structure, and selective signatures of TMS based on whole-genome sequencing of 55 TMS, 11 SAMM, and 197 public sheep genomes worldwide. - Source: PubMed
Publication date: 2026/01/31
Jiang BeixiangZeng JizeChi HuanpengShan JingfangZhang XueyingFeng QianjieLi FadiYue XiangpengFu Weiwei - The absence of effective biomarkers continues to limit early diagnostic accuracy and prognostic evaluation in patients with hepatocellular carcinoma (HCC). Aberrant sialylation (SI) has been demonstrated to contribute to therapeutic resistance and tumor progression. The aim of this investigation was to identify a sialylation-related gene (SRG) signature, evaluate its prognostic significance, and investigate associated immunological characteristics in HCC. - Source: PubMed
Publication date: 2025/12/15
Wang Guan-QingDu KangWang Yu-Peng - Acute kidney injury (AKI) can progress to chronic kidney disease (CKD), via a mechanism that is still largely unknown. We previously reported that glucosylceramide (GlcCer) acts as a damage-associated molecular pattern (DAMP) during AKI. Here, we demonstrate that renal GlcCer levels increase persistently during AKI, primarily due to oxidative stress-mediated downregulation of Ī²-1,4-galactosyltransferase 5 (B4galt5) in proximal tubules. Using mass spectrometry, we showed that GlcCer specifically accumulated in damaged proximal tubules. Among the enzymes involved in GlcCer metabolism, B4galt5 was predominantly expressed in proximal tubules and its expression was consistently downregulated across multiple AKI models. Knockdown of B4galt5 alone was sufficient to increase GlcCer levels in cultured proximal tubular cells. Moreover, in vivo administration of GlcCer combined with free cholesterol triggered inflammatory responses via the innate immune receptor macrophage-inducible C-type lectin (Mincle). These inflammatory responses were almost abolished in Mincle-deficient mice, suggesting a specific GlcCer-Mincle pathway. Our findings indicate that B4galt5 plays a critical role in GlcCer accumulation in necrotic tubules following AKI. Specifically, we propose that dying proximal tubules alter their glycolipid metabolism to generate DAMPs, highlighting B4galt5 as a potential therapeutic target for preventing the AKI-to-CKD transition. - Source: PubMed
Publication date: 2025/12/02
Osada AkinoriTanaka MiyakoSugiura YukiYuan XunmeiYamashita ShinjiOchi KozueKohda HiroIto AyakaGo ShioriOkajima TetsuyaKadomatsu KenjiYanagita MotokoFuruhashi KazuhiroMaruyama ShoichiSuganami Takayoshi