ST8SIA1 Antibody
- Known as:
- ST8SIA1 Antibody
- Catalog number:
- XW-8145
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- ST8SIA1 Antibody
Ask about this productRelated genes to: ST8SIA1 Antibody
- Gene:
- ST8SIA1 NIH gene
- Name:
- ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 1
- Previous symbol:
- SIAT8, SIAT8A
- Synonyms:
- -
- Chromosome:
- 12p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-09-12
- Date modifiied:
- 2016-10-05
Related products to: ST8SIA1 Antibody
Related articles to: ST8SIA1 Antibody
- GD3 synthase (GD3S) is a key enzyme in the production of gangliosides, sialylated membrane glycosphingolipids with essential physiological roles in mammalian brains. To elucidate the molecular bases of neuropathological findings associated with GD3S deficiency, we performed a multilayered analysis focused on the functionality of ion transporters Na/K-ATPase (NKA) and plasma membrane Ca-ATPase (PMCA) in the cortex and cerebellum of GD3S-deficient mice (GD3S). We examined global transcriptomes, NKA and PMCA gene and protein expression, the influence of membrane lipid composition on lipid raft integrity, and the activity of both ATPases, pairing them with an exploratory principal component analysis. Transcriptomic data reveal that sets of genes involved in ion transport and membrane dynamics are differentially expressed in the absence of GD3S, whereas qRT-PCR data confirm changes in gene expression of specific NKA and PMCA subunits or isoforms. Altered protein expression and significantly lower activity of both NKA and PMCA were found in the cerebral cortex of GD3S mice. Analysis of membrane cholesterol content revealed segregation of cholesterol into lipid rafts, which may lead to disordered membrane lipid architecture in GD3S deficiency. Additionally, our results confirm that an imbalance in membrane ganglioside composition leads to significant alterations in ion transporter NKA and PMCA activity. Furthermore, we experimentally restored the activity of both ATPases in cortical homogenates by administering exogenous b-series gangliosides, a finding that may aid in developing therapeutic strategies targeting deficits in GD3S and other enzymes of ganglioside biosynthesis. - Source: PubMed
Publication date: 2026/05/15
Puljko BornaHrvat Nikolina MačekIlic KatarinaUjevic AnaJosic EvaStojanović MarioRežen TadejaTacer Klementina FonRozman DamjanaBalog MartaHeffer MarijaKalanj-Bognar SvjetlanaMlinac-Jerkovic Kristina - This research aimed to explore key glycosylation-related genes (signature genes) and associated molecular mechanism on chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF), which further providing new perspectives for disease prognosis and diagnose. - Source: PubMed
Publication date: 2026/01/22
Yin Xiao LingZhai YingWang Lei - Pancreatic ductal adenocarcinoma (PDAC) is still an aggressive and rapidly progressive malignant tumor of the digestive system. Emerging treatment strategies have yielded limited benefits, primarily due to the high heterogeneity of tumors and the presence of various mechanisms of drug resistance. Ferroptosis is a newly discovered type of cell death that has emerged as a promising anti-tumor strategy, while our understanding of the interaction between ferroptosis and tumor glycosylation and immune remodeling remains limited. - Source: PubMed
Publication date: 2025/12/05
Tan HaoZhang HaitaoGao JiachengWang LeiLuan Xiaofeng - Gangliosides are sialic acid-enriched glycosphingolipids that play a vital role in regulating multiple signaling pathways during cancer progression. The diversity in their cell- and tissue-specific expression and dysregulations in cancer cells contributes to the unique pathophysiology of triple-negative breast cancer (TNBC). In this study, we follow up on our previously established hydrogel-mediated localized delivery of a combination of docetaxel (DTX) and carboplatin (CPT) (DTX-CPT-Gel therapy) that ensured effective tumor regression in multiple murine syngeneic and xenograft tumor models. Here, we demonstrate that DTX-CPT-Gel therapy downregulates GM3/GD3/GM1 gangliosides by targeting different ganglioside metabolic genes at the transcriptional and translational levels. DTX-CPT-Gel therapy-mediated alterations in ganglioside metabolism affect the activity of key growth factor receptor-mediated signaling pathways, including the epidermal growth factor receptor (EGFR) and cMET/hepatic growth factor receptor (HGFR), which positively impact tumor mitigation. Our work on DTX-CPT-Gel therapy, in continuum, highlights the potential of this therapy for TNBC treatment by intercepting multiple lipid-mediated signaling pathways and reinforces GD3 synthase/ST8SIA1 as a promising target for TNBC therapy. - Source: PubMed
Publication date: 2025/10/22
Ansari Mohammad NafeesKaur JasleenKhan AliKar AnimeshTripathi RajeshwariJain DollyAggarwal BhartiBajaj AvinashMukhopadhyay ArnabDasgupta Ujjaini - Sphingolipids play a crucial role in gut inflammation. Neutral ceramidase (NcDase) serves as a pivotal regulator of ceramide, the central intermediate in sphingolipid metabolism. The contribution of intestinal epithelial cells (IEC) NcDase to colitis is not well understood. Here, a protective mechanism by which IEC NcDase deficiency (Asah2) and its-related gangliosides prevent dextran sulfate sodium (DSS)-induced colitis in mice is described. Asah2 mice display reduced susceptibility to DSS-induced colitis and increase regulatory T (T) cells compared to Asah2 littermates. Deletion of IEC NcDase induces the upregulation of sialyltransferase ST8SIA1 and promotes the sialic-acid-containing ganglioside GD3 production. Siglec-E is a sialic-acid-binding lectin expresses predominantly on myeloid cells. Mechanistically, it is identified that GD3 is a functional ligand for Siglec-E on macrophages and found that GD3/Siglec-E interaction induced a rapid metabolic rewiring of macrophages that involved the production of IL-33, which contributes to the generation of ST2Foxp3 T cells. Finally, deletion of ST8SIA1 or administration of dietary GD3 induces or reduces mucosal inflammation, respectively. This work defines a critical role for ganglioside GD3 in the induction of colonic T cells and identifies an activating pathway that follows engagement of Siglec-E. - Source: PubMed
Publication date: 2025/11/07
Xu ZhishanLei ChaoSriwastva Mukesh KWang TingTuohongerbieke AmanguliSong XiaotongNoud CollinDerkson ShannonTan YiDryden GeraldMcClain Craig JDeng Zhongbin