ST8SIA1 Antibody
- Known as:
- ST8SIA1 Antibody
- Catalog number:
- XW-8145
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- ST8SIA1 Antibody
Related 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
- Pediatric malignancies are often closely linked to developmental cell states, differentiation trajectories, and restricted developmental windows. This relationship is especially evident in neural-crest-derived tumors, where malignant cells may retain, remodel, or reacquire glycosylation programs that normally regulate embryonic migration and lineage maturation. Using a pediatric developmental perspective, we consider tumor-associated sialylation as potentially reflecting retention of the developmental cell-of-origin glycome, reacquisition during malignant cell state plasticity, or cancer-specific remodeling. Neuroblastoma provides the strongest evidence linking these mechanisms to tumor biology and therapy. Polysialylated NCAM can support migratory and plastic phenotypes, ganglioside biosynthesis is coupled to adrenergic-mesenchymal cell state through cell state-dependent regulation of glycosyltransferases including ST8SIA1, and the developmentally enriched ganglioside GD2 creates an actionable therapeutic vulnerability. Selected neural-crest-derived tumors that also occur outside childhood are included as they may help distinguish lineage-associated mechanisms from features specific to pediatric malignancy. We examine sialoglycan-Siglec immune regulation, emerging glycan-directed therapies, and approaches for resolving sialylation across developmental and malignant cell states. This framework argues that pediatric neural-crest-derived tumors do not simply recapitulate embryonic glycosylation but selectively retain, remodel, or reacquire developmental sialylation programs that can influence plasticity, migration, immune evasion, and therapeutic response. - Source: PubMed
Publication date: 2026/09/17
Swami LaxmiSharma MeghaJanmeda PrachetaMandadapu PunarviJamal FauziaKumar PradeepHardiman Karin MStafman Laura L - Pathogenic immune-cardiac crosstalk underlies maladaptive remodeling in chronic heart failure, yet therapies directly targeting this axis are lacking. Glycoconjugates, which are crucial for signal transduction and extracellular matrix integrity, represent an underexploited therapeutic avenue. This study sought to define the role of glycoconjugate-metabolizing enzymes at the immune-cardiac interface and evaluate their translational potential. - Source: PubMed
Publication date: 2026/08/05
Zhou ChangzuanFu LishengYuan TianyouLi FangfangTang FanhuanWu XiaoyuYe YutongGao LongzheJin ChenyangZhang QitongXu LiangLiu ShaowenChen SongwenLi Jun - 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 transporters 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 BornaMaček Hrvat NikolinaIlic KatarinaUjevic AnaJosic EvaStojanović MarioRežen TadejaFon Tacer KlementinaRozman 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