Ask about this productRelated genes to: ST8SIA6 Blocking Peptide
- Gene:
- ST8SIA6 NIH gene
- Name:
- ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 6
- Previous symbol:
- SIAT8F
- Synonyms:
- -
- Chromosome:
- 10p12.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-22
- Date modifiied:
- 2017-12-06
Related products to: ST8SIA6 Blocking Peptide
Related articles to: ST8SIA6 Blocking Peptide
- Metabolic dysfunction-associated steatotic liver disease (MASLD) is a progressive hepatic metabolic disorder characterized by excessive fat accumulation in hepatocytes. MASLD can advance to metabolic dysfunction-associated steatohepatitis (MASH). These conditions often lead to hepatic fibrosis, cirrhosis and hepatocellular carcinoma (HCC) if not timely diagnosed and managed; thus, molecular phenotyping of MASLD and MASH conditions is highly desirable. The analyses were performed to identify distinct, differentially expressed genes, particularly noncoding ones, in MASLD and MASH patient samples, thereby expanding diagnostic and therapeutic options. - Source: PubMed
Publication date: 2026/07/16
Delgadillo Frida MPerez KarlaYang BarbaraDhandayuthapani SubramanianYallapu Murali MChauhan Subhash CRamos Enrique IGadad Shrikanth S - Sialic acids are terminal nine-carbon sugars that form sialoglycans on the glycocalyx of all vertebrate cell surfaces. In this exposed position, they fulfill various functions in the immune system, including involvement in host-pathogen interactions and control of immune cell activation. The synthesis of sialoglycans is catalyzed by sialyltransferases. One of these is ST8Sia6, which is known to catalyze the synthesis of α-2,8-linked di-sialyl motifs and to be upregulated in plasma cells. - Source: PubMed
Publication date: 2026/07/02
Brüchert RonjaHinzpeter-Schmidt MichaelRöder BettinaKrause MareikeBrey StefanieWinkler Thomas HBuettner Falk F RMühlenhoff MartinaNitschke Lars - Inflammatory bowel diseases (IBDs), including ulcerative colitis (UC) and Crohn's disease (CD), are characterized by chronic inflammation of the gastrointestinal tract. Pathogenesis of IBD is multifactorial and incompletely understood. Here, we show that the sialyltransferase ST8Sia6 regulates gut inflammation and homeostasis. ST8Sia6-deficient mice spontaneously accumulate activated immune cells in the small intestine and exhibit enhanced sensitivity to dextran sodium sulfate-induced colitis. ST8Sia6-knockout small bowel lamina propria T cells exhibit steady-state increases in T1 and pathogenic T17 programs and readily generate TNF-α upon in vitro stimulation. In addition, there are increased levels of inflammation-induced chemokines CCL3, CCL4, and CCL5 in ST8Sia6-deficient immune and epithelial cells. ST8Sia6-deficient T cells show altered glycosylation of CD43 and CD45. ST8Sia6 heterozygous mice show an intermediate phenotype, demonstrating that gut immune homeostasis is sensitive to ST8Sia6 expression levels. This work thus establishes a role for immune cell glycosylation by ST8Sia6 in IBD. - Source: PubMed
Publication date: 2026/05/13
Crotts Sydney BBarnes Jackson TAntonetti Regina MShapiro Michael JGades Naomi MFaubion William AKnoop Kathryn AShapiro Virginia Smith - 7-ketocholesterol (7-KC) is a highly abundant and biologically active lipid oxidation product that perturbs membrane integrity, sterol homeostasis, mitochondrial function, and redox balance. In parallel, tamoxifen, a cornerstone therapy for estrogen receptor-positive breast cancer, induces not only estrogen receptor antagonism but also pronounced metabolic and organelle-associated stress. Here, we investigated transcriptional responses of breast cancer cell line models to tamoxifen, 7-KC, and their combination. Tamoxifen elicited a shared antiproliferative response in MCF-7 and BT-20 cells, characterized by suppression of cell cycle progression, DNA replication, and mitosis. However, the downstream stress responses diverged markedly between the two models. MCF-7 cells activated adaptive programs, including unfolded protein response, autophagy, and metabolic reprogramming toward glycolysis, consistent with cytostatic survival. In contrast, BT-20 cells exhibited suppression of metabolic and redox pathways accompanied by inflammatory and apoptotic signaling, indicating impaired stress adaptation. Combined tamoxifen and 7-KC treatment further amplified these divergent stress-response phenotypes. Analysis of the correlation of 16 oppositely regulated genes with clinical data of breast cancer patients validated ST8SIA6 as the main candidate associated with adaptive stress tolerance. Overall, our findings indicate that the capacity to integrate metabolic and redox stress determines tumor cell type-specific responses to combined endocrine and oxysterol-induced stress in breast cancer. - Source: PubMed
Publication date: 2026/03/01
Seborova KarolinaKoucka KamilaTesarova TerezaKurucova MichaelaEhrlichova MarieHoly PetrHlavac ViktorSoucek PavelSpalenkova Alzbeta - - Source: PubMed
Publication date: 2026/01/22
Liu QingshanKe JianLuo Yu