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Ganglioside GM3 is known to participate in the induction of cell differentiation, modulation of cell proliferation, maintenance of fibroblast morphology, signal transduction, and integrin-mediated cell adhesion. Zusätzlich bieten wir Ihnen ST3 beta-Galactoside alpha-2,3-Sialyltransferase 5 Proteine (8) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 36 products:
Human Polyclonal ST3GAL5 Primary Antibody für FACS, IHC (p) - ABIN652016
Drasin, Guarnieri, Neelakantan, Kim, Cabrera, Wang, Zaberezhnyy, Gasparini, Cascione, Huebner, Tan, Ford: TWIST1-Induced miR-424 Reversibly Drives Mesenchymal Programming while Inhibiting Tumor Initiation. in Cancer research 2015
Human Polyclonal ST3GAL5 Primary Antibody für ELISA, WB - ABIN563853
Cheray, Petit, Forestier, Karayan-Tapon, Maftah, Jauberteau, Battu, Gallet, Lalloué: Glycosylation-related gene expression is linked to differentiation status in glioblastomas undifferentiated cells. in Cancer letters 2011
Human Polyclonal ST3GAL5 Primary Antibody für IHC, IHC (p) - ABIN4356109
Kurcon, Liu, Paradkar, Vaiana, Koppolu, Agrawal, Mahal: miRNA proxy approach reveals hidden functions of glycosylation. in Proceedings of the National Academy of Sciences of the United States of America 2015
While no differences in clinical characteristics were detected in patients possessing the functional promoter haplotypes of ST3GAL5, exophthalmic values were significantly lower in patients with the ST8SIA1 (zeige ST8SIA1 Antikörper) haplotype, which showed a significant increase in promoter activity
These cases broaden the phenotypic and genetic spectrum of GM3 synthase deficiency due to ST3GAL5 variants. Patients with intellectual disability or furthermore presenting with Rett-like phenotype should be suspected of GM3 synthase deficiency, a disorder of ganglioside biosynthesis.
Data suggest that ganglioside glycosyltransferases ST3GAL5, ST8SIA1 (zeige ST8SIA1 Antikörper), and B4GALNT1 (zeige B4GALNT1 Antikörper) are S-acylated at conserved cysteine residues located close to cytoplasmic border of their transmembrane domains; ST3Gal-II (zeige ST3GAL2 Antikörper) is acylated at conserved cysteine residue in N-terminal cytoplasmic tail; for B4GALNT1 (zeige B4GALNT1 Antikörper) and ST3Gal-II (zeige ST3GAL2 Antikörper), dimer formation controls their S-acylation status.
Studied the miRNA expression in human hepatocellular carcinoma cell lines; 13 differentially expressed miRNAs were identified between MHCC97-H and MHCC97-L cells; and the same results were found in clinical samples. Found that ST3GAL5 was the direct target of miR (zeige MLXIP Antikörper)-26a, miR (zeige MLXIP Antikörper)-548l and miR (zeige MLXIP Antikörper)-34a.
Serum deprivation triggers upregulation of hST3Gal V gene expression through Runx2 activation by BMP signaling in MG-63 cells.
this study indicated that sialylation involved in the development of MDR of AML (zeige RUNX1 Antikörper) cells probably through ST3GAL5 or ST8SIA4 (zeige ST8SIA4 Antikörper) regulating the activity of PI3K (zeige PIK3CA Antikörper)/Akt (zeige AKT1 Antikörper) signaling and the expression of P-gp (zeige ABCB4 Antikörper) and MRP1 (zeige MDM4 Antikörper).
Whole-exome sequencing of patients with salt and pepper syndrome shows a homozygous c.994G>A transition (p.E332K) in the ST3GAL5 gene.
GM3 synthase deficiency, responsible for early-onset epilepsy syndrome, leads to a secondary respiratory chain dysfunction.
Data demonstrate that valproic acid (VPA) transcriptionally regulates human GM3 synthase (hST3Gal V), which catalyzes ganglioside GM3 (zeige GRM6 Antikörper) biosynthesis in ARPE-19 human retinal pigment epithelial cells.
GM3 (zeige GRM6 Antikörper) exhibits the potential to regulate the allosteric structural transition from inactive to a signaling EGFR (zeige EGFR Antikörper) dimer, by preventing the autophosphorylation of the intracellular kinase (zeige GSK3b Antikörper) domain in response to ligand binding
These studies establish ganglioside GM3 (zeige GRM6 Antikörper) as a new candidate responsible for neuropathic pain and small fiber neuropathy in diabetes.
Functionally, the repression of St3gal5 suffices to elevate intercellular adhesion and expression of distinct junction-associated proteins, reminiscent of knockdown of Zeb1 (zeige ZEB1 Antikörper).
ganglioside GM3 synthase has a role in siRNA-based spherical nucleic acid reversal of impaired wound healing in diabetic mice
Results show that complete and partial deletion of the GM3 synthase gene exert distinct effects on the NP-C (Niemann-Pick disease Type C) phenotype.
genes involved in the sphingolipids metabolism may be modifiers of cystogenesis, and suggest GM3 synthase as a new anti-cystic therapeutic target.
Results suggest that complete, but not partial, inhibition of GM3 (zeige GRM6 Antikörper) synthesis results in robust activation of an alternate pathway that may compensate for the complete absence of the products of GM3 synthase.
the age at death of the npc1 (zeige NPC1 Antikörper)(-/-) mouse can be significantly influenced by many factors, including differences in strain background, other inactivating gene mutations in Siat9 and lxrbeta (zeige NR1H2 Antikörper)
GM3 synthase silencing suppressed lung metastasis in murine breast cancer cells. The molecular mechanism that underlies GM3 synthase mediated migration and invasion was inhibition of the phosphoinositide-3 kinase/Akt (zeige AKT1 Antikörper) pathway.
The defect of hearing ability of GM3 synthase null mice could be attributed to the functional disorganization of the organ of Corti, and the expression of gangliosides, especially GM3 (zeige GRM6 Antikörper), during the maturation of the cochlea.
zST3GalV-2 and mST3GalV are the enzymes responsible for the synthesis of GM4 in zebrafish and mice, respectively.
Ganglioside GM3 is known to participate in the induction of cell differentiation, modulation of cell proliferation, maintenance of fibroblast morphology, signal transduction, and integrin-mediated cell adhesion. The protein encoded by this gene is a type II membrane protein which catalyzes the formation of GM3 using lactosylceramide as the substrate. The encoded protein is a member of glycosyltransferase family 29 and may be localized to the Golgi apparatus. Mutation in this gene has been associated with Amish infantile epilepsy syndrome. Transcript variants encoding different isoforms have been found for this gene.
, GM3 synthase
, ST3Gal V
, alpha 2,3-sialyltransferase V
, ganglioside GM3 synthase
, lactosylceramide alpha-2,3-sialyltransferase
, sialyltransferase 9 (CMP-NeuAc:lactosylceramide alpha-2,3-sialyltransferase; GM3 synthase)
, sialyltransferase 9
, GM3-specific sialytransferase
, mST3Gal V
, sialyltransferase 9 (CMP-NeuAc:lactosylceramide alpha-2,3-sialyltransferase)