anti-ST3 beta-Galactoside alpha-2,3-Sialyltransferase 5 (ST3GAL5) Antibodies

Human ST3 beta-Galactoside alpha-2,3-Sialyltransferase 5 (ST3GAL5) interaction partners

1. 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 (show ST8SIA1 Antibodies) haplotype, which showed a significant increase in promoter activity

2. 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.

3. Data suggest that ganglioside glycosyltransferases ST3GAL5, ST8SIA1 (show ST8SIA1 Antibodies), and B4GALNT1 (show B4GALNT1 Antibodies) are S-acylated at conserved cysteine residues located close to cytoplasmic border of their transmembrane domains; ST3Gal-II (show ST3GAL2 Antibodies) is acylated at conserved cysteine residue in N-terminal cytoplasmic tail; for B4GALNT1 (show B4GALNT1 Antibodies) and ST3Gal-II (show ST3GAL2 Antibodies), dimer formation controls their S-acylation status.

4. 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 (show MLXIP Antibodies)-26a, miR (show MLXIP Antibodies)-548l and miR (show MLXIP Antibodies)-34a.

5. Serum deprivation triggers upregulation of hST3Gal V gene expression through Runx2 activation by BMP signaling in MG-63 cells.

6. this study indicated that sialylation involved in the development of MDR of AML (show RUNX1 Antibodies) cells probably through ST3GAL5 or ST8SIA4 (show ST8SIA4 Antibodies) regulating the activity of PI3K (show PIK3CA Antibodies)/Akt (show AKT1 Antibodies) signaling and the expression of P-gp (show ABCB4 Antibodies) and MRP1 (show MDM4 Antibodies).

7. Whole-exome sequencing of patients with salt and pepper syndrome shows a homozygous c.994G>A transition (p.E332K) in the ST3GAL5 gene.

8. GM3 synthase deficiency, responsible for early-onset epilepsy syndrome, leads to a secondary respiratory chain dysfunction.

9. Data demonstrate that valproic acid (VPA) transcriptionally regulates human GM3 synthase (hST3Gal V), which catalyzes ganglioside GM3 (show GRM6 Antibodies) biosynthesis in ARPE-19 human retinal pigment epithelial cells.

10. GM3 exhibits the potential to regulate the allosteric structural transition from inactive to a signaling EGFR dimer, by preventing the autophosphorylation of the intracellular kinase domain in response to ligand binding

Mouse (Murine) ST3 beta-Galactoside alpha-2,3-Sialyltransferase 5 (ST3GAL5) interaction partners

1. A new liver-specific c-type mRNA transcriptional variant of mouse ST3GAL5 protein has been identified.

2. We used GM2/GD2 synthase (B4galnt1 (show B4GALNT1 Antibodies))-deficient mice to immunize by liposomes embedded with GD1alpha or acidic glycolipid fractions from brain of St3gal5-deficient mice. Specificities of established mAbs as analyzed by enzyme-linked immunosorbent assay and thin-layer chromatography-immunostaining were very high among various gangliosides.

3. These studies establish ganglioside GM3 (show GRM6 Antibodies) as a new candidate responsible for neuropathic pain and small fiber neuropathy in diabetes.

4. Functionally, the repression of St3gal5 suffices to elevate intercellular adhesion and expression of distinct junction-associated proteins, reminiscent of knockdown of Zeb1 (show ZEB1 Antibodies).

5. ganglioside GM3 synthase has a role in siRNA-based spherical nucleic acid reversal of impaired wound healing in diabetic mice

6. 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.

7. genes involved in the sphingolipids metabolism may be modifiers of cystogenesis, and suggest GM3 synthase as a new anti-cystic therapeutic target.

8. Results suggest that complete, but not partial, inhibition of GM3 (show GRM6 Antibodies) synthesis results in robust activation of an alternate pathway that may compensate for the complete absence of the products of GM3 synthase.

9. the age at death of the npc1 (show NPC1 Antibodies)(-/-) mouse can be significantly influenced by many factors, including differences in strain background, other inactivating gene mutations in Siat9 and lxrbeta (show NR1H2 Antibodies)

10. 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 (show AKT1 Antibodies) pathway.