anti-UDP-N-Acetyl-alpha-D-Galactosamine:polypeptide N-Acetylgalactosaminyltransferase 3 (GalNAc-T3) (GALNT3) Antibodies

Mouse (Murine) UDP-N-Acetyl-alpha-D-Galactosamine:polypeptide N-Acetylgalactosaminyltransferase 3 (GalNAc-T3) (GALNT3) interaction partners

1. Overexpression of Galnt3 in chondrocytes causes dwarfism due to the increase of mucin (show SLC13A2 Antibodies)-type O-glycans and a reduction in chondroitin sulfates.

2. The stabilized Fgf23 (show FGF23 Antibodies)-Autosomal dominant hypophosphatemic rickets allele reversed the Galnt3-null phenotype and normalized total Fgf23 (show FGF23 Antibodies), serum phosphorus, and bone Fgf23 (show FGF23 Antibodies) mRNA.

3. The deficiency of Galnt3 results in a severe reduction of mucin (show SLC13A2 Antibodies)-type O-glycans in spermatids and causes impaired acrosome formation, leading to oligoasthenoteratozoospermia, and Galnt3 may also be involved in the process of fertilization.

4. A mouse with an N-Ethyl-N-nitrosourea (ENU) Induced Trp589Arg Galnt3 mutation represents a model for hyperphosphataemic familial tumoural calcinosis.

5. dietary phosphate restriction normalizes biochemical and skeletal phenotypes of Galnt3 knockout mice and, thus, can be an effective therapy for tumoral calcinosis.

6. Galnt3-deficient mice have a biochemical phenotype of tumoral calcinosis and provide in vivo evidence that Galnt3 plays an essential role in proper secretion of Fgf23 (show FGF23 Antibodies) in mice.

Human UDP-N-Acetyl-alpha-D-Galactosamine:polypeptide N-Acetylgalactosaminyltransferase 3 (GalNAc-T3) (GALNT3) interaction partners

1. Giantin (show GOLGB1 Antibodies)-knockout zebrafish exhibit hyperostosis and ectopic calcium deposits, recapitulating phenotypes of hyperphosphatemic familial tumoral calcinosis, a disease caused by mutations in GALNT3. These data reveal a new feature of Golgi homeostasis: the ability to regulate glycosyltransferase (show GTDC2 Antibodies) expression to generate a functional proteoglycome.

2. study supports an essential role of GALNT3 in Epithelial ovarian cancer dissemination, including its implication in modulating post-translational modifications and EOC metabolism

3. This study identified GALNT3 as a novel gene that rendered patients susceptible to coronary artery disease (CAD (show CAD Antibodies)), and the A allele of a disease-associated variant rs4621175 linked reduced CAD (show CAD Antibodies) risk through decreased GALNT3 expression.

4. Study indicates that loss of GALNT3 occurs in poorly differentiated PDAC, which is associated with the increased aggressiveness and altered glycosylation of ErbB (show EGFR Antibodies) family proteins.

5. The presence of lectin domain T3lec or T4lec during ppGalNAc-T2 and ppGalNAc-T3 catalytic reaction had a clear inhibitory effect on GalNAc-T (show B4GALNT1 Antibodies) activity.

6. GalNAc-T3 might play a role in the pathogenesis of early stage oral squamous cell carcinoma recurrence

7. MGAT5 (show MGAT5 Antibodies) expression is a potential independent adverse prognostic biomarker for recurrence and survival of patients with ccRCC after nephrectomy.

8. Two microRNAs (miRNAs), miR-17-3p and miR (show MLXIP Antibodies)-221, which target GalNAc transferase 3 (GALNT3) mRNA, are rapidly downregulated in human alveolar basal epithelial cells during the early stage of influenza A virus infection.

9. hyperphosphatemic familial tumoral calcinosis and hyperphosphatemic hyperostosis syndrome caused by a novel GALNT3 mutation

10. Polymorphisms of rs1863196, rs6710518, rs4667492, rs1349321 and rs6721582 (GALNT3) are associated with bone mineral density.GALNT3 may play a role in genetic susceptibility to postmenopausal osteoporosis in Chinese womeh.