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GalNAc-T3 was highly expressed by motile spermatozoa and the expression correlated positively with the classical semen parameters.
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Study shows that ZEB2 negatively regulates a GalNAc-transferase (GALNT3) that is involved in O-glycosylation adds another layer of complexity to the role of ZEB2 in cancer progression and metastasis.
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Giantin-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 expression to generate a functional proteoglycome.
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study supports an essential role of GALNT3 in Epithelial ovarian cancer dissemination, including its implication in modulating post-translational modifications and EOC metabolism
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The acetylated residues on ppGalNAc-T3 function as control points for enzyme activity, and high level of GlcNAc glycosides promote a synergistic regulatory mechanism, leading to a metabolically disordered state.
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This study identified GALNT3 as a novel gene that rendered patients susceptible to coronary artery disease (CAD), and the A allele of a disease-associated variant rs4621175 linked reduced CAD risk through decreased GALNT3 expression.
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Study indicates that loss of GALNT3 occurs in poorly differentiated PDAC, which is associated with the increased aggressiveness and altered glycosylation of ErbB family proteins.
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The presence of lectin domain T3lec or T4lec during ppGalNAc-T2 and ppGalNAc-T3 catalytic reaction had a clear inhibitory effect on GalNAc-T activity.
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GalNAc-T3 might play a role in the pathogenesis of early stage oral squamous cell carcinoma recurrence
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MGAT5 expression is a potential independent adverse prognostic biomarker for recurrence and survival of patients with ccRCC after nephrectomy.
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Two microRNAs (miRNAs), miR-17-3p and miR-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.
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hyperphosphatemic familial tumoral calcinosis and hyperphosphatemic hyperostosis syndrome caused by a novel GALNT3 mutation
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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.
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Data are indicative for a strong oncogenic potential of the GALNT3 gene in advanced EOC and identify this transferase as a novel EOC biomarker.
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Our data suggest that GalNAc-T3 expression may be a useful indicator of tumor differentiation in thyroid carcinomas.
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we integrated different computational tools to perform the in silico analysis of clinically significant mutations (nsSNPs/single amino acid change) at both functional and structural levels, found in human GALNT3, GALNT8, GALNT12, and GALNT13 genes.
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GalNac transferase transgenic knock-out mice neurons have significantly increased rates of axon degeneration.
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N-acetylgalactosaminyltransferases-3 expression independently predicts high-grade tumour and poor prognosis in patients with renal cell carcinomas.
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a novel homozygous missense mutation affecting highly conserved amino acids in GALNT3 in patients with hyperphosphatemic familial tumoral calcinosis
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GalNAc-T3 is likely involved in pancreatic carcinogenesis
