EC Number   |
General Information |
Reference |
|---|
   3.1.6.4 | malfunction |
deficiencies of N-acetylgalactosamine-6-sulfatase is associated with the mucopolysaccharidoses |
680928 |
| 3.1.6.4 | malfunction |
mucopolysaccharidosis IVA, MPS IVA, is an autosomal recessive disorder caused by N-acetylgalactosamine-6-sulfate sulfatase deficiency and leading to lysosomal accumulation of the glycosaminoglycans keratan sulfate and chondroitin-6-sulfate |
715797 |
| 3.1.6.4 | metabolism |
modification of expression of the enzyme regulates the content of chondroitin sulfate |
680928 |
| 3.1.6.4 | physiological function |
in post-natal ventral rat prostate, a distinct and reciprocal localization of arylsulfatase B and N-acetylgalactosamine-6-sulfatase is seen, with arylsulfatase B predominant in the stroma and N-acetylgalactosamine-6-sulfatase predominant in the epithelium. Estrogen treatment does not inhibit the increase in GALNS activity between days 5 and 30 |
730284 |
| 3.1.6.4 | physiological function |
in prostate stem cells, when N-acetylgalactosamine-4-sulfatase ARSB is reduced by silencing or galactosamine-N-acetyl-6-sulfatase GALNS is increased by overexpression, activity of non-receptor tyrosine phosphatase SHP2 declines, attributable to increased binding of SHP2 with C4S. This leads to increases in phospho-ERK1/2, Myc/Max nuclear DNA binding, DNA methyltransferase (DNMT) activity and expression, and methylation of the Dickkopf Wnt signaling pathway inhibitor (DKK)3 promoter and to reduced DKK3 expression. Since DKK3 negatively regulates Wnt/beta-catenin signaling, silencing of ARSB or overexpression of GALNS increases Wnt/beta-catenin signaling |
751772 |
| 3.1.6.4 | physiological function |
strain is able to grow on N-acetylglucosamine-6-sulfate, while N-acetylglucosamine-3-sulfate, N-acetylgalactosamine-3-sulfate, and N-acetylgalactosamine-6-sulfate do not support appreciable growth. Gene cluster Ats2 is required for N-acetylglucosamine-6-sulfate metabolism |
-, 749660 |
