3.1.6.4: N-acetylgalactosamine-6-sulfatase
This is an abbreviated version!
For detailed information about N-acetylgalactosamine-6-sulfatase, go to the full flat file.
Word Map on EC 3.1.6.4
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3.1.6.4
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mucopolysaccharidosis
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lysosomal
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morquio
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keratan
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glycosaminoglycans
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dysplasia
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chondroitin-6-sulfate
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sulfatases
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arylsulfatase
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elosulfase
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n-acetylgalactosamine-4-sulfatase
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medicine
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kyphoscoliosis
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odontoid
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sumf1
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synthesis
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sanfilippo
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pectus
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platyspondyly
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carinatum
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valgum
- 3.1.6.4
- mucopolysaccharidosis
- lysosomal
- morquio
- keratan
- glycosaminoglycans
- dysplasia
- chondroitin-6-sulfate
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sulfatases
- arylsulfatase
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elosulfase
- n-acetylgalactosamine-4-sulfatase
- medicine
-
kyphoscoliosis
-
odontoid
- sumf1
- synthesis
-
sanfilippo
-
pectus
-
platyspondyly
-
carinatum
-
valgum
Reaction
Synonyms
6-sulfatase, acetylgalactosamine 6-sulfatase, AtsA2, chondroitin sulfatase, chondroitinase, chondroitinsulfatase, galactose-6-sulfatase, galactose-6-sulfate sulfatase, GalNAc6S sulfatase, GALNS, N-acetylgalactosamine 6-sulfatase, N-acetylgalactosamine 6-sulphate sulphatase, N-acetylgalactosamine-6-sulfatase, N-acetylgalactosamine-6-sulfate sulfatase, sulfatase, acetylgalactosamine 6-, sulfatase, chondroitin
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General Information
General Information on EC 3.1.6.4 - N-acetylgalactosamine-6-sulfatase
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malfunction
metabolism
modification of expression of the enzyme regulates the content of chondroitin sulfate
physiological function
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
malfunction
deficiencies of N-acetylgalactosamine-6-sulfatase is associated with the mucopolysaccharidoses
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
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
physiological function
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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
physiological function
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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
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