Difference between revisions of "Part:BBa K5499002"

Revision as of 14:44, 29 September 2024

Iduronate-2-sulfatase (IDS)

Iduronate-2-sulfatase (IDS) is a lysosomal enzyme that splits the sulfate group in the C-2 positions from iduronic acid residues present in the mucopolysaccharides dermatan sulfate and heparan sulfate.

Usage and Biology

A Deficiency in this enzyme results in the accumulation of these glycosaminoglycans in the lysosomes and subsequently leads to the development of Hunter syndrome(or mucopolysaccharidosis type 2 ) in humans. The disorder is inherited as an X-linked recessive disease and has a broad spectrum of clinical phenotypes ranging from mild to severe forms. This heterogeneity has been postulated to reflect the presence of different mutations in the IDS gene.

Sequence and Features

Assembly Compatibility:

10
COMPATIBLE WITH RFC[10]
12
COMPATIBLE WITH RFC[12]
21
COMPATIBLE WITH RFC[21]
23
COMPATIBLE WITH RFC[23]
25
COMPATIBLE WITH RFC[25]
1000
COMPATIBLE WITH RFC[1000]

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 <partinfo>BBa_K5499002 short</partinfo>
-Iduronate-2-sulfatase (IDS) is a lysosomal enzyme that splits the sulfate group in the C-2 positions from iduronic acid residues present in the mucopolysaccharides dermatan sulfate and heparan sulfate.  A Deficiency in this enzyme results in the accumulation of these glycosaminoglycans in the lysosomes and subsequently leads to the development of Hunter syndrome(or mucopolysaccharidosis type 2 ) in humans.  The disorder is inherited as an X-linked recessive disease and has a broad spectrum of clinical phenotypes ranging from mild to severe forms.  This heterogeneity has been postulated to reflect the presence of different mutations in the IDS gene.
+Iduronate-2-sulfatase (IDS) is a lysosomal enzyme that splits the sulfate group in the C-2 positions from iduronic acid residues present in the mucopolysaccharides dermatan sulfate and heparan sulfate.
-<!-- Add more about the biology of this part here
+<!-- Add more about the biology of this part here-->
 ===Usage and Biology===
+A Deficiency in this enzyme results in the accumulation of these glycosaminoglycans in the lysosomes and subsequently leads to the development of Hunter syndrome(or mucopolysaccharidosis type 2 ) in humans.  The disorder is inherited as an X-linked recessive disease and has a broad spectrum of clinical phenotypes ranging from mild to severe forms.  This heterogeneity has been postulated to reflect the presence of different mutations in the IDS gene.
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