A major step on the road to understanding a unique posttranslational modification and its role in a genetic disease.

Abstract	The posttranslational conversion of cysteine to C(alpha)-formylglycine in the catalytic site of mammalian sulfatases is deficient in the rare but devastating disorder multiple sulfatase deficiency (MSD). Two papers in this issue of Cell report the cloning of a gene responsible for this activity.
Authors	Jacques U Baenziger
Journal	Cell (Cell) Vol. 113 Issue 4 Pg. 421-2 (May 16 2003) ISSN: 0092-8674 [Print] United States
PMID	12757700 (Publication Type: Comment, Journal Article, Review)
Chemical References	C(alpha)-formylglycine Sulfatases Alanine Glycine
Topics	Alanine (analogs & derivatives, metabolism) Animals Catalytic Domain (genetics) Gene Expression Regulation, Enzymologic (genetics) Glycine (analogs & derivatives, metabolism) Humans Mutation (genetics) Protein Processing, Post-Translational (genetics) Sphingolipidoses (enzymology, genetics) Sulfatases (deficiency, genetics)

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