Review
doi: 10.1016/s0092-8674(03)00354-4.
A major step on the road to understanding a unique posttranslational modification and its role in a genetic disease
Affiliations
- PMID: 12757700
- DOI: 10.1016/s0092-8674(03)00354-4
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Review
A major step on the road to understanding a unique posttranslational modification and its role in a genetic disease
Cell.
.
Free article
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.
Comment on
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Multiple sulfatase deficiency is caused by mutations in the gene encoding the human C(alpha)-formylglycine generating enzyme.Cell. 2003 May 16;113(4):435-44. doi: 10.1016/s0092-8674(03)00347-7. Cell. 2003. PMID: 12757705
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The multiple sulfatase deficiency gene encodes an essential and limiting factor for the activity of sulfatases.Cell. 2003 May 16;113(4):445-56. doi: 10.1016/s0092-8674(03)00348-9. Cell. 2003. PMID: 12757706
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