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.

journal_name

Cell

journal_title

Cell

authors

Baenziger JU

doi

10.1016/s0092-8674(03)00354-4

subject

Has Abstract

pub_date

2003-05-16 00:00:00

pages

421-2

issue

4

eissn

0092-8674

issn

1097-4172

pii

S0092867403003544

journal_volume

113

pub_type

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