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Article

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

Cell - 16 May 2003

Baenziger Jacques U

Abstract excerpt

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.

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 12757700
DOI: 10.1016/s0092-8674(03)00354-4

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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A major step on the road to understanding a unique posttranslational modification and its role in a genetic disease.PMID 12757700Read ↗

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