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Curr Opin Cell Biol. 2000 Jun;12(3):293-6.

The Mre11 complex and ATM: collaborating to navigate S phase.

Author information

1
University of Wisconsin Medical School, Madison, WI 53706, USA. jpetrini@facstaff.wisc.edu

Abstract

Recently, findings regarding a group of cancer predisposition and chromosome instability syndromes, Nijmegen breakage syndrome (NBS), the ataxia-telangiectasia-like disorder (A-TLD) and ataxia telangiectasia have shed light on the unexpected role of recombinational DNA repair proteins in DNA-damage-dependent cell-cycle regulation. Mutations in the Mre11 complex cause A-TLD and NBS. In addition, functions of the Mre11 complex have been biochemically linked to ATM, the large protein kinase that is defective in ataxia-telangiectasia cells by the observation that Nbs1 is a bona fide substrate of the ATM kinase.

PMID:
10801460
DOI:
10.1016/s0955-0674(00)00091-0
[Indexed for MEDLINE]

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