Abstract
ATR-Seckel syndrome and ataxia-teleangiectasia are autosomal recessive disorders associated with hematologic malignancies. They share the feature of genetic instability and are caused by defects in the DNA damage response: underlying causes are a hypomorphic ATR mutation and inactivating ATM mutations, respectively. A common substrate of ATM and ATR in the DNA damage response is the nuclear checkpoint kinase Chk1, which we have recently shown to localize to interphase centrosomes and thereby negatively regulate entry into mitosis by preventing premature activation of cyclin B-Cdk1 (
Nat Cell Biol
6
: 884
–891, 2004
Author notes
Corresponding author
2005, The American Society of Hematology
2005
This feature is available to Subscribers Only
Sign In or Create an Account Close Modal