Effect of DNA damage on a BRCA1 complex

Shang Li, Nicholas S. Y. Ting, Lei Zheng, Phang-Lang Chen and Wen-Hwa Lee ()
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Shang Li: University of Texas Health Science Center at San Antonio, Institute of Biotechnology
Nicholas S. Y. Ting: University of Texas Health Science Center at San Antonio, Institute of Biotechnology
Lei Zheng: University of Texas Health Science Center at San Antonio, Institute of Biotechnology
Phang-Lang Chen: University of Texas Health Science Center at San Antonio, Institute of Biotechnology
Wen-Hwa Lee: University of Texas Health Science Center at San Antonio, Institute of Biotechnology

Nature, 2001, vol. 414, issue 6859, 36-36

Abstract: Abstract Wu-Baer and Baer confirm our original observation that CtIP is phosphorylated in an ATM-dependent manner in response to γ-radiation. We have shown that phosphorylation by ATM kinase of CtIP at serine residues 664 and 745 is required to liberate DNA-damage-response genes such as GADD45 from repression. This is consistent with our more recent finding that overexpression in mammalian cells of a phosphorylated CtIP mutant with a double alanine substitution at serines 664 and 745 disrupts the radiation-induced cell-cycle checkpoint between G2 and M phases. The functional consequence of radiation-induced, ATM-dependent phosphorylation of CtIP is therefore clear.

Date: 2001
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DOI: 10.1038/35102121

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