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Effect of DNA damage on a BRCA1 complex

Author

Listed:
  • 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)

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.

Suggested Citation

  • Shang Li & Nicholas S. Y. Ting & Lei Zheng & Phang-Lang Chen & Wen-Hwa Lee, 2001. "Effect of DNA damage on a BRCA1 complex," Nature, Nature, vol. 414(6859), pages 36-36, November.
    • Handle: RePEc:nat:nature:v:414:y:2001:i:6859:d:10.1038_35102121
    DOI: 10.1038/35102121
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