MAD2L2 controls DNA repair at telomeres and DNA breaks by inhibiting 5′ end resection

Vera Boersma, Nathalie Moatti, Sandra Segura-Bayona, Marieke H. Peuscher, Jaco van der Torre, Brigitte A. Wevers, Alexandre Orthwein, Daniel Durocher and Jacqueline J. L. Jacobs ()
Additional contact information
Vera Boersma: The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands
Nathalie Moatti: The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands
Sandra Segura-Bayona: The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands
Marieke H. Peuscher: The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands
Jaco van der Torre: The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands
Brigitte A. Wevers: The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands
Alexandre Orthwein: The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada
Daniel Durocher: The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada
Jacqueline J. L. Jacobs: The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands

Nature, 2015, vol. 521, issue 7553, 537-540

Abstract: MAD2L2 regulates DNA repair at deprotected telomeres and at ionizing-radiation-induced double-stranded DNA breaks by inhibiting resection of the 5′ ends; the ends are thus shunted into the non-homologous end-joining pathway.

Date: 2015
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DOI: 10.1038/nature14216

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