ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

Mutations in the ATM tumor suppressor gene confer hypersensitivity to DNA-damaging chemotherapeutic agents. Here, the authors provide evidence that these hypersensitivities reflect a crucial role for ATM at damaged replication forks being to prevent toxic DNA end-joining leading to chromosome fusion...

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Autores principales: Gabriel Balmus, Domenic Pilger, Julia Coates, Mukerrem Demir, Matylda Sczaniecka-Clift, Ana C. Barros, Michael Woods, Beiyuan Fu, Fengtang Yang, Elisabeth Chen, Matthias Ostermaier, Tatjana Stankovic, Hannes Ponstingl, Mareike Herzog, Kosuke Yusa, Francisco Munoz Martinez, Stephen T. Durant, Yaron Galanty, Petra Beli, David J. Adams, Allan Bradley, Emmanouil Metzakopian, Josep V. Forment, Stephen P. Jackson
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2019
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Science
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Acceso en línea:https://doaj.org/article/c403db6b24d849f3aa73ce7778708c4a
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