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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Bibliographic Details
Main Authors: |
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 |
Format: | Article
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Language: | English |
Published: |
Nature Publishing Group
2019-01-01
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Series: | Nature Communications
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Online Access: | https://doi.org/10.1038/s41467-018-07729-2
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