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Harmonising the response to DSBs: a new string in the ATM bow

journal contribution
posted on 2023-06-07, 13:53 authored by M. Lobrich, Penny Jeggo
Ataxia telangiestasia mutated protein (ATM) is the major kinase that initiates the DNA damage signal transduction response following exposure to ionising radiation (IR) in mammalian cells. DNA non-homologous end-joining (NHEJ) is the most significant double strand break (DSB) repair pathway in mammalian cells. ATM-defective cell lines display cell cycle checkpoint defects and show pronounced radiosensitivity. ATM signalling was previously thought to be dispensable for NHEJ. This review discusses recent findings that ATM activates an end-processing mechanism dependent upon Artemis, a nuclease that also functions to cleave the hairpin intermediate generated during V(D)J recombination. ATM/Artemis-dependent end-processing is required for the repair of a sub-fraction (approximately 10%) of DSBs induced by IR and makes a significant contribution to survival following exposure to ionising radiation. This result represents a new role for ATM and demonstrates a novel cross communication between the DNA repair and signal transduction machinery.

History

Publication status

  • Published

Journal

DNA Repair

ISSN

1568-7864

Volume

7

Page range

749-759

Notes

GDSC124

Full text available

  • No

Peer reviewed?

  • Yes

Legacy Posted Date

2007-03-19

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    University of Sussex (Publications)

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