Lobrich, M. and Jeggo, Penny (2005) Harmonising the response to DSBs: a new string in the ATM bow. DNA Repair, 7. pp. 749-759. ISSN 1568-7864

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Abstract

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.

Item Type:	Article
Additional Information:	GDSC124
Depositing User:	Gee Wheatley
Date Deposited:	19 Mar 2007
Last Modified:	09 Sep 2019 15:56
URI:	http://sro.sussex.ac.uk/id/eprint/936
Google Scholar:	81 Citations

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