Title: ATR-dependent bystander effects in nontargeted cells

Authors: Susanne Burdak-Rothkamm, Kai Rothkamm, Kevin M. Prise

Addresses: Centre for Cancer Research and Cell Biology, Queen's University Belfast, 97 Lisburn Road, Belfast BT9 7BL, UK. ' Radiation Protection Division, Health Protection Agency, Chilton, OX11 0RQ, UK. ' Centre for Cancer Research and Cell Biology, Queen's University Belfast, 97 Lisburn Road, Belfast BT9 7BL, UK

Abstract: Ionising radiation-induced effects in nontargeted bystander cells may play an important role in low-dose cancer risk. Here, we briefly review the experimental systems used for bystander studies, the initiation and intercellular transmission of bystander signals and response mechanisms in recipient cells. Recent evidence that implicates the histone 2A variant X (H2AX) and the deoxyribonucleic acid (DNA) damage kinase ataxia telangiectasia and Rad3-related (ATR) in bystander signalling is highlighted and the implications of bystander responses for human radiation protection are discussed.

Keywords: low dose radiation; low radiation; risk assessment; radiation-induced bystander effect; bystander signalling; ataxia telangiectasia; Rad3; ATR; gamma-H2AX; DNA damage response; ionising radiation; cancer risk; radiation protection.

DOI: 10.1504/IJLR.2008.018814

International Journal of Low Radiation, 2008 Vol.5 No.1, pp.22 - 29

Published online: 18 Jun 2008 *

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