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Abstract
DNA double-strand breaks (DSBs) are the major lethal lesion induced by ionizing radiation
or by replication block. However, cells can take advantage of DSB-induced recombination
in order to generate genetic diversity in physiological processes such as meiosis
and V(D)J recombination. Two main alternative pathways compete for DSB repair: homologous
recombination (HR) and non-homologous end-joining (NHEJ). This review will briefly
present the mechanisms and the enzymatic complex for HR and NHEJ. The signalling of
the DSB through the ATM pathway will be presented. Then, we will focus on the case
of the RAD51 protein, which plays a pivotal role in HR and is conserved from bacteria
to humans. Post-translational regulation of RAD51 is presented. Two contrasting situations
are discussed: one with up-regulation (expression of the oncogene BCR/ABL) and one
with a down-regulation (expression of the oncogene BCL-2) of RAD51, associated with
apoptosis inhibition and tumour predisposition.
Copyright 2002 Elsevier Science Inc.