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      DNA double-strand break repair signalling: The case of RAD51 post-translational regulation

      , , ,
      Cellular Signalling
      Elsevier BV

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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.

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          Author and article information

          Journal
          Cellular Signalling
          Cellular Signalling
          Elsevier BV
          08986568
          December 2002
          December 2002
          : 14
          : 12
          : 969-975
          Article
          10.1016/S0898-6568(02)00052-9
          12359302
          e3ad5041-ac30-43f1-89ae-9613ff204777
          © 2002

          https://www.elsevier.com/tdm/userlicense/1.0/

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