Abstract
Double-strand DNA breaks (DSBs) fracture the chromosomes, generating genomic instability and chromosomal translocations which favor tumor transformation [1]. Cells use two mechanisms to repair these DSBs, Homologous Recombination (HR) and Non-Homologous End-Joining (NHEJ) [2]. NHEJ is the most frequent DNA repair pathway in mammalian cells but this is restricted to G0 and G1 phases of the cell cycle. During NHEJ the broken ends are processed with potential loss of genetic information, and the backbones ligated without using a template. In addition, the NHEJ system repairs programmed DSBs generated as intermediates during V(D)J recombination in lymphocytes. Several recessive human syndromes and diseases can be related to mutations of proteins that participate in these DNA repair pathways.
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Llorca, O., Rivera-Calzada, A., Spagnolo, L., Recuero-Checa, M.A., Pearl, L.H. (2008). 3D Structure of DNA Repair Macromolecular Complexes Participating in Non-Homologous End-Joining (NHEJ). In: Aretz, A., Hermanns-Sachweh, B., Mayer, J. (eds) EMC 2008 14th European Microscopy Congress 1–5 September 2008, Aachen, Germany. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-85228-5_18
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DOI: https://doi.org/10.1007/978-3-540-85228-5_18
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