作者: O. Llorca , A. Rivera-Calzada , L. Spagnolo , M. A. Recuero-Checa , L. H. Pearl
DOI: 10.1007/978-3-540-85228-5_18
关键词:
摘要: 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) Non-Homologous End-Joining (NHEJ) [2]. NHEJ is most frequent pathway in mammalian cells but this restricted G0 G1 phases of cell cycle. During broken ends are processed with potential loss genetic information, backbones ligated without using a template. In addition, system repairs programmed DSBs generated as intermediates during V(D)J recombination lymphocytes. Several recessive human syndromes diseases can be related mutations proteins that participate pathways.