The mechanism of non-homologous end-joining: a synopsis of synapsis.
Repair of DNA double-strand breaks (DSBs) by non-homologous end-joining (NHEJ) is required for resistance to genotoxic agents, such as ionizing radiation, but also for proper development of the vertebrate immune system. Much progress has been made in identifying the factors that are involved in this repair pathway. We are now entering the phase in which we begin to understand basic concepts of the reaction mechanism and regulation of non-homologous end-joining. This review concentrates on novel insights into damage recognition and subsequent tethering, processing and joining of DNA ends.
Weterings
Eric
E
Department of Cell Biology and Genetics, Erasmus Medical Center, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands.
van Gent
Dik C
DC
D000818:Animals; D004247:DNA / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D004249:DNA Damage; D000072481:DNA Ligase ATP; D011088:DNA Ligases / Q000378:metabolism; D004260:DNA Repair / Q000235:genetics / Q000276:immunology / Q000502:physiology*; D045643:DNA Repair Enzymes / Q000378:metabolism; D051747:DNA-Activated Protein Kinase; D004268:DNA-Binding Proteins / Q000378:metabolism; D005803:Genes, Immunoglobulin; D019672:Genes, T-Cell Receptor; D006801:Humans; D008954:Models, Biological; D009687:Nuclear Proteins; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism
D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; C101467:XRCC4 protein, human; D004247:DNA; D051747:DNA-Activated Protein Kinase; C497263:PRKDC protein, human; D017346:Protein Serine-Threonine Kinases; D011088:DNA Ligases; D045643:DNA Repair Enzymes; D000072481:DNA Ligase ATP