title: Mammalian DNA repair responses and genomic instability.
abstract: A cell responds to damage to its DNA in one of three ways: by tolerating the damage, by repairing the damage or by undergoing apoptosis. The latter two responses represent defenses against genomic instability and tumorigenesis resulting from unrepaired damage. There are multiple DNA repair pathways to cope with a variety of damage reflecting the importance of DNA repair in maintaining both cell viability and genomic stability. These include base excision repair, mismatch repair, double-strand break repair and nucleotide excision repair. Several signal transduction pathways are activated by DNA damage resulting in cell-cycle arrest. Cell-cycle arrest increases the time available for DNA repair before DNA replication and mutation fixation. Recently, there has been tremendous progress in our understanding of the molecular components repair processes and to examine recently observed interactions between DNA repair, signal transduction pathways and other cellular processes such as cell-cycle control, transcription, replication and recombination.
authors.affiliation: Laboratory of Molecular Genetics, National Institutes on Aging, National Institute of Health, Baltimore, MD 21224, USA.
authors.forename: C M
authors.initials: CM
authors.lastname: ap Rhys
authors.forename: V A
authors.initials: VA
authors.lastname: Bohr
mesh_terms: D000818:Animals; D002453:Cell Cycle / Q000502:physiology; D004247:DNA / Q000378:metabolism; D004260:DNA Repair / Q000235:genetics*; D016158:Genes, p53 / Q000235:genetics; D008322:Mammals / Q000378:metabolism; D008957:Models, Genetic; D009153:Mutagens / Q000009:adverse effects; D011827:Radiation; D015398:Signal Transduction / Q000502:physiology
chemical_list: D009153:Mutagens; D004247:DNA