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Repair and genetic consequences of endogenous DNA base damage in mammalian cells.

Annual review of genetics | Nov 30, 2004

Living organisms dependent on water and oxygen for their existence face the major challenge of faithfully maintaining their genetic material under a constant attack from spontaneous hydrolysis and active oxygen species and from other intracellular metabolites that can modify DNA bases. Repair of endogenous DNA base damage by the ubiquitous base-excision repair pathway largely accounts for the significant turnover of DNA even in nonreplicating cells, and must be sufficiently accurate and efficient to preserve genome stability compatible with long-term cellular viability. The size of the mammalian genome has necessitated an increased complexity of repair and diversification of key enzymes, as revealed by gene knock-out mouse models. The genetic instability characteristic of cancer cells may be due, in part, to mutations in genes whose products normally function to ensure DNA integrity.

Pubmed ID: 15568983 RIS Download

Mesh terms: Alkylation | Animals | Base Composition | Base Sequence | DNA Damage | DNA Glycosylases | DNA Repair | Deamination | Gene Targeting | Genome | Mice | Mice, Knockout | Mice, Transgenic | Models, Genetic | Mutagenesis | Oxidation-Reduction | Oxidative Stress | Uracil