Repair of genome destabilizing lesions.
Living organisms are constantly exposed to detrimental agents both from the environment (e.g. ionizing radiation, ultraviolet light, natural and synthetic chemicals) and from endogenous metabolic processes (e.g. oxidative and hydrolytic reactions), resulting in modifications of proteins, lipids and DNA. Proteins and lipids are degraded and resynthesized, but the DNA is replicated only during cell division, when DNA damage may result in mutation fixation. Thus the DNA damage generated has the potential to lead to carcinogenesis, cell death, or other genetic disorders in the absence of efficient error-free repair. Because modifications in DNA sequence or structure may be incompatible with its essential role in preservation and transmission of genetic information from generation to generation, exquisitely sensitive DNA repair pathways have evolved to maintain genomic stability and cell viability. This review focuses on the repair and processing of genome destabilizing lesions and helical distortions that differ significantly from the canonical B-form DNA in mammalian cells. In particular, we discuss the introduction and processing of site-specific lesions in mammalian cells with an emphasis on psoralen interstrand crosslinks.
Reddy
Madhava C
MC
Department of Carcinogenesis, The University of Texas M. D. Anderson Cancer Center, Science Park-Research Division, Smithville, Texas 78957, USA.
Vasquez
Karen M
KM
D000818:Animals; D003432:Cross-Linking Reagents / Q000627:therapeutic use; D004247:DNA / Q000378:metabolism; D004249:DNA Damage; D004260:DNA Repair; D005363:Ficusin / Q000494:pharmacology; D042822:Genomic Instability; D006609:High Mobility Group Proteins / Q000378:metabolism; D006801:Humans; D009369:Neoplasms / Q000188:drug therapy
D003432:Cross-Linking Reagents; D006609:High Mobility Group Proteins; C051802:triplex DNA; D004247:DNA; D005363:Ficusin