Molecular Controls of Cell Cycle Progression Following DNA Damage: Roles of P53 and Ataxia-Telangiectasia Gene Products

作者: Michael B. Kastan

DOI: 10.1007/978-1-4757-9217-1_8

关键词: DNA damageCell biologyDNA replicationAtaxia-telangiectasiaCarcinogenesisBiologyGeneticsDNA repairCell divisionDNANijmegen breakage syndrome

摘要: It has been suggested that exposure to environmental DNA damaging agents contributes the development of vast majority human tumors1. Therefore, an understanding molecular events involved in cellular responses such exposures should provide insights into mechanisms carcinogenesis. Much effort over past 25 years focused on how altered nucleotide bases are removed and linear integrity sequence is restored2. More recently, it become clear timing these repair processes relative various critical processes, as replication, may be important determinants for dictating consequences damage. For example, a cell which continues replicate its prior repairing lesions more likely result daughter cells have genetic information parental cell. would predicted develop changes contribute transformed phenotype (Figure 1).

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