Dual role of CDKs in DNA repair: to be, or not to be.
The maintenance of genome integrity is essential for the regulation of cell proliferation and differentiation. DNA must be accurately duplicated and segregated to daughter cells at cell division, a process that is primarily regulated by cyclin-dependent kinases (CDKs). During cell growth, however, it is inevitable that DNA breaks will occur due to endogenous and exogenous stresses. Interestingly, there is increasing evidence that the catalytic activities of CDKs play critical roles in the DNA damage response, especially in the case of damage repaired by the homologous recombination (HR) pathway. In this review, we outline current knowledge of CDK regulation and its roles both in the unperturbed cell cycle and in DNA damage responses, and discuss the physiological roles of CDKs in HR repair.
Yata
Keiko
K
Molecular Oncology Laboratories, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, UK.
Esashi
Fumiko
F
D000818:Animals; D024682:BRCA2 Protein / Q000378:metabolism; D002453:Cell Cycle; D002455:Cell Division; D018844:Cyclin-Dependent Kinases / Q000378:metabolism*; D053903:DNA Breaks, Double-Stranded; D004249:DNA Damage; D004260:DNA Repair / Q000502:physiology*; D006801:Humans; D051135:Rad51 Recombinase / Q000378:metabolism; D053484:RecQ Helicases / Q000378:metabolism; D011995:Recombination, Genetic; D051716:Replication Protein A / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
D024682:BRCA2 Protein; D051716:Replication Protein A; D016159:Tumor Suppressor Protein p53; D018844:Cyclin-Dependent Kinases; D051135:Rad51 Recombinase; D053484:RecQ Helicases