作者: Jeanette Heede Rudolph
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摘要: Radiation-induced DNA lesions lead to the activation of complex damage response pathways in mammalian cells. In one these p21 protein, a well-characterized cyclin dependent kinase inhibitor, is induced by TP53 after leading cell cycle arrest G1-phase. Independently its transactivation TP53, protein forms nuclear accumulations at heavy ion-induced [Jakob et al., 2000]. As shown this study, foci also arise exposure cells sparsely ionizing X-rays. an attempt elucidate functional role foci, their dependence on proliferating antigen (PCNA) demonstrated here. particular, requirement for interaction between and PCNA revealed. addition, kinetics PCNA- p21- be very similar, both proteins are part chromatin-bound fraction induction A possible involvement double- and/or single-strand break repair discussed.