KAP1 dictates p53 response induced by chemotherapeutic agents via Mdm2 interaction.
作者： Koji Okamoto , Issay Kitabayashi , Yoichi Taya
DOI: 10.1016/J.BBRC.2006.10.022
关键词: Cell growth 、 Camptothecin 、 Biology 、 In vivo 、 Cell biology 、 Gene silencing 、 Cell cycle checkpoint 、 Mdm2 、 Cell cycle 、 Gene
摘要: KAP1 recruits many proteins involved in gene silencing and functions as an integral part of co-repressor complex. was identified Mdm2-binding protein shown to form a complex with Mdm2 p53 vivo. We examined the role activation after treatment cells different types external stresses. reduction markedly enhanced induction p21, product target gene, actinomycin D or γ-irradiation, but not camptothecin. Treatment D, camptothecin, augmented interaction KAP1. Further, D-treated facilitated cell cycle arrest negatively affected clonal growth. Thus, levels promotes p53-dependent p21 inhibits proliferation cells. may serve therapeutic against cancer combination D.
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