紫外线损伤后，复制蛋白A与p53之间的相互作用以DNA修复依赖的方式被破坏。
Interaction between replication protein A and p53 is disrupted after UV damage in a DNA repair-dependent manner.
作者信息
Abramova N A, Russell J, Botchan M, Li R
机构信息
Department of Biochemistry, Health Sciences Center, University of Virginia, Charlottesville, VA 22908, USA.
出版信息
Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7186-91. doi: 10.1073/pnas.94.14.7186.
Abstract
Replication protein A (RPA) is required for both DNA replication and nucleotide excision repair. Previous studies have shown that RPA interacts with the tumor suppressor p53. Herein, we have mapped a 20-amino acid region in the N-terminal part of p53 that is essential for its binding to RPA. This region is distinct from the minimal activation domain of p53 previously identified. We also demonstrate that UV radiation of cells greatly reduces the ability of RPA to bind to p53. Interestingly, damage-induced hyperphosphorylated RPA does not associate with p53. Furthermore, down-regulation of the RPA/p53 interaction is dependent upon the capability of cells to perform global genome repair. On the basis of these data, we propose that RPA may participate in the coordination of DNA repair with the p53-dependent checkpoint control by sensing UV damage and releasing p53 to activate its downstream targets.
摘要
复制蛋白A（RPA）对于DNA复制和核苷酸切除修复均是必需的。先前的研究表明，RPA与肿瘤抑制因子p53相互作用。在此，我们已定位到p53 N端的一个20个氨基酸的区域，该区域对于其与RPA的结合至关重要。此区域不同于先前鉴定的p53最小激活域。我们还证明，细胞的紫外线辐射极大地降低了RPA与p53结合的能力。有趣的是，损伤诱导的超磷酸化RPA不与p53结合。此外，RPA/p53相互作用的下调取决于细胞进行全基因组修复的能力。基于这些数据，我们提出，RPA可能通过感知紫外线损伤并释放p53以激活其下游靶点，从而参与DNA修复与p53依赖性检查点控制的协调。
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