VRK1 与 p53 相互作用形成基础复合物，该复合物可被 UV 诱导的 DNA 损伤所激活。
VRK1 interacts with p53 forming a basal complex that is activated by UV-induced DNA damage.
机构信息
Experimental Therapeutics and Translational Oncology Program, Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC), Universidad de Salamanca, Salamanca, Spain.
Experimental Therapeutics and Translational Oncology Program, Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC), Universidad de Salamanca, Salamanca, Spain; Instituto de Investigación Biomédica de Salamanca (IBSAL), Hospital Universitario de Salamanca, Salamanca, Spain.
出版信息
FEBS Lett. 2014 Mar 3;588(5):692-700. doi: 10.1016/j.febslet.2014.01.040. Epub 2014 Jan 31.
DNA damage immediate cellular response requires the activation of p53 by kinases. We found that p53 forms a basal stable complex with VRK1, a Ser-Thr kinase that responds to UV-induced DNA damage by specifically phosphorylating p53. This interaction takes place through the p53 DNA binding domain, and frequent DNA-contact mutants of p53, such as R273H, R248H or R280K, do not disrupt the complex. UV-induced DNA damage activates VRK1, and is accompanied by phosphorylation of p53 at Thr-18 before it accumulates. We propose that the VRK1-p53 basal complex is an early-warning system for immediate cellular responses to DNA damage.
DNA 损伤的即刻细胞反应需要激酶激活 p53。我们发现 p53 与 VRK1 形成基础稳定复合物，VRK1 是一种 Ser-Thr 激酶，通过特异性磷酸化 p53 对 UV 诱导的 DNA 损伤做出反应。这种相互作用发生在 p53 的 DNA 结合域，并且 p53 的频繁 DNA 接触突变体，如 R273H、R248H 或 R280K，不会破坏复合物。UV 诱导的 DNA 损伤激活 VRK1，并伴随着 p53 在积累之前在 Thr-18 处的磷酸化。我们提出 VRK1-p53 基础复合物是对 DNA 损伤的即刻细胞反应的早期预警系统。
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