Ababneh M, Götz C, Montenarh M
Medizinische Biochemie und Molekularbiologie, Universität des Saarlandes, Gebäude 44, Homburg, 66421, Germany.
Biochem Biophys Res Commun. 2001 May 4;283(2):507-12. doi: 10.1006/bbrc.2001.4792.
We previously found that p53 binds to the catalytic subunit of the p34(cdc2)/cyclin B1-kinase. In the present study we analyzed the functional consequences of this interaction. Binding of wild-type p53 to p34(cdc2)/cyclin B1 results in a significant decrease of its histone H1 kinase activity. Binding of p53 to the kinase is a prerequisite for the inhibition because a mutant p53 which lacks the binding region fails to influence the enzymatic activity. Furthermore, by using C-terminal fragments of p53 it became obvious that also some other structural elements in the N-terminal region are necessary for the inhibitory effect. Our present study provides evidence that p53 might regulate cell-cycle checkpoints not only on the transcriptional level but also by binding to the cell-cycle regulating kinase p34(cdc2).
我们先前发现p53可与p34(cdc2)/细胞周期蛋白B1激酶的催化亚基结合。在本研究中，我们分析了这种相互作用的功能后果。野生型p53与p34(cdc2)/细胞周期蛋白B1结合会导致其组蛋白H1激酶活性显著降低。p53与该激酶的结合是抑制作用的前提条件，因为缺乏结合区域的突变型p53无法影响酶活性。此外，通过使用p53的C末端片段，很明显N末端区域的其他一些结构元件对于抑制作用也是必需的。我们目前的研究提供了证据，表明p53可能不仅在转录水平上调节细胞周期检查点，还通过与细胞周期调节激酶p34(cdc2)结合来进行调节。
