细胞周期蛋白依赖性激酶11（p46）亚型与RanBPM相互作用。
The cyclin-dependent kinase 11(p46) isoform interacts with RanBPM.
作者信息
Mikolajczyk Monika, Shi Jiaqi, Vaillancourt Richard R, Sachs Nancy A, Nelson Mark
机构信息
Department of Pathology, College of Medicine, University of Arizona, Tucson, AZ 85724, USA.
出版信息
Biochem Biophys Res Commun. 2003 Oct 10;310(1):14-8. doi: 10.1016/j.bbrc.2003.08.116.
We identified Ran-binding protein (RanBPM) as an interacting partner of the caspase-processed C-terminal domain of cyclin-dependent kinase 11 (CDK11(p46)) by using the yeast two-hybrid system. CDK11(p110) protein kinases are members of the cyclin-dependent kinase superfamily. During staurosporine-, Fas-, and tumor necrosis factor alpha-induced apoptosis caspase-processed activated CDK11(p46) is generated from larger CDK11(p110) isoforms. CDK11(p46) promotes apoptosis when it is ectopically expressed in human cells. However, the mechanism of signal transduction through CDK11(p46) is still unclear. In this study, we demonstrate that CDK11(p46) directly interacts with RanBPM in vitro and in human cells. RanBPM contains a conserved SPRY (repeats in splA and Ryr) domain and is localized both in the nucleus and cytoplasm. The SPRY domain of RanBPM is responsible for the association between CDK11(p46) and RanBPM. Furthermore, we show that CDK11(46) phosphorylates RanBPM.
我们通过酵母双杂交系统鉴定出Ran结合蛋白（RanBPM）是细胞周期蛋白依赖性激酶11（CDK11(p46)）经半胱天冬酶处理后的C末端结构域的相互作用伴侣。CDK11(p110)蛋白激酶是细胞周期蛋白依赖性激酶超家族的成员。在星形孢菌素、Fas和肿瘤坏死因子α诱导的细胞凋亡过程中，较大的CDK11(p110)异构体可产生经半胱天冬酶处理后激活的CDK11(p46)。当CDK11(p46)在人类细胞中异位表达时，它会促进细胞凋亡。然而，通过CDK11(p46)进行信号转导的机制仍不清楚。在本研究中，我们证明CDK11(p46)在体外和人类细胞中都能直接与RanBPM相互作用。RanBPM包含一个保守的SPRY（splA和Ryr中的重复序列）结构域，定位于细胞核和细胞质中。RanBPM的SPRY结构域负责CDK11(p46)与RanBPM之间的结合。此外，我们还表明CDK11(46)可使RanBPM磷酸化。
Zotero 插件