Susaki Etsuo, Nakayama Keiichi I
Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Cell Cycle. 2007 Dec 15;6(24):3015-20. doi: 10.4161/cc.6.24.5087. Epub 2007 Sep 19.
The nuclear export and rapid degradation of p27(Kip1) at the G(0)-G(1) transition are critical events for effective progression of the cell cycle. Several pathways have been proposed at the molecular level for the export of this cyclin-dependent kinase inhibitor from the nucleus. However, the addition of each new pathway renders the situation more complicated. We recently showed that cyclin D2 links growth signals to the cytoplasmic translocation and degradation of p27 at the G(0)-G(1) transition. Here we describe our findings and discuss how the multiple potential mechanisms for p27 translocation that precedes its degradation might be integrated in the context of growth stimulation and G(1) progression.
在G(0)-G(1)期转换时,p27(Kip1)的核输出及快速降解是细胞周期有效进展的关键事件。在分子水平上,已经提出了几种将这种细胞周期蛋白依赖性激酶抑制剂从细胞核输出的途径。然而,每增加一条新途径都会使情况变得更加复杂。我们最近发现,细胞周期蛋白D2在G(0)-G(1)期转换时将生长信号与p27的细胞质转运及降解联系起来。在此,我们描述我们的发现,并讨论在生长刺激和G(1)期进展的背景下,p27降解之前的多种潜在转运机制可能如何整合。