Multiple mechanisms for p27(Kip1) translocation and degradation

Abstract

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.