Multiple mechanisms for p27(Kip1) translocation and degradation.
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.
Susaki
Etsuo
E
Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Nakayama
Keiichi I
KI
D021581:Active Transport, Cell Nucleus; D000818:Animals; D002453:Cell Cycle / Q000502:physiology*; D018797:Cell Cycle Proteins / Q000502:physiology; D002467:Cell Nucleus / Q000378:metabolism; D002478:Cells, Cultured; D056742:Cyclin D2; D050760:Cyclin-Dependent Kinase Inhibitor p27 / Q000378:metabolism / Q000502:physiology*; D016213:Cyclins / Q000378:metabolism; D003593:Cytoplasm / Q000502:physiology; D051379:Mice; D021381:Protein Transport; D016192:Resting Phase, Cell Cycle / Q000502:physiology; D015398:Signal Transduction
C486196:Ccnd2 protein, mouse; D018797:Cell Cycle Proteins; D056742:Cyclin D2; D016213:Cyclins; D050760:Cyclin-Dependent Kinase Inhibitor p27