p21Cip1Promotes Cyclin D1 Nuclear Accumulation via Direct Inhibition of Nuclear Export
作者： Jodi R. Alt , Andrew B. Gladden , J. Alan Diehl
关键词: Cancer research 、 Null cell 、 Cyclin A2 、 GSK-3 、 Cyclin A 、 Cyclin D1 、 Chemistry 、 In vivo 、 Cell biology 、 Nuclear export signal 、 Cyclin 、 Biochemistry 、 Molecular biology
摘要: There is increasing evidence that p21Cip1 and p27Kip1 are requisite positive regulators of cyclin D1·CDK4 assembly nuclear accumulation. Both Cip Kip proteins can promote accumulation D1, but the underlying mechanism has not been elucidated. We now provide promotes D1 complexes via inhibition export. In vivo, we demonstrate inhibit glycogen synthase kinase 3β-triggered export phosphorylation-dependent nucleocytoplasmic shuttling. Furthermore, find in p21/p27 null cells be restored through CRM1-depenendent The ability to correlates with its bind Thr-286-phosphorylated thereby prevents D1·CRM1 association.
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