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• W2115692032 endingPage "1583" @default.
• W2115692032 startingPage "1571" @default.
• W2115692032 abstract "The widely prevailing view that the cyclin-dependent kinase inhibitors (CKIs) are solely negative regulators of cyclin-dependent kinases (CDKs) is challenged here by observations that normal up-regulation of cyclin D- CDK4 in mitogen-stimulated fibroblasts depends redundantly upon p21(Cip1) and p27(Kip1). Primary mouse embryonic fibroblasts that lack genes encoding both p21 and p27 fail to assemble detectable amounts of cyclin D-CDK complexes, express cyclin D proteins at much reduced levels, and are unable to efficiently direct cyclin D proteins to the cell nucleus. Restoration of CKI function reverses all three defects and thereby restores cyclin D activity to normal physiological levels. In the absence of both CKIs, the severe reduction in cyclin D-dependent kinase activity was well tolerated and had no overt effects on the cell cycle." @default.
• W2115692032 created "2016-06-24" @default.
• W2115692032 creator A5054879064 @default.
• W2115692032 date "1999-03-15" @default.
• W2115692032 modified "2023-10-14" @default.
• W2115692032 title "The p21Cip1 and p27Kip1 CDK `inhibitors' are essential activators of cyclin D-dependent kinases in murine fibroblasts" @default.
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• W2115692032 doi "https://doi.org/10.1093/emboj/18.6.1571" @default.
• W2115692032 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1171245" @default.
• W2115692032 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10075928" @default.
• W2115692032 hasPublicationYear "1999" @default.
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