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pubmed-article:10074425pubmed:abstractTextThe ability of cyclin-dependent kinases (CDKs) to promote cell proliferation is opposed by cyclin-dependent kinase inhibitors (CKIs), proteins that bind tightly to cyclin-CDK complexes and block the phosphorylation of exogenous substrates. Mice with targeted CKI gene deletions have only subtle proliferative abnormalities, however, and cells prepared from these mice seem remarkably normal when grown in vitro. One explanation may be the operation of compensatory pathways that control CDK activity and cell proliferation when normal pathways are inactivated. We have used mice lacking the CKIs p21(Cip1) and p27(Kip1) to investigate this issue, specifically with respect to CDK regulation by mitogens.lld:pubmed
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pubmed-article:10074425pubmed:articleTitleA new pathway for mitogen-dependent cdk2 regulation uncovered in p27(Kip1)-deficient cells.lld:pubmed
pubmed-article:10074425pubmed:affiliationCancer Biology Group Amgen Inc. Thousand Oaks California USA.lld:pubmed
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pubmed-article:10074425pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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