Overcoming inhibitions: subversion of CKI function by viral cyclins.
DNA tumour viruses deregulate the mammalian cell cycle to provide a better environment for their replication. Studies of such deregulation have led to the identification of key regulatory steps that normally control the G1-S phase transition of the cell cycle. The balance between the activities of G1-specific cyclin-CDK complexes and their inhibitors is critical. Recent studies suggest that certain herpesviruses disrupt this balance: the viruses encode a cyclin that generates active complexes even in the presence of high inhibitor levels.
Swanton
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Gene Regulation Laboratory, ICRF, PO Box 123, Lincoln's Inn Fields, London, UK WC2A 3PX.
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Mann
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McDonald
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Jones
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D002453:Cell Cycle; D018797:Cell Cycle Proteins; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000502:physiology; D050759:Cyclin-Dependent Kinase Inhibitor p21; D050760:Cyclin-Dependent Kinase Inhibitor p27; D018844:Cyclin-Dependent Kinases / Q000037:antagonists & inhibitors*; D016213:Cyclins / Q000502:physiology*; D006564:Herpesviridae / Q000472:pathogenicity / Q000502:physiology*; D006801:Humans; D008869:Microtubule-Associated Proteins / Q000502:physiology; D008954:Models, Biological; D008958:Models, Molecular; D025521:Tumor Suppressor Proteins; D014779:Virus Replication
C493956:CDKN1A protein, human; D018797:Cell Cycle Proteins; D019941:Cyclin-Dependent Kinase Inhibitor p16; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D008869:Microtubule-Associated Proteins; D025521:Tumor Suppressor Proteins; D050760:Cyclin-Dependent Kinase Inhibitor p27; D018844:Cyclin-Dependent Kinases