Inhibiting CDK inhibitors: new lessons from DNA tumor viruses.
The ability of viral oncoproteins to inactivate the retinoblastoma and p53 tumor suppressors provides mechanisms for bypassing the normal inhibitory activities of cyclin-dependent-kinase inhibitors (CKIs). Recent studies point to novel mechanisms for inhibiting the activities of the CKIs p21CIP1 and p27KIP1 activity. Such mechanisms involve the binding of viral oncoproteins or other proteins to these CKIs and suggest a model in which the cell-cycle activities of p21CIP1 are coordinated through protein-protein interactions.
Funk
J O
JO
Dept of Dermatology, Friedrich-Alexander-University, Erlangen, Germany. funk@derma.med.uni-erlangen.de
Galloway
D A
DA
D002453:Cell Cycle; D018797:Cell Cycle Proteins; D050759:Cyclin-Dependent Kinase Inhibitor p21; D050760:Cyclin-Dependent Kinase Inhibitor p27; D018844:Cyclin-Dependent Kinases / Q000037:antagonists & inhibitors*; D016213:Cyclins / Q000502:physiology; D006801:Humans; D008869:Microtubule-Associated Proteins / Q000502:physiology; D008954:Models, Biological; D027383:Papillomaviridae / Q000502:physiology; D016160:Retinoblastoma Protein / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000502:physiology; D025521:Tumor Suppressor Proteins; D014764:Viral Proteins / Q000502:physiology
C493956:CDKN1A protein, human; D018797:Cell Cycle Proteins; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D008869:Microtubule-Associated Proteins; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; D014764:Viral Proteins; D050760:Cyclin-Dependent Kinase Inhibitor p27; D018844:Cyclin-Dependent Kinases