Cdk2 dethroned as master of S phase entry.
The prevailing view of cdk2 as a critical regulator of cell cycle progression and optimal therapeutic target in cancer cells is now challenged by the observation that tumor cells deficient in cdk2 protein and kinase activity are not impaired in proliferation.
Hinds
Philip W
PW
Department of Pathology, Harvard Medical School, Boston, MA 02115, USA. phil_hinds@hms.harvard.edu
D000818:Animals; D042846:CDC2-CDC28 Kinases; D002455:Cell Division; D019927:Cyclin E / Q000235:genetics; D051357:Cyclin-Dependent Kinase 2; D018844:Cyclin-Dependent Kinases / Q000502:physiology*; D020868:Gene Silencing; D006801:Humans; D009369:Neoplasms / Q000235:genetics; D017346:Protein Serine-Threonine Kinases / Q000502:physiology*; D016160:Retinoblastoma Protein / Q000235:genetics; D016196:S Phase / Q000502:physiology*; D015398:Signal Transduction
D019927:Cyclin E; D016160:Retinoblastoma Protein; D017346:Protein Serine-Threonine Kinases; D042846:CDC2-CDC28 Kinases; C495894:CDK2 protein, human; D051357:Cyclin-Dependent Kinase 2; D018844:Cyclin-Dependent Kinases