v-Jun overrides the mitogen dependence of S-phase entry by deregulating retinoblastoma protein phosphorylation and E2F-pocket protein interactions as a consequence of enhanced cyclin E-cdk2 catalytic activity.

Journal article

v-Jun accelerates G(1) progression and shares the capacity of the Myc, E2F, and E1A oncoproteins to sustain S-phase entry in the absence of mitogens; however, how it does so is unknown. To gain insight into the mechanism, we investigated how v-Jun affects mitogen-dependent processes which control the G(1)/S transition. We show that v-Jun enables cells to express cyclin A and cyclin A-cdk2 kinase activity in the absence of growth factors and that deregulation of cdk2 is required for S-phase en...

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Authors: Clark, W; Black, E; MacLaren, A; Kruse, U; LaThangue, N

• Publication status: Published
• Journal: Molecular and cellular biology
• Volume: 20
• Issue: 7
• Pages: 2529-2542
• Publication date: 2000-04-01
• DOI: 10.1128/mcb.20.7.2529-2542.2000
• EISSN: 1098-5549
• ISSN: 0270-7306
• Language: English
• Keywords: CDC2-CDC28 Kinases; G1 Phase; Cell Division; Cyclin-Dependent Kinase Inhibitor p16; Fibroblasts; Cyclins; Phosphorylation; Oncogene Proteins; Animals; Chick Embryo; Transformation, Genetic; Cell Cycle; S Phase; Microinjections; Plasmids; Retinoblastoma Protein; Mitogens; Cyclin-Dependent Kinases; Carrier Proteins; Cyclin-Dependent Kinase 2; Oncogene Protein p65(gag-jun); Protein-Serine-Threonine Kinases