Deregulated expression of G1 cyclins and their cognate cdk partners is often found in human tumor cells.
2
These findings argue against the proposed necessity of complete Rb inactivation by sequential phosphorylation by D- and E-type cyclin-cdk complexes.
3
We have studied the role of a conserved hydrophobic patch on the surface of cyclin A in substrate recognition by cyclin A-cdk2.
4
In addition, the concomitant expression of Np95 and of cycE-cdk2 was alone sufficient to induce S phase in TD cells.
5
Shortening of G1 phase temporally correlated with more rapid degradation of the cdk inhibitor p27Kip1 and with premature activation of cyclin A-dependent cdk2.