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The candidate tumor suppressor ING1b can stabilize p53 by disrupting the regulation of p53 by MDM2.
TLDR
It is shown that ING1b could stimulate the activity of p53 by increasing the level and stability of the p53 protein, and similarly to MDM2, ING 1b binds to the NH(2)-terminal region of p 53. Expand
G1 versus G2 cell cycle arrest after adriamycin‐induced damage in mouse Swiss3T3 cells
TLDR
It is shown that adriamycin was capable of inducing a G1 cell cycle arrest, both during the G0‐G1 transition and during theG1 phase of the normal cell cycle, and was relatively tight and correlated with the Thr‐14/Tyr‐15 phosphorylation of cyclin B‐Cdc2 complexes. Expand
How Many Mutant p53 Molecules Are Needed To Inactivate a Tetramer?
TLDR
Surprisingly, these experiments reveal that DNA binding-defective p53 mutants (R249S and R273H) are very ineffective in impairing the transcriptional activity of p53: at least three mutants are required to inactivate a tetramer. Expand
MDM2 and MDMX bind and stabilize the p53-related protein p73
TLDR
In striking contrast to p53, the half-life of p73 was found to be increased by binding to MDM2, and the growth suppression functions of p 73 and the induction of endogenous p21, a major mediator of the p53-dependent growth arrest pathway, were enhanced in the presence ofMDM2. Expand
On the concentrations of cyclins and cyclin-dependent kinases in extracts of cultured human cells.
TLDR
It is formally demonstrated that CDC2 and CDK2 are in excess of their cyclin partners, and the concentration of the CDK inhibitor p21(CIP1/WAF1) induced after DNA damage is sufficient to overcome the cyclin-CDK2 complexes in MCF-7 cells. Expand
Cyclin F Is Degraded during G2-M by Mechanisms Fundamentally Different from Other Cyclins*
TLDR
Although cyclin F is degraded at similar time as the mitotic cyclins, the underlying mechanisms are entirely distinct and appear to involve metalloproteases. Expand
ING1b decreases cell proliferation through p53‐dependent and ‐independent mechanisms
TLDR
Data indicate that ING1 has a subtle antiproliferative effect even in the absence of p53, and ING 1b enhances the DNA damage responses through p53‐dependent and ‐independent mechanisms. Expand
Topoisomerase poisons differentially activate DNA damage checkpoints through ataxia-telangiectasia mutated-dependent and -independent mechanisms.
TLDR
Different mechanisms are involved in the activation of different cell cycle checkpoints at different concentrations of Adriamycin and camptothecin, indicating that the involvement of ATM following treatment with Topo poisons differs extensively with dosage and for differentcell cycle checkpoints. Expand
Differential Contribution of Inhibitory Phosphorylation of CDC2 and CDK2 for Unperturbed Cell Cycle Control and DNA Integrity Checkpoints*
TLDR
It is found that inhibitory phosphorylation plays a major role in the regulation of CDC2 but only a minor role for CDK2 during the unperturbed cell cycle of HeLa cells and during the DNA damage checkpoint. Expand
Differential Mode of Regulation of the Checkpoint Kinases CHK1 and CHK2 by Their Regulatory Domains*
TLDR
Comparisons of how the regulatory domains of human CHK1 and CHK2 modulate the respective kinase activities reveal the very different mode of regulation between CHK 1 andCHK2. Expand
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