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A more recent version of this article appeared on November 9, 2001
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Papers In Press, published online ahead of print September 14, 2001
J. Biol. Chem, 10.1074/jbc.M106460200
Submitted on July 10, 2001
Revised on September 14, 2001
Accepted on September 13, 2001

Involvement of the interaction between p21 and PCNA for the maintenance of G2/M arrest after DNA damage

Tomoaki Ando, Takumi Kawabe, Hirotaka Ohara, Bernard Ducommun, Makoto Itoh, and Takashi Okamoto

Molecular Genetics, Nagoya City University Medical School, Nagoya, Aichi 467-8601

Corresponding Author: tokamoto{at}med.nagoya-cu.ac.jp

Although a major effect of p21, a cyclin-dependent kinase inhibitor, is considered to be exerted during G1 phase of the cell cycle, p21 gene knock-out studies suggested its involvement in G2/M checkpoint as well. Here we demonstrate evidences that p21 is required for the cell cycle arrest at G2 upon DNA damage. We found that expression of wild-type p21 (p21WT), not mutant p21 (p21PCNA-) lacking the interaction with proliferating cell nuclear antigen (PCNA), caused G2 cell cycle arrest in p53-deficient DLD1 colon cancer cell line after the DNA damage by treatment with cis-diamminedichloroplatinum (II) (CDDP). We also found that p21WT was associated with Cdc2/cyclin B1 together with PCNA. Furthermore, coimmunoprecipitation experiments revealed that PCNA interacted with Cdc25C at G2-M transition and this interaction was abolished when p21WT was expressed presumably due to the competition between p21 WT and Cdc25C in the binding to PCNA. These findings suggest that p21 plays a regulatory role in the maintenance of cell cycle arrest at G2 by blocking the interaction of Cdc25C with PCNA.


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