Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2050479 | FEBS Letters | 2007 | 6 Pages |
Abstract
When cells progressing in G1 phase are irradiated with UV light, two damage checkpoint pathways are activated: CHK1–Cdc25A and p53–p21WAF1/CIP1, both targeting Cdk2 but the latter inducing long lasting inactivation. In similarly irradiated S phase cells, however, p21WAF1/CIP1-dependent checkpoint is largely inactive. We report here that p21-dependent checkpoint can effectively be activated and induce a prolonged S phase arrest with similarly extended inactivation of Cdk2 by association of p21 if mid-S phase cells are damaged with a base-modifying agent instead of UV light, indicating that the poor utilization of p21-dependent checkpoint is not an innate property of S phase cells.
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Authors
Qiuming Kan, Shigeki Jinno, Hanako Yamamoto, Hiroto Okayama,