p53-dependent Chk1 phosphorylation is required for maintenance of prolonged G arrest
Radiation Research, ISSN: 0033-7587, Vol: 168, Issue: 6, Page: 706-715
2007
- 8Citations
- 10Captures
Metric Options: Counts1 Year3 YearSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations8
- Citation Indexes8
- CrossRef4
- Captures10
- Readers10
- 10
Article Description
Targeting checkpoint kinases has been shown to have a potential chemosensitizing effect in cancer treatment. However, inhibitors of such kinases preferentially abrogate the DNA damage-induced G checkpoint in p53 as opposed to p53 cells. The mechanisms by which p53 (TP53) can prevent abrogation of the G checkpoint are unclear. Using normal human diploid p53 and p53 fibroblasts as model systems, we have compared the effects of three checkpoint inhibitors, caffeine, staurosporine and UCN-01, on γ-radiation-induced G arrest. The G arrest in p53 cells was abrogated by caffeine, but not by staurosporine and UCN-01, whereas the G arrest in p53 cells was sensitive to all three inhibitors. Chk2 (CHEK1) phosphorylation was maintained in the presence of all three inhibitors in both p53 and p53 cells. Chk1 phosphorylation was maintained only in the presence of staurosporine and UCN-01 in p53 cells. In the presence of caffeine Chk1 phosphorylation was inhibited regardless of p53 status. The pathway of Chk1 phosphorylation → Cdc25A degradation → inhibition of cyclin B1/Cdk1 activity → G arrest is accordingly resistant to staurosporine and UCN-01 in p53 cells. Moreover, sustained phosphorylation of Chk1 in the presence of staurosporine and UCN-01 is strongly related to phosphorylation of p53. The present study suggests the unique role of Chk1 in preventing abrogation of the G checkpoint in p53 cells. © 2007 by Radiation Research Society.
Bibliographic Details
Provide Feedback
Have ideas for a new metric? Would you like to see something else here?Let us know