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An ATM-independent S-phase checkpoint response involves CHK1 pathwayAfter exposure to genotoxic stress, proliferating cells actively slow down the DNA replication through a S-phase checkpoint to provide time for repair. We report that in addition to the ataxia-telangiectasia mutated (ATM)-dependent pathway that controls the fast response, there is an ATM-independent pathway that controls the slow response to regulate the S-phase checkpoint after ionizing radiation in mammalian cells. The slow response of S-phase checkpoint, which is resistant to wortmannin, sensitive to caffeine and UCN-01, and related to cyclin-dependent kinase phosphorylation, is much stronger in CHK1 overexpressed cells, and it could be abolished by Chk1 antisense oligonucleotides. These results provide evidence that the ATM-independent slow response of S-phase checkpoint involves CHK1 pathway.
Document ID
20040088401
Document Type
Reprint (Version printed in journal)
Authors
Zhou, Xiang-Yang (Kimmel Cancer Center of Jefferson Medical College, Thomas Jefferson University Philadelphia, Pennsylvania 19107, United States)
Wang, Xiang
Hu, Baocheng
Guan, Jun
Iliakis, George
Wang, Ya
Date Acquired
August 21, 2013
Publication Date
March 15, 2002
Publication Information
Publication: Cancer research
Volume: 62
Issue: 6
ISSN: 0008-5472
Subject Category
Life Sciences (General)
Funding Number(s)
CONTRACT_GRANT: CA76203
CONTRACT_GRANT: CA56706
CONTRACT_GRANT: T32-CA09137
CONTRACT_GRANT: P30-CA56036
Distribution Limits
Public
Copyright
Other
Keywords
Non-NASA Center
NASA Discipline Radiation Health