CHK1 Affecting Cell Radiosensitivity is Independent of Non-Homologous End Joining

CHK1 is one of the most important checkpoint proteins in mammalian cells for responding to DNA damage. Cells defective in CHK1 are sensitive to ionizing radiation (IR). The mechanism by which CHK1 protects cells from IR-induced killing remains unclear. DNA double strand breaks (DSBs) induced by IR a...

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Bibliographic Details
Published in:Cell cycle (Georgetown, Tex.) Tex.), 2005-02, Vol.4 (2), p.299-302
Main Authors: Wang, Hongyan, Hu, Baocheng, Liu, Ronghua, Wang, Ya
Format: Article
Language:English
Subjects:
Binding
Biology
Bioscience
Calcium
Cancer
Cell
Cycle
Landes
Organogenesis
Proteins
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Summary:CHK1 is one of the most important checkpoint proteins in mammalian cells for responding to DNA damage. Cells defective in CHK1 are sensitive to ionizing radiation (IR). The mechanism by which CHK1 protects cells from IR-induced killing remains unclear. DNA double strand breaks (DSBs) induced by IR are critical lesions for cell survival. Two major complementary DNA DSBs repair pathways exist in mammalian cells, homologous recombination repair (HRR) and non-homologous end joining (NHEJ). By using CHK1 kinase dead human cell lines established in our laboratory, we show here that although these human cell lines have different CHK1 activities with different sensitivities to IR-induced killing and G2 accumulation, all these cell lines show similar inductions and rejoining rates of DNA DSBs. These results indicate that the different radiosensitivities and G2 checkpoint responses in these cell lines are independent of NHEJ, suggesting that CHK1-regulated checkpoint facilitates HRR and therefore protects cells from IR-induced killing.
ISSN:1538-4101
1551-4005
DOI:10.4161/cc.4.2.1415