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Brief Report
CHK1 Affecting Cell Radiosensitivity is Independent of Non-Homologous End Joining
Hongyan Wang, Baocheng Hu, Ronghua Liu and Ya Wang
volume 4 | issue 2
february 2005Pages: 300 - 303
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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.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.