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1 December 2007 Ionizing Radiation Sensitivity of DNA Polymerase Lambda-Deficient Cells
Christie Vermeulen, Barbara Bertocci, Adrian C. Begg, Conchita Vens
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Abstract

Vermeulen, C., Bertocci, B., Begg, A. C. and Vens, C. Ionizing Radiation Sensitivity of DNA Polymerase Lambda-Deficient Cells. Radiat. Res. 168, 683–688 (2007).

Ionizing radiation induces a diverse spectrum of DNA lesions, including strand breaks and oxidized bases. In mammalian cells, ionizing radiation-induced lesions are targets of non-homologous end joining, homologous recombination, and base excision repair. In vitro assays show a potential involvement of DNA polymerase lambda in non-homologous end joining and base excision repair. In this study, we investigated whether DNA polymerase lambda played a significant role in determining ionizing radiation sensitivity. Despite increased sensitivity to hydrogen peroxide, lambda-deficient mouse embryonic fibroblasts displayed equal survival after exposure to ionizing radiation compared to their wild-type counterparts. In addition, we found increased sensitivity to the topoisomerase inhibitors camptothecin and etoposide in the absence of polymerase lambda. These results do not reveal a major role for DNA polymerase lambda in determining radiosensitivity in vivo.

Christie Vermeulen, Barbara Bertocci, Adrian C. Begg, and Conchita Vens "Ionizing Radiation Sensitivity of DNA Polymerase Lambda-Deficient Cells," Radiation Research 168(6), 683-688, (1 December 2007). https://doi.org/10.1667/RR1057R.1
Received: 10 April 2007; Accepted: 1 July 2007; Published: 1 December 2007
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