The Rad9 protein enhances survival and promotes DNA repair following exposure to ionizing radiation |
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Authors: | Brandt Patrick D Helt Christopher E Keng Peter C Bambara Robert A |
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Institution: | Department of Biochemistry and Biophysics, School of Medicine and Dentistry, The University of Rochester, NY 14642, USA. |
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Abstract: | Following DNA damage cells initiate cell cycle checkpoints to allow time to repair sustained lesions. Rad9, Rad1, and Hus1 proteins form a toroidal complex, termed the 9-1-1 complex, that is involved in checkpoint signaling. 9-1-1 shares high structural similarity to the DNA replication protein proliferating cell nuclear antigen (PCNA) and 9-1-1 has been shown in vitro to stimulate steps of the repair process known as long patch base excision repair. Using a system that allows conditional repression of the Rad9 protein in human cell culture, we show that Rad9, and by extension, the 9-1-1 complex, enhances cell survival, is required for efficient exit from G2-phase arrest, and stimulates the repair of damaged DNA following ionizing radiation. These data provide in vivo evidence that the human 9-1-1 complex participates in DNA repair in addition to its previously described role in DNA damage sensing. |
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Keywords: | Rad9 9-1-1 complex DNA damage Cell cycle checkpoints Base excision repair |
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