Journal
DNA REPAIR
Volume 3, Issue 8-9, Pages 909-918Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.dnarep.2004.03.021
Keywords
DNA-dependent protein kinase; DNA double-strand breaks; non-homologous end joining; phosphorylation; telomere maintenance; apoptosis; innate immunity
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Funding
- NCI NIH HHS [CA86936, CA50519, CA92584] Funding Source: Medline
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The DNA-dependent protein kinase (DNA-PK) plays a critical role in DNA double-strand break (DSB) repair and in V(D)J recombination. DNA-PK also plays a very important role in triggering apoptosis in response to severe DNA damage or critically shortened telomeres. Paradoxically, components of the DNA-PK complex are present at the mammalian telomere where they function in capping chromosome ends to prevent them from being mistaken for double-strand breaks. In addition, DNA-PK appears to be involved in mounting an innate immune response to bacterial DNA and to viral infection. As DNA-PK localizes very rapidly to DNA breaks and phosphorylates itself and other damage-responsive proteins, it appears that DNA-PK serves as both a sensor and a transducer of DNA-damage signals. The many roles of DNA-PK in the mammalian cell are discussed in this review with particular emphasis on recent advances in our understanding of the phosphorylation events that take place during the activation of DNA-PK at DNA breaks. (C) 2004 Elsevier B.V. All rights reserved.
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