Role of non-homologous end joining in the repair of DNA double-strand breaks

Sandeep Burma, Benjamin Chen, David J. Chen

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Of the various types of DNA damage that can occur within the mammalian cell nucleus, the DNA double-strand break (DSB) is perhaps the most dangerous. DSBs are induced by ionizing radiation, chemotherapeutic drugs, as well as by the byproducts of cellular metabolism. Understanding exactly how a mammalian cell responds to and repairs a DSB is very important because, on one hand, DSBs cause cancer while, on the other hand, DSBs are induced by chemotherapeutic agents to treat the disease. Of the two main mechanisms by which cells can repair DSBs, NHEJ (non-homologous end joining) and HR (homologous repair), NHEJ is the predominant repair pathway in mammalian cells. In this chapter we describe the main steps in the NHEJ pathway of repair highlighting major recent discoveries, and also provide a perspective on the link between defective NHEJ and human disease.

Original languageEnglish (US)
Title of host publicationDNA Repair, Genetic Instability, and Cancer
PublisherWorld Scientific Publishing Co.
Pages157-175
Number of pages19
ISBN (Print)9789812706782, 9789812700148
DOIs
StatePublished - Jan 1 2007

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

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    Burma, S., Chen, B., & Chen, D. J. (2007). Role of non-homologous end joining in the repair of DNA double-strand breaks. In DNA Repair, Genetic Instability, and Cancer (pp. 157-175). World Scientific Publishing Co.. https://doi.org/10.1142/9789812706782_0006