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DNA Repair (Amst). 2014 May;17:21-9. doi: 10.1016/j.dnarep.2014.02.020. Epub 2014 Mar 27.

DNA-PK: a dynamic enzyme in a versatile DSB repair pathway.

Author information

1
Division of Molecular Radiation Biology, Department of Radiation Oncology, University of Texas Southwestern Medical Center, 2201 Inwood Road, Dallas, TX 75390, United States.
2
Division of Molecular Radiation Biology, Department of Radiation Oncology, University of Texas Southwestern Medical Center, 2201 Inwood Road, Dallas, TX 75390, United States. Electronic address: david.chen@utsouthwestern.edu.

Abstract

DNA double stranded breaks (DSBs) are the most cytoxic DNA lesion as the inability to properly repair them can lead to genomic instability and tumorigenesis. The prominent DSB repair pathway in humans is non-homologous end-joining (NHEJ). In the simplest sense, NHEJ mediates the direct re-ligation of the broken DNA molecule. However, NHEJ is a complex and versatile process that can repair DSBs with a variety of damages and ends via the utilization of a significant number of proteins. In this review we will describe the important factors and mechanisms modulating NHEJ with emphasis given to the versatility of this repair process and the DNA-PK complex.

KEYWORDS:

DNA double strand breaks; DNA ligase IV; DNA-PKcs; Ku70/80; Non-homologous end-joining; XLF; XRCC4

PMID:
24680878
PMCID:
PMC4032623
DOI:
10.1016/j.dnarep.2014.02.020
[Indexed for MEDLINE]
Free PMC Article
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