Format

Send to

Choose Destination
J Biol Chem. 2018 Jul 6;293(27):10536-10546. doi: 10.1074/jbc.TM117.000375. Epub 2018 Mar 12.

Repair of DNA double-strand breaks by mammalian alternative end-joining pathways.

Author information

1
From the Departments of Internal Medicine and Molecular Genetics and Microbiology, University of New Mexico Comprehensive Cancer Center, University of New Mexico, Albuquerque, New Mexico 87131.
2
From the Departments of Internal Medicine and Molecular Genetics and Microbiology, University of New Mexico Comprehensive Cancer Center, University of New Mexico, Albuquerque, New Mexico 87131 atomkinson@salud.unm.edu.

Abstract

Alternative end-joining (a-EJ) pathways, which repair DNA double-strand breaks (DSBs), are initiated by end resection that generates 3' single strands. This reaction is shared, at least in part, with homologous recombination but distinguishes a-EJ from the major nonhomologous end-joining pathway. Although the a-EJ pathways make only a minor and poorly understood contribution to DSB repair in nonmalignant cells, there is growing interest in these pathways, as they generate genomic rearrangements that are hallmarks of cancer cells. Here, we review and discuss the current understanding of the mechanisms and regulation of a-EJ pathways, the role of a-EJ in human disease, and the potential utility of a-EJ as a therapeutic target in cancer.

KEYWORDS:

DNA damage; DNA endonuclease; DNA ligation; DNA polymerase; alternative end-joining pathway; chromosomes; deletions; double-strand break; genomic instability; microhomology; single-strand annealing; translocation

PMID:
29530982
PMCID:
PMC6036210
[Available on 2019-07-06]
DOI:
10.1074/jbc.TM117.000375

Supplemental Content

Full text links

Icon for HighWire
Loading ...
Support Center