Double-Strand Breaks Repair by Non-Homologous DNA End Joining in Mammalian Cells

Author(s): Mariusz Malinowski, Elzbieta Pastwa

Journal Name: Current Genomics

Volume 7 , Issue 5 , 2006

Become EABM
Become Reviewer
Call for Editor


DNA double-strand breaks (DSBs) are a common form of DNA damage and double-strand break rejoining is a fundamental mechanism of genome protection to prevent chromosomal fragmentation, translocation and deletions. DSBs may be induced by exogenous agents, such as ionizing radiation, but also occur spontaneously during cellular processes e.g. in the rearrangement of gene segments during V(D)J [variable (V), diversity (D), joining (J)] recombination. The ge-nomic instability resulting from incorrectly repaired DSBs can lead to carcinogenesis, while unrepaired may carry on even to cell death. To repair this potentially lethal damage cells developed several different types of repair act on the DSBs e.g. homologous recombination repair (HRR), non-homologous DNA end joining (NHEJ), and single-strand annealing (SSA).The most essential in mammalian cells is NHEJ, whereas HRR and SSA significantly contributes to DSBs repair in lower eukaryotes. At least six distinct proteins are known to be required for NHEJ, i ncluding Ku70, Ku80, DNA-PKcs, XRCC4, DNA ligase IV, and Artemis. In this review we highlight classical and up-to-date aspects and present understanding of the molecular mechanisms of NHEJ in the maintenance of genome integrity.

Keywords: Non-homologous DNA end joining, NHEJ, DNA double-strand breaks repair, DNA-PK, DNA-PKcs, Ku70, Ku80, XRCC4, ligase IV, Artemis

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2006
Published on: 01 March, 2012
Page: [311 - 322]
Pages: 12
DOI: 10.2174/138920206778604386
Price: $65

Article Metrics

PDF: 1