Abstract
DNA double-strand breaks (DSBs) are introduced in cells by ionizing radiation and reactive oxygen species. In addition, they are commonly generated during V(D)J recombination, an essential aspect of the developing immune system. Failure to effectively repair these DSBs can result in chromosome breakage, cell death, onset of cancer, and defects in the immune system of higher vertebrates. Fortunately, all mammalian cells possess two enzymatic pathways that mediate the repair of DSBs: homologous recombination and non-homologous end-joining (NHEJ). The NHEJ process utilizes enzymes that capture both ends of the broken DNA molecule, bring them together in a synaptic DNA-protein complex, and finally repair the DNA break. In this review, all the known enzymes that play a role in the NHEJ process are discussed and a working model for the co-operation of these enzymes during DSB repair is presented.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 114-124 |
| Number of pages | 11 |
| Journal | Cell Research |
| Volume | 18 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jan 2008 |
| Externally published | Yes |
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Keywords
- Artemis
- ATM
- Cernunnos
- DNA double-strand break
- DNA-PK
- DSB
- Ku70/80
- Ligase IV
- NHEJ
- Non-homologous end-joining
- V(D)J recombination
- XLF
- XRCC4
ASJC Scopus subject areas
- Cell Biology
Cite this
The endless tale of non-homologous end-joining. / Weterings, Eric -; Chen, David J.
In: Cell Research, Vol. 18, No. 1, 01.2008, p. 114-124.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The endless tale of non-homologous end-joining
AU - Weterings, Eric -
AU - Chen, David J.
PY - 2008/1
Y1 - 2008/1
N2 - DNA double-strand breaks (DSBs) are introduced in cells by ionizing radiation and reactive oxygen species. In addition, they are commonly generated during V(D)J recombination, an essential aspect of the developing immune system. Failure to effectively repair these DSBs can result in chromosome breakage, cell death, onset of cancer, and defects in the immune system of higher vertebrates. Fortunately, all mammalian cells possess two enzymatic pathways that mediate the repair of DSBs: homologous recombination and non-homologous end-joining (NHEJ). The NHEJ process utilizes enzymes that capture both ends of the broken DNA molecule, bring them together in a synaptic DNA-protein complex, and finally repair the DNA break. In this review, all the known enzymes that play a role in the NHEJ process are discussed and a working model for the co-operation of these enzymes during DSB repair is presented.
AB - DNA double-strand breaks (DSBs) are introduced in cells by ionizing radiation and reactive oxygen species. In addition, they are commonly generated during V(D)J recombination, an essential aspect of the developing immune system. Failure to effectively repair these DSBs can result in chromosome breakage, cell death, onset of cancer, and defects in the immune system of higher vertebrates. Fortunately, all mammalian cells possess two enzymatic pathways that mediate the repair of DSBs: homologous recombination and non-homologous end-joining (NHEJ). The NHEJ process utilizes enzymes that capture both ends of the broken DNA molecule, bring them together in a synaptic DNA-protein complex, and finally repair the DNA break. In this review, all the known enzymes that play a role in the NHEJ process are discussed and a working model for the co-operation of these enzymes during DSB repair is presented.
KW - Artemis
KW - ATM
KW - Cernunnos
KW - DNA double-strand break
KW - DNA-PK
KW - DSB
KW - Ku70/80
KW - Ligase IV
KW - NHEJ
KW - Non-homologous end-joining
KW - V(D)J recombination
KW - XLF
KW - XRCC4
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UR - http://www.scopus.com/inward/citedby.url?scp=38049125555&partnerID=8YFLogxK
U2 - 10.1038/cr.2008.3
DO - 10.1038/cr.2008.3
M3 - Article
VL - 18
SP - 114
EP - 124
JO - Cell Research
JF - Cell Research
SN - 1001-0602
IS - 1
ER -