Abstract
Cell death linked to DNA damage has been implicated in various diseases caused by environmental stress and infection. Severe DNA damage, which is beyond the capacity of the DNA repair proteins, triggers apoptosis. Accumulation of DNA damage has been proposed to be a principal mechanism of infection, inflammation, cancer, and aging. The most deleterious form of DNA damage is double-strand breaks (DSBs), where ataxia-telangiectasia-mutated (ATM) is the main transducer of the double-strand DNA break signal. Once the DNA is damaged, the DNA repair protein Ku70/80 translocates into the nucleus, a process which may be mediated by ataxia-telangiectasia-mutated, a member of the phosphoinositide-3-kinase-like family. The function and stability of Artemis may also be regulated by ataxia-telangiectasia-mutated through its phosphorylation upon the occurrence of DNA damage. Interestingly, both Artemis and Ku70/80 are substrates of DNA-dependent protein kinase (DNA-PK), another member of the phosphoinositide-3-kinase-like family. In this review, we show how Ku and Artemis function in the DNA damage response and the ataxia-telangiectasia-mutated signaling pathway and discuss potential applications of agents targeting these DNA damage response molecules in the treatment of inflammation and cancer.
| Original language | English |
|---|---|
| Pages (from-to) | 598-603 |
| Number of pages | 6 |
| Journal | International Journal of Biochemistry and Cell Biology |
| Volume | 40 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - 2008 Jan 14 |
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All Science Journal Classification (ASJC) codes
- Biochemistry
- Cell Biology
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Ku, Artemis, and ataxia-telangiectasia-mutated : Signalling networks in DNA damage. / Morio, Tomohiro; Kim, Hyeyoung.
In: International Journal of Biochemistry and Cell Biology, Vol. 40, No. 4, 14.01.2008, p. 598-603.Research output: Contribution to journal › Short survey
TY - JOUR
T1 - Ku, Artemis, and ataxia-telangiectasia-mutated
T2 - Signalling networks in DNA damage
AU - Morio, Tomohiro
AU - Kim, Hyeyoung
PY - 2008/1/14
Y1 - 2008/1/14
N2 - Cell death linked to DNA damage has been implicated in various diseases caused by environmental stress and infection. Severe DNA damage, which is beyond the capacity of the DNA repair proteins, triggers apoptosis. Accumulation of DNA damage has been proposed to be a principal mechanism of infection, inflammation, cancer, and aging. The most deleterious form of DNA damage is double-strand breaks (DSBs), where ataxia-telangiectasia-mutated (ATM) is the main transducer of the double-strand DNA break signal. Once the DNA is damaged, the DNA repair protein Ku70/80 translocates into the nucleus, a process which may be mediated by ataxia-telangiectasia-mutated, a member of the phosphoinositide-3-kinase-like family. The function and stability of Artemis may also be regulated by ataxia-telangiectasia-mutated through its phosphorylation upon the occurrence of DNA damage. Interestingly, both Artemis and Ku70/80 are substrates of DNA-dependent protein kinase (DNA-PK), another member of the phosphoinositide-3-kinase-like family. In this review, we show how Ku and Artemis function in the DNA damage response and the ataxia-telangiectasia-mutated signaling pathway and discuss potential applications of agents targeting these DNA damage response molecules in the treatment of inflammation and cancer.
AB - Cell death linked to DNA damage has been implicated in various diseases caused by environmental stress and infection. Severe DNA damage, which is beyond the capacity of the DNA repair proteins, triggers apoptosis. Accumulation of DNA damage has been proposed to be a principal mechanism of infection, inflammation, cancer, and aging. The most deleterious form of DNA damage is double-strand breaks (DSBs), where ataxia-telangiectasia-mutated (ATM) is the main transducer of the double-strand DNA break signal. Once the DNA is damaged, the DNA repair protein Ku70/80 translocates into the nucleus, a process which may be mediated by ataxia-telangiectasia-mutated, a member of the phosphoinositide-3-kinase-like family. The function and stability of Artemis may also be regulated by ataxia-telangiectasia-mutated through its phosphorylation upon the occurrence of DNA damage. Interestingly, both Artemis and Ku70/80 are substrates of DNA-dependent protein kinase (DNA-PK), another member of the phosphoinositide-3-kinase-like family. In this review, we show how Ku and Artemis function in the DNA damage response and the ataxia-telangiectasia-mutated signaling pathway and discuss potential applications of agents targeting these DNA damage response molecules in the treatment of inflammation and cancer.
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UR - http://www.scopus.com/inward/citedby.url?scp=39649099566&partnerID=8YFLogxK
U2 - 10.1016/j.biocel.2007.12.007
DO - 10.1016/j.biocel.2007.12.007
M3 - Short survey
C2 - 18243767
AN - SCOPUS:39649099566
VL - 40
SP - 598
EP - 603
JO - International Journal of Biochemistry and Cell Biology
JF - International Journal of Biochemistry and Cell Biology
SN - 1357-2725
IS - 4
ER -