Ku, Artemis, and ataxia-telangiectasia-mutated: Signalling networks in DNA damage

Tomohiro Morio, Hyeyoung Kim

Research output: Contribution to journalShort survey

27 Citations (Scopus)

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 languageEnglish
Pages (from-to)598-603
Number of pages6
JournalInternational Journal of Biochemistry and Cell Biology
Volume40
Issue number4
DOIs
Publication statusPublished - 2008 Jan 14

Fingerprint

Ataxia Telangiectasia
DNA Damage
DNA
1-Phosphatidylinositol 4-Kinase
DNA Repair
DNA-Activated Protein Kinase
Inflammation
Phosphatidylinositols
Double-Stranded DNA Breaks
Repair
Infection
Phosphotransferases
Transducers
Neoplasms
Proteins
Cell Death
Phosphorylation
Apoptosis
Cell death
Aging of materials

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Cell Biology

Cite this

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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.",
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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 journalShort survey

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