Nitric oxide upregulates expression of DNA-PKcs to protect cells from DNA-damaging anti-tumour agents.
- Publication Type:
- Journal Article
- Citation:
- Nat Cell Biol, 2000, 2 (6), pp. 339 - 345
- Issue Date:
- 2000-06
Closed Access
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2009002941OK.pdf | 338.41 kB | Adobe PDF |
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Xu, W | en_US |
dc.contributor.author | Liu, L | en_US |
dc.contributor.author | Smith, GC | en_US |
dc.contributor.author | Charles, LG | en_US |
dc.date.issued | 2000-06 | en_US |
dc.identifier.citation | Nat Cell Biol, 2000, 2 (6), pp. 339 - 345 | en_US |
dc.identifier.issn | 1465-7392 | en_US |
dc.identifier.uri | http://hdl.handle.net/10453/13348 | |
dc.description.abstract | Nitric-oxide synthase (NOS) activity has been detected in many human tumours, although its function is unclear. Here we show that exposure of cells to nitric oxide (NO) results in a 4-5-fold increase in expression of the DNA-dependent protein-kinase catalytic subunit (DNA-PKcs), one of the key enzymes involved in repairing double-stranded DNA breaks. This NO-mediated increase in enzymatically active DNA-PK not only protects cells from the toxic effects of NO, but also provides crossprotection against clinically important DNA-damaging agents, such as X-ray radiation, adriamycin, bleomycin and cisplatin. The NO-mediated increase in DNA-PKcs described here demonstrates the presence of a new and highly effective NO-mediated mechanism for DNA repair. | en_US |
dc.language | eng | en_US |
dc.relation.ispartof | Nat Cell Biol | en_US |
dc.relation.isbasedon | 10.1038/35014028 | en_US |
dc.subject.classification | Developmental Biology | en_US |
dc.subject.mesh | Cell Line | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | DNA Damage | en_US |
dc.subject.mesh | Cisplatin | en_US |
dc.subject.mesh | Nitric Oxide | en_US |
dc.subject.mesh | Doxorubicin | en_US |
dc.subject.mesh | Ecdysterone | en_US |
dc.subject.mesh | Protein-Serine-Threonine Kinases | en_US |
dc.subject.mesh | Bleomycin | en_US |
dc.subject.mesh | DNA-Binding Proteins | en_US |
dc.subject.mesh | Nuclear Proteins | en_US |
dc.subject.mesh | DNA | en_US |
dc.subject.mesh | RNA, Messenger | en_US |
dc.subject.mesh | Nitric Oxide Donors | en_US |
dc.subject.mesh | Antineoplastic Agents | en_US |
dc.subject.mesh | Cell Survival | en_US |
dc.subject.mesh | DNA Repair | en_US |
dc.subject.mesh | Enzyme Induction | en_US |
dc.subject.mesh | Up-Regulation | en_US |
dc.subject.mesh | Catalytic Domain | en_US |
dc.subject.mesh | Sp1 Transcription Factor | en_US |
dc.subject.mesh | Nitric Oxide Synthase | en_US |
dc.subject.mesh | DNA-Activated Protein Kinase | en_US |
dc.subject.mesh | Nitric Oxide Synthase Type II | en_US |
dc.subject.mesh | Promoter Regions, Genetic | en_US |
dc.title | Nitric oxide upregulates expression of DNA-PKcs to protect cells from DNA-damaging anti-tumour agents. | en_US |
dc.type | Journal Article | |
utslib.citation.volume | 6 | en_US |
utslib.citation.volume | 2 | en_US |
utslib.location.activity | England | en_US |
utslib.for | 0601 Biochemistry and Cell Biology | en_US |
utslib.for | 06 Biological Sciences | en_US |
utslib.for | 11 Medical and Health Sciences | en_US |
dc.location.activity | ISI:000087454000015 | en_US |
pubs.embargo.period | Not known | en_US |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Strength - ithree - Institute of Infection, Immunity and Innovation | |
utslib.copyright.status | closed_access | |
pubs.issue | 6 | en_US |
pubs.publication-status | Published | en_US |
pubs.volume | 2 | en_US |
Abstract:
Nitric-oxide synthase (NOS) activity has been detected in many human tumours, although its function is unclear. Here we show that exposure of cells to nitric oxide (NO) results in a 4-5-fold increase in expression of the DNA-dependent protein-kinase catalytic subunit (DNA-PKcs), one of the key enzymes involved in repairing double-stranded DNA breaks. This NO-mediated increase in enzymatically active DNA-PK not only protects cells from the toxic effects of NO, but also provides crossprotection against clinically important DNA-damaging agents, such as X-ray radiation, adriamycin, bleomycin and cisplatin. The NO-mediated increase in DNA-PKcs described here demonstrates the presence of a new and highly effective NO-mediated mechanism for DNA repair.
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