Source:http://linkedlifedata.com/resource/pubmed/id/17213819
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
27
|
| pubmed:dateCreated |
2007-6-7
|
| pubmed:abstractText |
Octamer transcription factor-1 (Oct-1) has recently been shown to function as a stress sensor that promotes cell survival subsequent to DNA damage. Here, we show that the survival signal imparted by Oct-1 following exposure to ionizing radiation (IR) is dependent upon DNA-dependent protein kinase (DNA-PK)-dependent phosphorylation of a cluster of 13 specific ser/thr residues within the N-terminal transcriptional regulatory domain of Oct-1. Although IR treatment did not affect the recruitment of Oct-1 to the histone H2B promoter, the recruitment of RNA polymerase II, TATA-binding protein and histone H4 acetylation were strongly reduced, consistent with a decrease in Oct-1 transcriptional regulatory potential following IR exposure. Ser/Thr-Ala substitution of 13 sites present in Oct-1 transcriptional regulatory domain eliminated Oct-1 phosphorylation subsequent to IR exposure. Further, these substitutions prevented Oct-1 from rescuing the survival of IR-treated Oct-1-/- murine embryonic fibroblasts, providing a direct link between DNA-PK-dependent phosphorylation and the contribution of Oct-1 to cell survival. These results implicate Oct-1 as a primary effector in a DNA-PK-dependent cell survival pathway that is activated by double-stranded DNA breaks.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Activated Protein Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/Histones,
http://linkedlifedata.com/resource/pubmed/chemical/Octamer Transcription Factor-1,
http://linkedlifedata.com/resource/pubmed/chemical/Serine,
http://linkedlifedata.com/resource/pubmed/chemical/Threonine
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jun
|
| pubmed:issn |
0950-9232
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
7
|
| pubmed:volume |
26
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
3980-8
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| pubmed:dateRevised |
2009-11-19
|
| pubmed:meshHeading |
pubmed-meshheading:17213819-3T3 Cells,
pubmed-meshheading:17213819-Amino Acid Sequence,
pubmed-meshheading:17213819-Amino Acid Substitution,
pubmed-meshheading:17213819-Animals,
pubmed-meshheading:17213819-Binding Sites,
pubmed-meshheading:17213819-Blotting, Western,
pubmed-meshheading:17213819-Cell Line,
pubmed-meshheading:17213819-Cell Line, Tumor,
pubmed-meshheading:17213819-Cell Survival,
pubmed-meshheading:17213819-DNA Damage,
pubmed-meshheading:17213819-DNA-Activated Protein Kinase,
pubmed-meshheading:17213819-Dose-Response Relationship, Radiation,
pubmed-meshheading:17213819-Histones,
pubmed-meshheading:17213819-Humans,
pubmed-meshheading:17213819-Mice,
pubmed-meshheading:17213819-Mice, Knockout,
pubmed-meshheading:17213819-Molecular Sequence Data,
pubmed-meshheading:17213819-Octamer Transcription Factor-1,
pubmed-meshheading:17213819-Phosphorylation,
pubmed-meshheading:17213819-Promoter Regions, Genetic,
pubmed-meshheading:17213819-Protein Binding,
pubmed-meshheading:17213819-Serine,
pubmed-meshheading:17213819-Threonine,
pubmed-meshheading:17213819-Transfection
|
| pubmed:year |
2007
|
| pubmed:articleTitle |
DNA-PK phosphorylation sites on Oct-1 promote cell survival following DNA damage.
|
| pubmed:affiliation |
Department of Medicine, The Ottawa Health Research Institute, University of Ottawa, Ottawa, Ontario, Canada. cschild-poulter@robarts.ca
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|