| pubmed-article:17213819 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17213819 | lifeskim:mentions | umls-concept:C1442824 | lld:lifeskim |
| pubmed-article:17213819 | lifeskim:mentions | umls-concept:C0007620 | lld:lifeskim |
| pubmed-article:17213819 | lifeskim:mentions | umls-concept:C0012860 | lld:lifeskim |
| pubmed-article:17213819 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
| pubmed-article:17213819 | lifeskim:mentions | umls-concept:C1519063 | lld:lifeskim |
| pubmed-article:17213819 | pubmed:issue | 27 | lld:pubmed |
| pubmed-article:17213819 | pubmed:dateCreated | 2007-6-7 | lld:pubmed |
| pubmed-article:17213819 | 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. | lld:pubmed |
| pubmed-article:17213819 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17213819 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17213819 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17213819 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17213819 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17213819 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17213819 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17213819 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17213819 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17213819 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:17213819 | pubmed:issn | 0950-9232 | lld:pubmed |
| pubmed-article:17213819 | pubmed:author | pubmed-author:SharpP APA | lld:pubmed |
| pubmed-article:17213819 | pubmed:author | pubmed-author:ShioNN | lld:pubmed |
| pubmed-article:17213819 | pubmed:author | pubmed-author:Schild-Poulte... | lld:pubmed |
| pubmed-article:17213819 | pubmed:author | pubmed-author:TantinDD | lld:pubmed |
| pubmed-article:17213819 | pubmed:author | pubmed-author:SoubeyrandSS | lld:pubmed |
| pubmed-article:17213819 | pubmed:author | pubmed-author:YarymowichN... | lld:pubmed |
| pubmed-article:17213819 | pubmed:author | pubmed-author:HachéR J GRJ | lld:pubmed |
| pubmed-article:17213819 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17213819 | pubmed:day | 7 | lld:pubmed |
| pubmed-article:17213819 | pubmed:volume | 26 | lld:pubmed |
| pubmed-article:17213819 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17213819 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17213819 | pubmed:pagination | 3980-8 | lld:pubmed |
| pubmed-article:17213819 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:17213819 | pubmed:meshHeading | pubmed-meshheading:17213819... | lld:pubmed |
| pubmed-article:17213819 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17213819 | pubmed:articleTitle | DNA-PK phosphorylation sites on Oct-1 promote cell survival following DNA damage. | lld:pubmed |
| pubmed-article:17213819 | pubmed:affiliation | Department of Medicine, The Ottawa Health Research Institute, University of Ottawa, Ottawa, Ontario, Canada. cschild-poulter@robarts.ca | lld:pubmed |
| pubmed-article:17213819 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17213819 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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