| pubmed-article:18243662 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18243662 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
| pubmed-article:18243662 | lifeskim:mentions | umls-concept:C0031715 | lld:lifeskim |
| pubmed-article:18243662 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
| pubmed-article:18243662 | lifeskim:mentions | umls-concept:C0034538 | lld:lifeskim |
| pubmed-article:18243662 | lifeskim:mentions | umls-concept:C0040624 | lld:lifeskim |
| pubmed-article:18243662 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:18243662 | lifeskim:mentions | umls-concept:C0244988 | lld:lifeskim |
| pubmed-article:18243662 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:18243662 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:18243662 | pubmed:dateCreated | 2008-2-19 | lld:pubmed |
| pubmed-article:18243662 | pubmed:abstractText | DNA damage by ionizing radiation (IR) can induce activations of both NF-kappaB and p53 through the upstream kinase ataxia telangiectasia mutated (ATM). NF-kappaB activation could also be signaled through two distinct or overlapped pathways; IkappaB kinases (IKKs)-IkappaBalpha and Akt-glycogen synthase kinase-3 (GSK-3). In the present study, however, we show that activation of Akt1 and the subsequent phosphorylation and inactivation of GSK-3beta by IR could also occur in ATM-deficient AT5BIVA cells as well as in normal MRC5CV1 fibroblasts. Similarly, lithium chloride (LiCl) was found to increase the phosphorylation of GSK-3beta independently of ATM. Transfection with either wild-type or kinase dead mutant GSK-3beta to the cells further indicated that phosphorylations of Akt1 and GSK-3beta were closely associated with the transcriptional transactivation of NF-kappaB in response to ionizing radiation. On the other hand, LiCl, having no effect on caspase-3 activation, significantly increased p53 phosphorylation and apoptotic death of the normal MRC5CV1 cells while IR, activating both caspase-3 and p53, profoundly affected AT5BIVA cell death. Hence, our data suggest that although ATM-mediated IKK-IkappaBalpha pathway might be a typical pathway for IR-induced NF-kappaB activation, GSK-3beta phosphorylation could also partially contribute to the transcriptional transactivation of NF-kappaB in an ATM-independent manner and that GSK-3beta phosphorylation could induce ATM-mediated cell apoptosis through the activation of p53. | lld:pubmed |
| pubmed-article:18243662 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18243662 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18243662 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18243662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18243662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:18243662 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18243662 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:18243662 | pubmed:issn | 0898-6568 | lld:pubmed |
| pubmed-article:18243662 | pubmed:author | pubmed-author:JungMiraM | lld:pubmed |
| pubmed-article:18243662 | pubmed:author | pubmed-author:KimBo YeonBY | lld:pubmed |
| pubmed-article:18243662 | pubmed:author | pubmed-author:AhnJong... | lld:pubmed |
| pubmed-article:18243662 | pubmed:author | pubmed-author:KimMin SooMS | lld:pubmed |
| pubmed-article:18243662 | pubmed:author | pubmed-author:KimSun OkSO | lld:pubmed |
| pubmed-article:18243662 | pubmed:author | pubmed-author:HeLongL | lld:pubmed |
| pubmed-article:18243662 | pubmed:author | pubmed-author:KimKyung AKA | lld:pubmed |
| pubmed-article:18243662 | pubmed:author | pubmed-author:SokDai EunDE | lld:pubmed |
| pubmed-article:18243662 | pubmed:author | pubmed-author:KwonOsongO | lld:pubmed |
| pubmed-article:18243662 | pubmed:author | pubmed-author:ChaEun... | lld:pubmed |
| pubmed-article:18243662 | pubmed:author | pubmed-author:YoonByung... | lld:pubmed |
| pubmed-article:18243662 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18243662 | pubmed:volume | 20 | lld:pubmed |
| pubmed-article:18243662 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18243662 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18243662 | pubmed:pagination | 602-12 | lld:pubmed |
| pubmed-article:18243662 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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| pubmed-article:18243662 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18243662 | pubmed:articleTitle | Ionizing radiation can induce GSK-3beta phosphorylation and NF-kappaB transcriptional transactivation in ATM-deficient fibroblasts. | lld:pubmed |
| pubmed-article:18243662 | pubmed:affiliation | Korea Research Institute of Bioscience and Biotechnology, Yuseong, Daejeon, 305-806, Republic of Korea. | lld:pubmed |
| pubmed-article:18243662 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18243662 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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