| pubmed-article:12223490 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12223490 | lifeskim:mentions | umls-concept:C0023418 | lld:lifeskim |
| pubmed-article:12223490 | lifeskim:mentions | umls-concept:C0887899 | lld:lifeskim |
| pubmed-article:12223490 | lifeskim:mentions | umls-concept:C0031715 | lld:lifeskim |
| pubmed-article:12223490 | lifeskim:mentions | umls-concept:C1155312 | lld:lifeskim |
| pubmed-article:12223490 | lifeskim:mentions | umls-concept:C1367731 | lld:lifeskim |
| pubmed-article:12223490 | lifeskim:mentions | umls-concept:C1150587 | lld:lifeskim |
| pubmed-article:12223490 | lifeskim:mentions | umls-concept:C1705632 | lld:lifeskim |
| pubmed-article:12223490 | pubmed:issue | 46 | lld:pubmed |
| pubmed-article:12223490 | pubmed:dateCreated | 2002-11-11 | lld:pubmed |
| pubmed-article:12223490 | pubmed:abstractText | Oxidative stress induces JNK activation, which leads to apoptosis through mitochondria-dependent caspase activation. However, little is known about the mechanism by which JNK alters mitochondrial function. In this study, we investigated the role of phosphorylation of myeloid cell leukemia 1 (Mcl-1), an anti-apoptotic member of the Bcl-2 family, in oxidative stress-induced apoptosis. We found that JNK phosphorylated Ser-121 and Thr-163 of Mcl-1 in response to stimulation with H(2)O(2) and that transfection of unphosphorylatable Mcl-1 resulted in an enhanced anti-apoptotic activity in response to stimulation with H(2)O(2). JNK-dependent phosphorylation and thus inactivation of Mcl-1 may be one of the mechanisms through which oxidative stress induces cellular damage. | lld:pubmed |
| pubmed-article:12223490 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12223490 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12223490 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12223490 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12223490 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:12223490 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:12223490 | pubmed:author | pubmed-author:UmezawaAkihir... | lld:pubmed |
| pubmed-article:12223490 | pubmed:author | pubmed-author:TeradaYoshioY | lld:pubmed |
| pubmed-article:12223490 | pubmed:author | pubmed-author:IchijoHidenor... | lld:pubmed |
| pubmed-article:12223490 | pubmed:author | pubmed-author:TakedaKohsuke... | lld:pubmed |
| pubmed-article:12223490 | pubmed:author | pubmed-author:HataJunichiJ | lld:pubmed |
| pubmed-article:12223490 | pubmed:author | pubmed-author:InoshitaSeiji... | lld:pubmed |
| pubmed-article:12223490 | pubmed:author | pubmed-author:HataiTakikoT | lld:pubmed |
| pubmed-article:12223490 | pubmed:author | pubmed-author:SanoMakotoM | lld:pubmed |
| pubmed-article:12223490 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12223490 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:12223490 | pubmed:volume | 277 | lld:pubmed |
| pubmed-article:12223490 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12223490 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12223490 | pubmed:pagination | 43730-4 | lld:pubmed |
| pubmed-article:12223490 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:12223490 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12223490 | pubmed:articleTitle | Phosphorylation and inactivation of myeloid cell leukemia 1 by JNK in response to oxidative stress. | lld:pubmed |
| pubmed-article:12223490 | pubmed:affiliation | Laboratory of Cell Signaling, Department of Hard Tissue Engineering, Division of Bio-Matrix, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Japan. | lld:pubmed |
| pubmed-article:12223490 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12223490 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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