pubmed-article:17964427 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17964427 | lifeskim:mentions | umls-concept:C0031727 | lld:lifeskim |
pubmed-article:17964427 | lifeskim:mentions | umls-concept:C0162610 | lld:lifeskim |
pubmed-article:17964427 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
pubmed-article:17964427 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:17964427 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
pubmed-article:17964427 | pubmed:issue | 11 | lld:pubmed |
pubmed-article:17964427 | pubmed:dateCreated | 2007-10-29 | lld:pubmed |
pubmed-article:17964427 | pubmed:abstractText | Here we use a large-scale RNAi suppression screen to identify additional kinases playing a role in the activation of SKN-1 in response to oxidative stress. The SKN-1 transcription factor specifies cell fate of the EMS blastomere at the four-cell stage in the nematode Caenorhabditis elegans and also directs transcription of many genes responding to oxidative stress, including glutathione S-transferase, NAD(P)H:quinone oxidoreductase, and superoxide dismutase. SKN-1 localizes to the nucleus and directs transcription following exposure to paraquat, heat, hyperbaric oxygen, and sodium azide. Previous studies have identified GSK-3 as an inhibitor of SKN-1 nuclear localization, in the absence of stress, and PMK-1 as an activator of SKN-1 during periods of oxidative stress. Through this screen we have identified four kinases, MKK-4, IKK epsilon-1, NEKL-2, and PDHK-2, which are necessary for the nuclear localization of SKN-1 in response to oxidative stress. Inhibition of two of these kinases results in shorter life span and increased sensitivity to stress. | lld:pubmed |
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pubmed-article:17964427 | pubmed:language | eng | lld:pubmed |
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pubmed-article:17964427 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17964427 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17964427 | pubmed:month | Dec | lld:pubmed |
pubmed-article:17964427 | pubmed:issn | 0891-5849 | lld:pubmed |
pubmed-article:17964427 | pubmed:author | pubmed-author:JohnsonThomas... | lld:pubmed |
pubmed-article:17964427 | pubmed:author | pubmed-author:VenturaNatasc... | lld:pubmed |
pubmed-article:17964427 | pubmed:author | pubmed-author:KellAlisonA | lld:pubmed |
pubmed-article:17964427 | pubmed:author | pubmed-author:KahnNateN | lld:pubmed |
pubmed-article:17964427 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17964427 | pubmed:day | 1 | lld:pubmed |
pubmed-article:17964427 | pubmed:volume | 43 | lld:pubmed |
pubmed-article:17964427 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17964427 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17964427 | pubmed:pagination | 1560-6 | lld:pubmed |
pubmed-article:17964427 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
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pubmed-article:17964427 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17964427 | pubmed:articleTitle | Activation of SKN-1 by novel kinases in Caenorhabditis elegans. | lld:pubmed |
pubmed-article:17964427 | pubmed:affiliation | Institute for Behavioral Genetics, University of Colorado at Boulder, Box 447, Boulder, CO 80309, USA. | lld:pubmed |
pubmed-article:17964427 | pubmed:publicationType | Journal Article | lld:pubmed |
entrez-gene:177343 | entrezgene:pubmed | pubmed-article:17964427 | lld:entrezgene |
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