pubmed-article:17714076 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17714076 | lifeskim:mentions | umls-concept:C0040648 | lld:lifeskim |
pubmed-article:17714076 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
pubmed-article:17714076 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:17714076 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:17714076 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:17714076 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:17714076 | lifeskim:mentions | umls-concept:C0162610 | lld:lifeskim |
pubmed-article:17714076 | lifeskim:mentions | umls-concept:C1515877 | lld:lifeskim |
pubmed-article:17714076 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:17714076 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:17714076 | pubmed:dateCreated | 2007-12-7 | lld:pubmed |
pubmed-article:17714076 | pubmed:abstractText | SKN-1 in the nematode worm Caenorhabditis elegans is functionally orthologous to mammalian NRF2 [NF-E2 (nuclear factor-E2)-related factor 2], a protein regulating response to oxidative stress. We have examined both the expression and activity of SKN-1 in response to a variety of oxidative stressors and to down-regulation of specific gene targets by RNAi (RNA interference). We used an SKN-1-GFP (green fluorescent protein) translational fusion to record changes in both skn-1 expression and SKN-1 nuclear localization, and a gst-4-GFP transcriptional fusion to measure SKN-1 transcriptional activity. GST-4 (glutathione transferase-4) is involved in the Phase II oxidative stress response and its expression is lost in an skn-1(zu67) mutant. In the present study, we show that the regulation of skn-1 is tied to the protein-degradation machinery of the cell. RNAi-targeted removal of most proteasome subunits in C. elegans caused nuclear localization of SKN-1 and, in some cases, induced transcription of gst-4. Most intriguingly, RNAi knockdown of proteasome core subunits caused nuclear localization of SKN-1 and induced gst-4, whereas RNAi knockdown of proteasome regulatory subunits resulted in nuclear localization of SKN-1 but did not induce gst-4. RNAi knockdown of ubiquitin-specific hydrolases and chaperonin components also caused nuclear localization of SKN-1 and, in some cases, also induced gst-4 transcription. skn-1 activation by proteasome dysfunction could be occurring by one or several mechanisms: (i) the reduced processivity of dysfunctional proteasomes may allow oxidatively damaged by-products to build up, which, in turn, activate the skn-1 stress response; (ii) dysfunctional proteasomes may activate the skn-1 stress response by blocking the constitutive turnover of SKN-1; and (iii) dysfunctional proteasomes may activate an unidentified signalling pathway that feeds back to control the skn-1 stress response. | lld:pubmed |
pubmed-article:17714076 | pubmed:language | eng | lld:pubmed |
pubmed-article:17714076 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17714076 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17714076 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17714076 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17714076 | pubmed:month | Jan | lld:pubmed |
pubmed-article:17714076 | pubmed:issn | 1470-8728 | lld:pubmed |
pubmed-article:17714076 | pubmed:author | pubmed-author:JohnsonThomas... | lld:pubmed |
pubmed-article:17714076 | pubmed:author | pubmed-author:ReaShane LSL | lld:pubmed |
pubmed-article:17714076 | pubmed:author | pubmed-author:KellAlisonA | lld:pubmed |
pubmed-article:17714076 | pubmed:author | pubmed-author:KahnNate WNW | lld:pubmed |
pubmed-article:17714076 | pubmed:author | pubmed-author:MoyleSarahS | lld:pubmed |
pubmed-article:17714076 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:17714076 | pubmed:day | 1 | lld:pubmed |
pubmed-article:17714076 | pubmed:volume | 409 | lld:pubmed |
pubmed-article:17714076 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17714076 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17714076 | pubmed:pagination | 205-13 | lld:pubmed |
pubmed-article:17714076 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:17714076 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:17714076 | pubmed:articleTitle | Proteasomal dysfunction activates the transcription factor SKN-1 and produces a selective oxidative-stress response in Caenorhabditis elegans. | lld:pubmed |
pubmed-article:17714076 | pubmed:affiliation | Institute for Behavioral Genetics, University of Colorado at Boulder, Box 447, Boulder, CO 80309, USA. | lld:pubmed |
pubmed-article:17714076 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17714076 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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