| pubmed-article:20816092 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20816092 | lifeskim:mentions | umls-concept:C0038435 | lld:lifeskim |
| pubmed-article:20816092 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:20816092 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
| pubmed-article:20816092 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:20816092 | lifeskim:mentions | umls-concept:C0162610 | lld:lifeskim |
| pubmed-article:20816092 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:20816092 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:20816092 | pubmed:dateCreated | 2010-9-6 | lld:pubmed |
| pubmed-article:20816092 | pubmed:abstractText | The insulin-like signaling (ILS) pathway regulates metabolism and is known to modulate adult life span in C. elegans. Altered stress responses and resistance to a wide range of stressors are also associated with changes in ILS and contribute to enhanced longevity. The transcription factors DAF-16 and HSF-1 are key effectors of the longevity phenotype. We demonstrate that increased intrinsic thermotolerance, due to lower ILS, is not dependent on stress-induced transcriptional responses but instead requires active protein translation. Translation profiling experiments reveal genes that are posttranscriptionally regulated in response to altered ILS during heat shock in a DAF-16-dependent manner. Furthermore, several novel proteins are specifically required for ILS effects on thermotolerance. We propose that lowered ILS results in metabolic and physiological changes. These DAF-16-induced changes precondition a translational response under acute stress to modulate survival. | lld:pubmed |
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| pubmed-article:20816092 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20816092 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20816092 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20816092 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20816092 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:20816092 | pubmed:issn | 1932-7420 | lld:pubmed |
| pubmed-article:20816092 | pubmed:author | pubmed-author:MelovSimonS | lld:pubmed |
| pubmed-article:20816092 | pubmed:author | pubmed-author:LithgowGordon... | lld:pubmed |
| pubmed-article:20816092 | pubmed:author | pubmed-author:RogersAric... | lld:pubmed |
| pubmed-article:20816092 | pubmed:author | pubmed-author:LinkChristoph... | lld:pubmed |
| pubmed-article:20816092 | pubmed:author | pubmed-author:BushAshley... | lld:pubmed |
| pubmed-article:20816092 | pubmed:author | pubmed-author:HubbardAlan... | lld:pubmed |
| pubmed-article:20816092 | pubmed:author | pubmed-author:KapahiPankajP | lld:pubmed |
| pubmed-article:20816092 | pubmed:author | pubmed-author:AlavezSilvest... | lld:pubmed |
| pubmed-article:20816092 | pubmed:author | pubmed-author:McCollGawainG | lld:pubmed |
| pubmed-article:20816092 | pubmed:copyrightInfo | 2010 Elsevier Inc. All rights reserved. | lld:pubmed |
| pubmed-article:20816092 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20816092 | pubmed:day | 8 | lld:pubmed |
| pubmed-article:20816092 | pubmed:volume | 12 | lld:pubmed |
| pubmed-article:20816092 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20816092 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20816092 | pubmed:pagination | 260-72 | lld:pubmed |
| pubmed-article:20816092 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:20816092 | pubmed:meshHeading | pubmed-meshheading:20816092... | lld:pubmed |
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| pubmed-article:20816092 | pubmed:meshHeading | pubmed-meshheading:20816092... | lld:pubmed |
