| pubmed-article:19627265 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19627265 | lifeskim:mentions | umls-concept:C0023980 | lld:lifeskim |
| pubmed-article:19627265 | lifeskim:mentions | umls-concept:C0242606 | lld:lifeskim |
| pubmed-article:19627265 | lifeskim:mentions | umls-concept:C0162610 | lld:lifeskim |
| pubmed-article:19627265 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
| pubmed-article:19627265 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:19627265 | pubmed:dateCreated | 2009-7-24 | lld:pubmed |
| pubmed-article:19627265 | pubmed:abstractText | Oxidative stress has been hypothesized to play a role in normal aging. The response to oxidative stress is regulated by the SKN-1 transcription factor, which also is necessary for intestinal development in Caenorhabditis elegans. Almost a thousand genes including the antioxidant and heat-shock responses, as well as genes responsible for xenobiotic detoxification were induced by the oxidative stress which was found using transcriptome analysis. There were also 392 down-regulated genes including many involved in metabolic homeostasis, organismal development, and reproduction. Many of these oxidative stress-induced transcriptional changes are dependent on SKN-1 action; the induction of the heat-shock response is not. When RNAi to inhibit genes was used, most had no effect on either resistance to oxidative stress or longevity; however two SKN-1-dependent genes, nlp-7 and cup-4, that were up-regulated by oxidative stress were found to be required for resistance to oxidative stress and for normal lifespan. nlp-7 encodes a neuropeptide-like protein, expressed in neurons, while cup-4 encodes a coelomocyte-specific, ligand-gated ion channel. RNAi of nlp-7 or cup-4 increased sensitivity to oxidative stress and reduced lifespan. Among down-regulated genes, only inhibition of ent-1, a nucleoside transporter, led to increased resistance to oxidative stress; inhibition had no effect on lifespan. In contrast, RNAi of nhx-2, a Na(+)/H(+) exchanger, extended lifespan significantly without affecting sensitivity to oxidative stress. These findings showed that a transcriptional shift from growth and maintenance towards the activation of cellular defense mechanisms was caused by the oxidative stress; many of these transcriptional alterations are SKN-1 dependent. | lld:pubmed |
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| pubmed-article:19627265 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19627265 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19627265 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19627265 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19627265 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19627265 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:19627265 | pubmed:issn | 1474-9726 | lld:pubmed |
| pubmed-article:19627265 | pubmed:author | pubmed-author:JohnsonThomas... | lld:pubmed |
| pubmed-article:19627265 | pubmed:author | pubmed-author:ParkSang-KyuS... | lld:pubmed |
| pubmed-article:19627265 | pubmed:author | pubmed-author:TedescoPatric... | lld:pubmed |
| pubmed-article:19627265 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19627265 | pubmed:volume | 8 | lld:pubmed |
| pubmed-article:19627265 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19627265 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19627265 | pubmed:pagination | 258-69 | lld:pubmed |
| pubmed-article:19627265 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
| pubmed-article:19627265 | pubmed:meshHeading | pubmed-meshheading:19627265... | lld:pubmed |
| pubmed-article:19627265 | pubmed:meshHeading | pubmed-meshheading:19627265... | lld:pubmed |
| pubmed-article:19627265 | pubmed:meshHeading | pubmed-meshheading:19627265... | lld:pubmed |
| pubmed-article:19627265 | pubmed:meshHeading | pubmed-meshheading:19627265... | lld:pubmed |
| pubmed-article:19627265 | pubmed:meshHeading | pubmed-meshheading:19627265... | lld:pubmed |
| pubmed-article:19627265 | pubmed:meshHeading | pubmed-meshheading:19627265... | lld:pubmed |
| pubmed-article:19627265 | pubmed:meshHeading | pubmed-meshheading:19627265... | lld:pubmed |
| pubmed-article:19627265 | pubmed:meshHeading | pubmed-meshheading:19627265... | lld:pubmed |
| pubmed-article:19627265 | pubmed:meshHeading | pubmed-meshheading:19627265... | lld:pubmed |
| pubmed-article:19627265 | pubmed:meshHeading | pubmed-meshheading:19627265... | lld:pubmed |
| pubmed-article:19627265 | pubmed:meshHeading | pubmed-meshheading:19627265... | lld:pubmed |
| pubmed-article:19627265 | pubmed:meshHeading | pubmed-meshheading:19627265... | lld:pubmed |
| pubmed-article:19627265 | pubmed:meshHeading | pubmed-meshheading:19627265... | lld:pubmed |
| pubmed-article:19627265 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19627265 | pubmed:articleTitle | Oxidative stress and longevity in Caenorhabditis elegans as mediated by SKN-1. | lld:pubmed |
| pubmed-article:19627265 | pubmed:affiliation | Institute for Behavioral Genetics, University of Colorado, Box 447, Boulder, CO 80309, USA. sangkyu@colorado.edu | lld:pubmed |
| pubmed-article:19627265 | pubmed:publicationType | Journal Article | lld:pubmed |
