DC Field | Value | Language |
---|---|---|
dc.contributor.author | Zhang, Peichuan | ko |
dc.contributor.author | Judy, Meredith | ko |
dc.contributor.author | Lee, Seung-Jae | ko |
dc.contributor.author | Kenyon, Cynthia | ko |
dc.date.accessioned | 2019-03-19T01:28:56Z | - |
dc.date.available | 2019-03-19T01:28:56Z | - |
dc.date.created | 2019-03-06 | - |
dc.date.issued | 2013-01 | - |
dc.identifier.citation | CELL METABOLISM, v.17, no.1, pp.85 - 100 | - |
dc.identifier.issn | 1550-4131 | - |
dc.identifier.uri | http://hdl.handle.net/10203/251706 | - |
dc.description.abstract | In long-lived C. elegans insulin/IGF-1 pathway mutants, the life-extending FOXO transcription factor DAF-16 is present throughout the animal, but we find that its activity in a single tissue can delay the aging of other tissues and extend the animal's life span. To better understand the topography of DAF-16 action among the tissues, we analyzed a collection of DAF-16-regulated genes. DAF-16 regulated most of these genes in a cell-autonomous fashion, often using tissue-specific GATA factors to direct their expression to specific tissues. DAF-16 could also act cell nonautonomously to influence gene expression. DAF-16 affected gene expression in other cells, at least in part, via the lipid-gene regulator MDT-15. DAF-16, and probably MDT-15, could act cell nonautonomously in the endoderm to ameliorate the paralysis caused by expressing Alzheimer's A beta protein in muscles. These findings suggest that MDT-15-dependent intercellular signals, possibly lipid signals, can help to coordinate tissue physiology, enhance proteostasis, and extend life in response to DAF-16/FOXO activity. | - |
dc.language | English | - |
dc.publisher | CELL PRESS | - |
dc.title | Direct and Indirect Gene Regulation by a Life-Extending FOXO Protein in C. elegans: Roles for GATA Factors and Lipid Gene Regulators | - |
dc.type | Article | - |
dc.identifier.wosid | 000313998800011 | - |
dc.identifier.scopusid | 2-s2.0-84872143888 | - |
dc.type.rims | ART | - |
dc.citation.volume | 17 | - |
dc.citation.issue | 1 | - |
dc.citation.beginningpage | 85 | - |
dc.citation.endingpage | 100 | - |
dc.citation.publicationname | CELL METABOLISM | - |
dc.identifier.doi | 10.1016/j.cmet.2012.12.013 | - |
dc.contributor.localauthor | Lee, Seung-Jae | - |
dc.contributor.nonIdAuthor | Zhang, Peichuan | - |
dc.contributor.nonIdAuthor | Judy, Meredith | - |
dc.contributor.nonIdAuthor | Kenyon, Cynthia | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordPlus | BETA-AMYLOID PEPTIDE | - |
dc.subject.keywordPlus | CAENORHABDITIS-ELEGANS | - |
dc.subject.keywordPlus | TRANSCRIPTION FACTOR | - |
dc.subject.keywordPlus | SIGNALING PATHWAY | - |
dc.subject.keywordPlus | INSULIN-RECEPTOR | - |
dc.subject.keywordPlus | SPAN EXTENSION | - |
dc.subject.keywordPlus | FAT-BODY | - |
dc.subject.keywordPlus | DAF-16 | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | LONGEVITY | - |
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