Yeast as a model to understand the interaction between genotype and the response to calorie restriction.
Identifieur interne : 001094 ( Main/Exploration ); précédent : 001093; suivant : 001095Yeast as a model to understand the interaction between genotype and the response to calorie restriction.
Auteurs : Jennifer Schleit [États-Unis] ; Brian M. Wasko ; Matt KaeberleinSource :
- FEBS letters [ 1873-3468 ] ; 2012.
Descripteurs français
- KwdFr :
- MESH :
- génétique : Levures.
- physiologie : Levures.
- Animaux, Génotype, Longévité, Modèles biologiques, Restriction calorique.
English descriptors
- KwdEn :
- MESH :
- genetics : Yeasts.
- physiology : Yeasts.
- Animals, Caloric Restriction, Genotype, Longevity, Models, Biological.
Abstract
Calorie restriction is reported to enhance survival and delay the onset of age-related decline in many different species. Several proteins have been proposed to play a role in mediating the response to calorie restriction, including the target of rapamycin kinase, sirtuins, and AMP kinase. An enhanced mechanistic understanding of calorie restriction has popularized the concept of "calorie restriction mimetics", drugs that mimic the beneficial effects of caloire restriction without requiring a reduction in nutrient intake. In theory, such drugs should delay the onset and progression of multiple age-related diseases, similar to calorie restriction in mammals. Despite the potential benefits of such calorie restriction mimetics, however, relatively little is known about the interaction between genetic variation and individual response to calorie restriction. Limited evidence from model systems indicates that genotype plays a large role in determining both the magnitude and direction of effect that calorie restriction has on longevity. Here we present an overview of these data from the perspective of using yeast as a model to study aging and describe an approach we are taking to further characterize the molecular mechanisms underlying genotype-dependent responses to calorie restriction.
DOI: 10.1016/j.febslet.2012.07.038
PubMed: 22828279
PubMed Central: PMC4016815
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Here we present an overview of these data from the perspective of using yeast as a model to study aging and describe an approach we are taking to further characterize the molecular mechanisms underlying genotype-dependent responses to calorie restriction.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22828279</PMID><DateCompleted><Year>2012</Year><Month>10</Month><Day>23</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-3468</ISSN><JournalIssue CitedMedium="Internet"><Volume>586</Volume><Issue>18</Issue><PubDate><Year>2012</Year><Month>Aug</Month><Day>31</Day></PubDate></JournalIssue><Title>FEBS letters</Title><ISOAbbreviation>FEBS Lett</ISOAbbreviation></Journal><ArticleTitle>Yeast as a model to understand the interaction between genotype and the response to calorie restriction.</ArticleTitle><Pagination><MedlinePgn>2868-73</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.febslet.2012.07.038</ELocationID><Abstract><AbstractText>Calorie restriction is reported to enhance survival and delay the onset of age-related decline in many different species. Several proteins have been proposed to play a role in mediating the response to calorie restriction, including the target of rapamycin kinase, sirtuins, and AMP kinase. An enhanced mechanistic understanding of calorie restriction has popularized the concept of "calorie restriction mimetics", drugs that mimic the beneficial effects of caloire restriction without requiring a reduction in nutrient intake. In theory, such drugs should delay the onset and progression of multiple age-related diseases, similar to calorie restriction in mammals. Despite the potential benefits of such calorie restriction mimetics, however, relatively little is known about the interaction between genetic variation and individual response to calorie restriction. Limited evidence from model systems indicates that genotype plays a large role in determining both the magnitude and direction of effect that calorie restriction has on longevity. Here we present an overview of these data from the perspective of using yeast as a model to study aging and describe an approach we are taking to further characterize the molecular mechanisms underlying genotype-dependent responses to calorie restriction.</AbstractText><CopyrightInformation>Copyright © 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. 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