RapamycinFungusV1, Main, Exploration, bibRecord, 000A06

Stress resistance and lifespan are increased in C. elegans but decreased in S. cerevisiae by mafr-1/maf1 deletion.

Identifieur interne : 000A06 ( Main/Exploration ); précédent : 000A05; suivant : 000A07

Stress resistance and lifespan are increased in C. elegans but decreased in S. cerevisiae by mafr-1/maf1 deletion.

Auteurs : Ying Cai [République populaire de Chine] ; Yue-Hua Wei [République populaire de Chine]

Source :

Oncotarget [ 1949-2553 ] ; 2016.

RBID : pubmed:26934328

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Autophagy (MeSH), Caenorhabditis elegans (physiology), Caenorhabditis elegans Proteins (genetics), Caenorhabditis elegans Proteins (metabolism), Caloric Restriction (MeSH), Humans (MeSH), Longevity (genetics), Repressor Proteins (deficiency), Repressor Proteins (genetics), Repressor Proteins (metabolism), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (physiology), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Transcription Factors (deficiency), Transcription Factors (genetics), Transcription Factors (metabolism).
MESH :
- chemical , deficiency : Repressor Proteins, Transcription Factors.
- chemical , genetics : Caenorhabditis elegans Proteins, Repressor Proteins, Saccharomyces cerevisiae Proteins, Transcription Factors.
- chemical , metabolism : Caenorhabditis elegans Proteins, Repressor Proteins, Saccharomyces cerevisiae Proteins, Transcription Factors.
- genetics : Longevity, Saccharomyces cerevisiae.
- physiology : Caenorhabditis elegans, Saccharomyces cerevisiae.
- Animals, Autophagy, Caloric Restriction, Humans.

Abstract

Maf1 is a conserved effector of the mechanistic target of rapamycin (mTOR), an aging promoting kinase. However, whether Maf1 is required for lifespan extension caused by mTOR inhibition, such as dietary restriction (DR) or calorie restriction (CR) remains elusive. Here we show that deletion of maf1 in the budding yeast S. cerevisiae but not mafr-1 in C. elegans prevents DR or CR to extend lifespan. Interestingly, mafr-1 deletion increases stress tolerance and extends lifespan. MAFR-1 is phosphorylated in a mTOR-dependent manner and mafr-1 deletion alleviates the inhibition of tRNA synthesis caused by reduced mTOR activity. We find that the opposite effect of mafr-1 deletion on lifespan is due to an enhancement of stress response, including oxidative stress response, mitochondrial unfolded protein response (UPRmt) and autophagy. mafr-1 deletion also attenuates the paralysis of a C. elegans model of Alzheimer's disease. Our study reveals distinct mechanisms of lifespan regulation by Maf1 and MAFR-1.

DOI: 10.18632/oncotarget.7769
PubMed: 26934328
PubMed Central: PMC4905441

Affiliations:

République populaire de Chine

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000A91
to stream Main, to step Curation: 000A91

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Stress resistance and lifespan are increased in C. elegans but decreased in S. cerevisiae by mafr-1/maf1 deletion.</title>
<author><name sortKey="Cai, Ying" sort="Cai, Ying" uniqKey="Cai Y" first="Ying" last="Cai">Ying Cai</name>
<affiliation wicri:level="1"><nlm:affiliation>Shanghai Ninth People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shanghai Ninth People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai</wicri:regionArea>
<wicri:noRegion>Shanghai</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Wei, Yue Hua" sort="Wei, Yue Hua" uniqKey="Wei Y" first="Yue-Hua" last="Wei">Yue-Hua Wei</name>
<affiliation wicri:level="1"><nlm:affiliation>Shanghai Ninth People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shanghai Ninth People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai</wicri:regionArea>
<wicri:noRegion>Shanghai</wicri:noRegion>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2016">2016</date>
<idno type="RBID">pubmed:26934328</idno>
<idno type="pmid">26934328</idno>
<idno type="doi">10.18632/oncotarget.7769</idno>
<idno type="pmc">PMC4905441</idno>
<idno type="wicri:Area/Main/Corpus">000A91</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000A91</idno>
<idno type="wicri:Area/Main/Curation">000A91</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000A91</idno>
<idno type="wicri:Area/Main/Exploration">000A91</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">Stress resistance and lifespan are increased in C. elegans but decreased in S. cerevisiae by mafr-1/maf1 deletion.</title>
<author><name sortKey="Cai, Ying" sort="Cai, Ying" uniqKey="Cai Y" first="Ying" last="Cai">Ying Cai</name>
<affiliation wicri:level="1"><nlm:affiliation>Shanghai Ninth People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shanghai Ninth People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai</wicri:regionArea>
<wicri:noRegion>Shanghai</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Wei, Yue Hua" sort="Wei, Yue Hua" uniqKey="Wei Y" first="Yue-Hua" last="Wei">Yue-Hua Wei</name>
<affiliation wicri:level="1"><nlm:affiliation>Shanghai Ninth People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shanghai Ninth People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai</wicri:regionArea>
<wicri:noRegion>Shanghai</wicri:noRegion>
</affiliation>
</author>
</analytic>
<series><title level="j">Oncotarget</title>
<idno type="eISSN">1949-2553</idno>
<imprint><date when="2016" type="published">2016</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Autophagy (MeSH)</term>
<term>Caenorhabditis elegans (physiology)</term>
<term>Caenorhabditis elegans Proteins (genetics)</term>
<term>Caenorhabditis elegans Proteins (metabolism)</term>
<term>Caloric Restriction (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Longevity (genetics)</term>
<term>Repressor Proteins (deficiency)</term>
<term>Repressor Proteins (genetics)</term>
<term>Repressor Proteins (metabolism)</term>
<term>Saccharomyces cerevisiae (genetics)</term>
<term>Saccharomyces cerevisiae (physiology)</term>
<term>Saccharomyces cerevisiae Proteins (genetics)</term>
<term>Saccharomyces cerevisiae Proteins (metabolism)</term>
<term>Transcription Factors (deficiency)</term>
<term>Transcription Factors (genetics)</term>
<term>Transcription Factors (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Autophagie (MeSH)</term>
<term>Caenorhabditis elegans (physiologie)</term>
<term>Facteurs de transcription (déficit)</term>
<term>Facteurs de transcription (génétique)</term>
<term>Facteurs de transcription (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Longévité (génétique)</term>
<term>Protéines de Caenorhabditis elegans (génétique)</term>
<term>Protéines de Caenorhabditis elegans (métabolisme)</term>
<term>Protéines de Saccharomyces cerevisiae (génétique)</term>
<term>Protéines de Saccharomyces cerevisiae (métabolisme)</term>
<term>Protéines de répression (déficit)</term>
<term>Protéines de répression (génétique)</term>
<term>Protéines de répression (métabolisme)</term>
<term>Restriction calorique (MeSH)</term>
<term>Saccharomyces cerevisiae (génétique)</term>
<term>Saccharomyces cerevisiae (physiologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Repressor Proteins</term>
<term>Transcription Factors</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Caenorhabditis elegans Proteins</term>
<term>Repressor Proteins</term>
<term>Saccharomyces cerevisiae Proteins</term>
<term>Transcription Factors</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caenorhabditis elegans Proteins</term>
<term>Repressor Proteins</term>
<term>Saccharomyces cerevisiae Proteins</term>
<term>Transcription Factors</term>
</keywords>
<keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Facteurs de transcription</term>
<term>Protéines de répression</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Longevity</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteurs de transcription</term>
<term>Longévité</term>
<term>Protéines de Caenorhabditis elegans</term>
<term>Protéines de Saccharomyces cerevisiae</term>
<term>Protéines de répression</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteurs de transcription</term>
<term>Protéines de Caenorhabditis elegans</term>
<term>Protéines de Saccharomyces cerevisiae</term>
<term>Protéines de répression</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Caenorhabditis elegans</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Caenorhabditis elegans</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Autophagy</term>
<term>Caloric Restriction</term>
<term>Humans</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Autophagie</term>
<term>Humains</term>
<term>Restriction calorique</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Maf1 is a conserved effector of the mechanistic target of rapamycin (mTOR), an aging promoting kinase. However, whether Maf1 is required for lifespan extension caused by mTOR inhibition, such as dietary restriction (DR) or calorie restriction (CR) remains elusive. Here we show that deletion of maf1 in the budding yeast S. cerevisiae but not mafr-1 in C. elegans prevents DR or CR to extend lifespan. Interestingly, mafr-1 deletion increases stress tolerance and extends lifespan. MAFR-1 is phosphorylated in a mTOR-dependent manner and mafr-1 deletion alleviates the inhibition of tRNA synthesis caused by reduced mTOR activity. We find that the opposite effect of mafr-1 deletion on lifespan is due to an enhancement of stress response, including oxidative stress response, mitochondrial unfolded protein response (UPRmt) and autophagy. mafr-1 deletion also attenuates the paralysis of a C. elegans model of Alzheimer's disease. Our study reveals distinct mechanisms of lifespan regulation by Maf1 and MAFR-1. </div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26934328</PMID>
<DateCompleted><Year>2017</Year>
<Month>11</Month>
<Day>30</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1949-2553</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>7</Volume>
<Issue>10</Issue>
<PubDate><Year>2016</Year>
<Month>Mar</Month>
<Day>08</Day>
</PubDate>
</JournalIssue>
<Title>Oncotarget</Title>
<ISOAbbreviation>Oncotarget</ISOAbbreviation>
</Journal>
<ArticleTitle>Stress resistance and lifespan are increased in C. elegans but decreased in S. cerevisiae by mafr-1/maf1 deletion.</ArticleTitle>
<Pagination><MedlinePgn>10812-26</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.18632/oncotarget.7769</ELocationID>
<Abstract><AbstractText>Maf1 is a conserved effector of the mechanistic target of rapamycin (mTOR), an aging promoting kinase. However, whether Maf1 is required for lifespan extension caused by mTOR inhibition, such as dietary restriction (DR) or calorie restriction (CR) remains elusive. Here we show that deletion of maf1 in the budding yeast S. cerevisiae but not mafr-1 in C. elegans prevents DR or CR to extend lifespan. Interestingly, mafr-1 deletion increases stress tolerance and extends lifespan. MAFR-1 is phosphorylated in a mTOR-dependent manner and mafr-1 deletion alleviates the inhibition of tRNA synthesis caused by reduced mTOR activity. We find that the opposite effect of mafr-1 deletion on lifespan is due to an enhancement of stress response, including oxidative stress response, mitochondrial unfolded protein response (UPRmt) and autophagy. mafr-1 deletion also attenuates the paralysis of a C. elegans model of Alzheimer's disease. Our study reveals distinct mechanisms of lifespan regulation by Maf1 and MAFR-1. </AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cai</LastName>
<ForeName>Ying</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Shanghai Ninth People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wei</LastName>
<ForeName>Yue-Hua</ForeName>
<Initials>YH</Initials>
<AffiliationInfo><Affiliation>Shanghai Ninth People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>P40 OD010440</GrantID>
<Acronym>OD</Acronym>
<Agency>NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Oncotarget</MedlineTA>
<NlmUniqueID>101532965</NlmUniqueID>
<ISSNLinking>1949-2553</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D029742">Caenorhabditis elegans Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C104954">MAF1 protein, S cerevisiae</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C520535">MAF1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D012097">Repressor Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D029701">Saccharomyces cerevisiae Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017173" MajorTopicYN="N">Caenorhabditis elegans</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D029742" MajorTopicYN="N">Caenorhabditis elegans Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D031204" MajorTopicYN="N">Caloric Restriction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008136" MajorTopicYN="N">Longevity</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012097" MajorTopicYN="N">Repressor Proteins</DescriptorName>
<QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D029701" MajorTopicYN="N">Saccharomyces cerevisiae Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName>
<QualifierName UI="Q000172" MajorTopicYN="Y">deficiency</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Gerotarget</Keyword>
<Keyword MajorTopicYN="N">Maf1</Keyword>
<Keyword MajorTopicYN="N">autophagy</Keyword>
<Keyword MajorTopicYN="N">calorie restriction</Keyword>
<Keyword MajorTopicYN="N">lifespan</Keyword>
<Keyword MajorTopicYN="N">stress response</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year>
<Month>09</Month>
<Day>24</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2016</Year>
<Month>02</Month>
<Day>18</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2016</Year>
<Month>3</Month>
<Day>3</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2016</Year>
<Month>3</Month>
<Day>5</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2017</Year>
<Month>12</Month>
<Day>1</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">26934328</ArticleId>
<ArticleId IdType="pii">7769</ArticleId>
<ArticleId IdType="doi">10.18632/oncotarget.7769</ArticleId>
<ArticleId IdType="pmc">PMC4905441</ArticleId>
</ArticleIdList>
<ReferenceList><Reference><Citation>Nat Rev Mol Cell Biol. 2006 Feb;7(2):85-96</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16493415</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 2010 Aug;30(15):3749-57</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20516213</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2011 Sep 2;146(5):682-95</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21884931</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Cycle. 2010 Feb 15;9(4):683-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20139716</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Aging (Albany NY). 2014 Feb;6(2):118-30</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24642473</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Genes Dev. 2015 May 1;29(9):934-47</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25934505</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Aging Cell. 2006 Dec;5(6):515-24</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17096674</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS Genet. 2014 Dec 11;10 (12 ):e1004789</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25502566</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Rep. 2014 Dec 24;9(6):2180-91</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25497095</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Aging (Albany NY). 2015 Feb;7(2):133-43</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25720796</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS Genet. 2012;8(7):e1002792</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22829775</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Aging (Albany NY). 2013 Jun;5(6):474-84</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23817674</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Aging (Albany NY). 2013 Jul;5(7):507-14</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23924667</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2012 Jan 24;109 (4):1139-44</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22228302</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Trends Biochem Sci. 2007 Feb;32(2):51-3</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17174096</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Methods Mol Biol. 2007;371:89-95</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17634576</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>FEMS Yeast Res. 2009 Feb;9(1):32-44</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19054128</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 2013 Jan 17;493(7432):338-45</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23325216</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Cell Sci. 2010 Aug 1;123(Pt 15):2533-42</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20940129</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2002 Jul 26;110(2):177-89</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12150926</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Gerontol A Biol Sci Med Sci. 1996 Nov;51(6):B392-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8914487</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Aging Cell. 2011 Oct;10(5):735-48</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21443682</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS Genet. 2010 Jul 15;6(7):e1001024</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20657825</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Curr Biol. 2007 Oct 9;17(19):1646-56</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17900900</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Clin Endocrinol Metab. 2003 Aug;88(8):3664-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12915652</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell. 2004 Apr 9;14(1):1-15</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15068799</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nucleus. 2010 Mar-Apr;1(2):162-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21326948</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 1995 Sep 26;92(20):9368-72</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7568134</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Science. 2003 Sep 5;301(5638):1387-91</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12958363</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Aging (Albany NY). 2015 Jun;7(6):419-34</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26142908</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>EMBO J. 2009 Aug 5;28(15):2220-30</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19574957</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Aging (Albany NY). 2011 Dec;3(12):1130-41</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22246147</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Aging (Albany NY). 2009 Jul 20;1(7):586-97</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20157541</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Metab. 2012 May 2;15(5):713-24</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22560223</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2010 Jun 29;107(26):11823-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20543138</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 2009 Jul 16;460(7253):392-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19587680</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Cycle. 2009 Dec 15;8(24):4085-90</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19823048</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2011 Jun 21;108(25):10190-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21646527</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>EMBO J. 2012 Apr 18;31(8):1916-30</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22367393</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Mol Life Sci. 2007 Jun;64(11):1323-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17396225</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Gene. 1997 Feb 7;185(2):291-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9055829</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Science. 1996 Jul 5;273(5271):59-63</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8658196</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2006 Feb 7;103(6):1768-73</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16446459</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS One. 2012;7(4):e34929</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22514691</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Aging Cell. 2011 Apr;10(2):185-90</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21176090</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Aging Cell. 2009 Jun;8(3):258-69</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19627265</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochim Biophys Acta. 2013 Mar-Apr;1829(3-4):376-84</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23201230</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochim Biophys Acta. 2013 Feb;1833(2):410-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22445420</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 2007 Nov;27(21):7693-702</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17785443</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Metab. 2007 Apr;5(4):265-77</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17403371</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Aging (Albany NY). 2014 Jan;6(1):48-57</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24481314</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Science. 2005 Oct 14;310(5746):314-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16224023</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Aging Cell. 2014 Oct;13(5):869-78</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25040785</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biol Rev Camb Philos Soc. 2015 Feb;90(1):167-81</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24673778</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Curr Biol. 2011 Sep 27;21(18):1507-14</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21906946</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Aging (Albany NY). 2010 Sep;2(9):535-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20876940</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Genet. 2003 Jan;33(1):40-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12447374</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS Genet. 2012;8(6):e1002699</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22685415</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2009 Mar 6;136(5):939-51</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19249087</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biogerontology. 2013 Aug;14(4):353-63</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23740528</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2008 Mar 21;132(6):1025-38</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18358814</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 1998 Oct 27;95(22):13091-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9789046</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Cai, Ying" sort="Cai, Ying" uniqKey="Cai Y" first="Ying" last="Cai">Ying Cai</name>
</noRegion>
<name sortKey="Wei, Yue Hua" sort="Wei, Yue Hua" uniqKey="Wei Y" first="Yue-Hua" last="Wei">Yue-Hua Wei</name>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000A06 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000A06 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Bois
   |area=    RapamycinFungusV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:26934328
   |texte=   Stress resistance and lifespan are increased in C. elegans but decreased in S. cerevisiae by mafr-1/maf1 deletion.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i   -Sk "pubmed:26934328" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd   \
       | NlmPubMed2Wicri -a RapamycinFungusV1

This area was generated with Dilib version V0.6.38.
Data generation: Thu Nov 19 21:55:41 2020. Site generation: Thu Nov 19 22:00:39 2020

	Serveur d'exploration sur la rapamycine et les champignons
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur la rapamycine et les champignons

Stress resistance and lifespan are increased in C. elegans but decreased in S. cerevisiae by mafr-1/maf1 deletion.

Stress resistance and lifespan are increased in C. elegans but decreased in S. cerevisiae by mafr-1/maf1 deletion.

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki