Evaluation of mTOR function by a gain-of-function approach.
Identifieur interne : 001526 ( Main/Exploration ); précédent : 001525; suivant : 001527Evaluation of mTOR function by a gain-of-function approach.
Auteurs : Yoichiro Ohne [Japon] ; Terunao Takahara ; Tatsuya MaedaSource :
- Cell cycle (Georgetown, Tex.) [ 1551-4005 ] ; 2009.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Humains (MeSH), Interférence par ARN (MeSH), Lignée cellulaire (MeSH), Mutation (MeSH), Protein kinases (génétique), Protein kinases (métabolisme), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Sirolimus (métabolisme), Sérine-thréonine kinases TOR (MeSH).
- MESH :
- génétique : Protein kinases, Saccharomyces cerevisiae.
- métabolisme : Protein kinases, Saccharomyces cerevisiae, Sirolimus.
- Animaux, Humains, Interférence par ARN, Lignée cellulaire, Mutation, Sérine-thréonine kinases TOR.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Protein Kinases.
- chemical , metabolism : Protein Kinases, Sirolimus.
- genetics : Saccharomyces cerevisiae.
- metabolism : Saccharomyces cerevisiae.
- Animals, Cell Line, Humans, Mutation, RNA Interference, TOR Serine-Threonine Kinases.
Abstract
The mammalian target of rapamycin (mTOR), a member of the phosphoinositide 3-kinase related kinase (PIKK) family, plays a central role in the regulation of cell growth. The cellular function of mTOR has been proposed based solely on loss-of-function analyses using the specific inhibitor rapamycin or RNAi-mediated knockdown. There have been recent reports of mTOR mutants with enhanced activity that were isolated by genetic screening in yeast. These isolated mTOR mutants exhibited enhanced kinase activity in vitro, and when expressed in cells, prevented the dephosphorylation of known mTOR substrates. The application of these mutants in gain-of-function analyses has enabled a re-evaluation of the function of mTOR. Although these studies confirmed many of the proposed mTOR functions some unexpected observations urged a reconsideration of the regulatory mechanisms and the physiological function of the mTOR pathway. Hyperactive mTOR mutants are thus valuable tools for analysis of the activation mechanism as well as the in vivo function of mTOR.
DOI: 10.4161/cc.8.4.7660
PubMed: 19182527
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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cellulaire</term><term>Mutation</term><term>Sérine-thréonine kinases TOR</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The mammalian target of rapamycin (mTOR), a member of the phosphoinositide 3-kinase related kinase (PIKK) family, plays a central role in the regulation of cell growth. The cellular function of mTOR has been proposed based solely on loss-of-function analyses using the specific inhibitor rapamycin or RNAi-mediated knockdown. There have been recent reports of mTOR mutants with enhanced activity that were isolated by genetic screening in yeast. These isolated mTOR mutants exhibited enhanced kinase activity in vitro, and when expressed in cells, prevented the dephosphorylation of known mTOR substrates. The application of these mutants in gain-of-function analyses has enabled a re-evaluation of the function of mTOR. Although these studies confirmed many of the proposed mTOR functions some unexpected observations urged a reconsideration of the regulatory mechanisms and the physiological function of the mTOR pathway. Hyperactive mTOR mutants are thus valuable tools for analysis of the activation mechanism as well as the in vivo function of mTOR.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19182527</PMID><DateCompleted><Year>2009</Year><Month>03</Month><Day>30</Day></DateCompleted><DateRevised><Year>2020</Year><Month>09</Month><Day>30</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1551-4005</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><Issue>4</Issue><PubDate><Year>2009</Year><Month>Feb</Month><Day>15</Day></PubDate></JournalIssue><Title>Cell cycle (Georgetown, Tex.)</Title><ISOAbbreviation>Cell Cycle</ISOAbbreviation></Journal><ArticleTitle>Evaluation of mTOR function by a gain-of-function approach.</ArticleTitle><Pagination><MedlinePgn>573-9</MedlinePgn></Pagination><Abstract><AbstractText>The mammalian target of rapamycin (mTOR), a member of the phosphoinositide 3-kinase related kinase (PIKK) family, plays a central role in the regulation of cell growth. The cellular function of mTOR has been proposed based solely on loss-of-function analyses using the specific inhibitor rapamycin or RNAi-mediated knockdown. There have been recent reports of mTOR mutants with enhanced activity that were isolated by genetic screening in yeast. These isolated mTOR mutants exhibited enhanced kinase activity in vitro, and when expressed in cells, prevented the dephosphorylation of known mTOR substrates. The application of these mutants in gain-of-function analyses has enabled a re-evaluation of the function of mTOR. Although these studies confirmed many of the proposed mTOR functions some unexpected observations urged a reconsideration of the regulatory mechanisms and the physiological function of the mTOR pathway. Hyperactive mTOR mutants are thus valuable tools for analysis of the activation mechanism as well as the in vivo function of mTOR.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ohne</LastName><ForeName>Yoichiro</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Institute of Molecular and Cellular Biosciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Takahara</LastName><ForeName>Terunao</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Maeda</LastName><ForeName>Tatsuya</ForeName><Initials>T</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2009</Year><Month>02</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Cell Cycle</MedlineTA><NlmUniqueID>101137841</NlmUniqueID><ISSNLinking>1551-4005</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 2.7.-</RegistryNumber><NameOfSubstance UI="D011494">Protein Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="C546842">MTOR protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>W36ZG6FT64</RegistryNumber><NameOfSubstance UI="D020123">Sirolimus</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011494" MajorTopicYN="N">Protein Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D034622" MajorTopicYN="Y">RNA Interference</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>2</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>2</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>3</Month><Day>31</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19182527</ArticleId><ArticleId IdType="pii">7660</ArticleId><ArticleId IdType="doi">10.4161/cc.8.4.7660</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Japon</li></country><region><li>Région de Kantō</li></region><settlement><li>Tokyo</li></settlement><orgName><li>Université de Tokyo</li></orgName></list><tree><noCountry><name sortKey="Maeda, Tatsuya" sort="Maeda, Tatsuya" uniqKey="Maeda T" first="Tatsuya" last="Maeda">Tatsuya Maeda</name><name sortKey="Takahara, Terunao" sort="Takahara, Terunao" uniqKey="Takahara T" first="Terunao" last="Takahara">Terunao Takahara</name></noCountry><country name="Japon"><region name="Région de Kantō"><name sortKey="Ohne, Yoichiro" sort="Ohne, Yoichiro" uniqKey="Ohne Y" first="Yoichiro" last="Ohne">Yoichiro Ohne</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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