RapamycinFungusV1, Main, Exploration, bibRecord, 001067

Chemical genetics of rapamycin-insensitive TORC2 in S. cerevisiae.

Identifieur interne : 001067 ( Main/Exploration ); précédent : 001066; suivant : 001068

Chemical genetics of rapamycin-insensitive TORC2 in S. cerevisiae.

Auteurs : Joseph I. Kliegman [États-Unis] ; Dorothea Fiedler [États-Unis] ; Colm J. Ryan [Irlande (pays)] ; Yi-Fan Xu [États-Unis] ; Xiao-Yang Su [États-Unis] ; David Thomas [États-Unis] ; Max C. Caccese [États-Unis] ; Ada Cheng [États-Unis] ; Michael Shales [États-Unis] ; Joshua D. Rabinowitz [États-Unis] ; Nevan J. Krogan [États-Unis] ; Kevan M. Shokat [États-Unis]

Source :

Cell reports [ 2211-1247 ] ; 2013.

RBID : pubmed:24360963

Descripteurs français

KwdFr :
- Délétion de gène (MeSH), Phosphatidylinositol 3-kinases (génétique), Phosphatidylinositol 3-kinases (métabolisme), Protéines de Saccharomyces cerevisiae (antagonistes et inhibiteurs), Protéines de Saccharomyces cerevisiae (génétique), Protéines de Saccharomyces cerevisiae (métabolisme), Protéines du cycle cellulaire (antagonistes et inhibiteurs), Protéines du cycle cellulaire (génétique), Protéines du cycle cellulaire (métabolisme), Saccharomyces cerevisiae (effets des médicaments et des substances chimiques), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Sirolimus (pharmacologie), Tests de criblage à haut débit (méthodes), Voie des pentoses phosphates (MeSH), Épistasie (MeSH).
MESH :
- antagonistes et inhibiteurs : Protéines de Saccharomyces cerevisiae, Protéines du cycle cellulaire.
- effets des médicaments et des substances chimiques : Saccharomyces cerevisiae.
- génétique : Phosphatidylinositol 3-kinases, Protéines de Saccharomyces cerevisiae, Protéines du cycle cellulaire, Saccharomyces cerevisiae.
- métabolisme : Phosphatidylinositol 3-kinases, Protéines de Saccharomyces cerevisiae, Protéines du cycle cellulaire, Saccharomyces cerevisiae.
- méthodes : Tests de criblage à haut débit.
- pharmacologie : Sirolimus.
- Délétion de gène, Voie des pentoses phosphates, Épistasie.

English descriptors

KwdEn :
- Cell Cycle Proteins (antagonists & inhibitors), Cell Cycle Proteins (genetics), Cell Cycle Proteins (metabolism), Epistasis, Genetic (MeSH), Gene Deletion (MeSH), High-Throughput Screening Assays (methods), Pentose Phosphate Pathway (MeSH), Phosphatidylinositol 3-Kinases (genetics), Phosphatidylinositol 3-Kinases (metabolism), Phosphoinositide-3 Kinase Inhibitors (MeSH), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (antagonists & inhibitors), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Sirolimus (pharmacology).
MESH :
- chemical , antagonists & inhibitors : Cell Cycle Proteins, Saccharomyces cerevisiae Proteins.
- chemical , genetics : Cell Cycle Proteins, Saccharomyces cerevisiae Proteins.
- chemical , metabolism : Cell Cycle Proteins, Saccharomyces cerevisiae Proteins.
- drug effects : Saccharomyces cerevisiae.
- genetics : Phosphatidylinositol 3-Kinases, Saccharomyces cerevisiae.
- metabolism : Phosphatidylinositol 3-Kinases, Saccharomyces cerevisiae.
- methods : High-Throughput Screening Assays.
- chemical , pharmacology : Sirolimus.
- Epistasis, Genetic, Gene Deletion, Pentose Phosphate Pathway, Phosphoinositide-3 Kinase Inhibitors.

Abstract

Current approaches for identifying synergistic targets use cell culture models to see if the combined effect of clinically available drugs is better than predicted by their individual efficacy. New techniques are needed to systematically and rationally identify targets and pathways that may be synergistic targets. Here, we created a tool to screen and identify molecular targets that may synergize with new inhibitors of target of rapamycin (TOR), a conserved protein that is a major integrator of cell proliferation signals in the nutrient-signaling pathway. Although clinical results from TOR complex 1 (TORC1)-specific inhibition using rapamycin analogs have been disappointing, trials using inhibitors that also target TORC2 have been promising. To understand this increased therapeutic efficacy and to discover secondary targets for combination therapy, we engineered Tor2 in S. cerevisiae to accept an orthogonal inhibitor. We used this tool to create a chemical epistasis miniarray profile (ChE-MAP) by measuring interactions between the chemically inhibited Tor2 kinase and a diverse library of deletion mutants. The ChE-MAP identified known TOR components and distinguished between TORC1- and TORC2-dependent functions. The results showed a TORC2-specific interaction with the pentose phosphate pathway, a previously unappreciated TORC2 function that suggests a role for the complex in balancing the high energy demand required for ribosome biogenesis.

DOI: 10.1016/j.celrep.2013.11.040
PubMed: 24360963
PubMed Central: PMC4007695

Affiliations:

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

to stream Main, to step Corpus: 000F19
to stream Main, to step Curation: 000F19

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en">Chemical genetics of rapamycin-insensitive TORC2 in S. cerevisiae.</title>
<author><name sortKey="Kliegman, Joseph I" sort="Kliegman, Joseph I" uniqKey="Kliegman J" first="Joseph I" last="Kliegman">Joseph I. Kliegman</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, San Francisco, CA 94158</wicri:regionArea>
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<country xml:lang="fr">Irlande (pays)</country>
<wicri:regionArea>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158, USA; School of Computer Science and Informatics, University College Dublin, Dublin 4</wicri:regionArea>
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<author><name sortKey="Su, Xiao Yang" sort="Su, Xiao Yang" uniqKey="Su X" first="Xiao-Yang" last="Su">Xiao-Yang Su</name>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Thomas, David" sort="Thomas, David" uniqKey="Thomas D" first="David" last="Thomas">David Thomas</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Chemistry, Princeton University, Princeton, NJ 08540</wicri:regionArea>
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<author><name sortKey="Caccese, Max C" sort="Caccese, Max C" uniqKey="Caccese M" first="Max C" last="Caccese">Max C. Caccese</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, San Francisco, CA 94158, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, San Francisco, CA 94158</wicri:regionArea>
<placeName><region type="state">Californie</region>
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<author><name sortKey="Cheng, Ada" sort="Cheng, Ada" uniqKey="Cheng A" first="Ada" last="Cheng">Ada Cheng</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158</wicri:regionArea>
<placeName><region type="state">Californie</region>
</placeName>
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<author><name sortKey="Shales, Michael" sort="Shales, Michael" uniqKey="Shales M" first="Michael" last="Shales">Michael Shales</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158</wicri:regionArea>
<placeName><region type="state">Californie</region>
</placeName>
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<author><name sortKey="Rabinowitz, Joshua D" sort="Rabinowitz, Joshua D" uniqKey="Rabinowitz J" first="Joshua D" last="Rabinowitz">Joshua D. Rabinowitz</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Chemistry, Princeton University, Princeton, NJ 08540</wicri:regionArea>
<placeName><region type="state">New Jersey</region>
<settlement type="city">Princeton (New Jersey)</settlement>
</placeName>
<orgName type="university">Université de Princeton</orgName>
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<author><name sortKey="Krogan, Nevan J" sort="Krogan, Nevan J" uniqKey="Krogan N" first="Nevan J" last="Krogan">Nevan J. Krogan</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158, USA; J. David Gladstone Institutes, San Francisco, CA 94158, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158, USA; J. David Gladstone Institutes, San Francisco, CA 94158</wicri:regionArea>
<placeName><region type="state">Californie</region>
</placeName>
</affiliation>
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<author><name sortKey="Shokat, Kevan M" sort="Shokat, Kevan M" uniqKey="Shokat K" first="Kevan M" last="Shokat">Kevan M. Shokat</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, San Francisco, CA 94158, USA. Electronic address: kevan.shokat@ucsf.edu.</nlm:affiliation>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Cycle Proteins (antagonists & inhibitors)</term>
<term>Cell Cycle Proteins (genetics)</term>
<term>Cell Cycle Proteins (metabolism)</term>
<term>Epistasis, Genetic (MeSH)</term>
<term>Gene Deletion (MeSH)</term>
<term>High-Throughput Screening Assays (methods)</term>
<term>Pentose Phosphate Pathway (MeSH)</term>
<term>Phosphatidylinositol 3-Kinases (genetics)</term>
<term>Phosphatidylinositol 3-Kinases (metabolism)</term>
<term>Phosphoinositide-3 Kinase Inhibitors (MeSH)</term>
<term>Saccharomyces cerevisiae (drug effects)</term>
<term>Saccharomyces cerevisiae (genetics)</term>
<term>Saccharomyces cerevisiae (metabolism)</term>
<term>Saccharomyces cerevisiae Proteins (antagonists & inhibitors)</term>
<term>Saccharomyces cerevisiae Proteins (genetics)</term>
<term>Saccharomyces cerevisiae Proteins (metabolism)</term>
<term>Sirolimus (pharmacology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Délétion de gène (MeSH)</term>
<term>Phosphatidylinositol 3-kinases (génétique)</term>
<term>Phosphatidylinositol 3-kinases (métabolisme)</term>
<term>Protéines de Saccharomyces cerevisiae (antagonistes et inhibiteurs)</term>
<term>Protéines de Saccharomyces cerevisiae (génétique)</term>
<term>Protéines de Saccharomyces cerevisiae (métabolisme)</term>
<term>Protéines du cycle cellulaire (antagonistes et inhibiteurs)</term>
<term>Protéines du cycle cellulaire (génétique)</term>
<term>Protéines du cycle cellulaire (métabolisme)</term>
<term>Saccharomyces cerevisiae (effets des médicaments et des substances chimiques)</term>
<term>Saccharomyces cerevisiae (génétique)</term>
<term>Saccharomyces cerevisiae (métabolisme)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Tests de criblage à haut débit (méthodes)</term>
<term>Voie des pentoses phosphates (MeSH)</term>
<term>Épistasie (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Cell Cycle Proteins</term>
<term>Saccharomyces cerevisiae Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cell Cycle Proteins</term>
<term>Saccharomyces cerevisiae Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cell Cycle Proteins</term>
<term>Saccharomyces cerevisiae Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Protéines de Saccharomyces cerevisiae</term>
<term>Protéines du cycle cellulaire</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Phosphatidylinositol 3-Kinases</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Phosphatidylinositol 3-kinases</term>
<term>Protéines de Saccharomyces cerevisiae</term>
<term>Protéines du cycle cellulaire</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Phosphatidylinositol 3-Kinases</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>High-Throughput Screening Assays</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Phosphatidylinositol 3-kinases</term>
<term>Protéines de Saccharomyces cerevisiae</term>
<term>Protéines du cycle cellulaire</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="méthodes" xml:lang="fr"><term>Tests de criblage à haut débit</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Epistasis, Genetic</term>
<term>Gene Deletion</term>
<term>Pentose Phosphate Pathway</term>
<term>Phosphoinositide-3 Kinase Inhibitors</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Délétion de gène</term>
<term>Voie des pentoses phosphates</term>
<term>Épistasie</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Current approaches for identifying synergistic targets use cell culture models to see if the combined effect of clinically available drugs is better than predicted by their individual efficacy. New techniques are needed to systematically and rationally identify targets and pathways that may be synergistic targets. Here, we created a tool to screen and identify molecular targets that may synergize with new inhibitors of target of rapamycin (TOR), a conserved protein that is a major integrator of cell proliferation signals in the nutrient-signaling pathway. Although clinical results from TOR complex 1 (TORC1)-specific inhibition using rapamycin analogs have been disappointing, trials using inhibitors that also target TORC2 have been promising. To understand this increased therapeutic efficacy and to discover secondary targets for combination therapy, we engineered Tor2 in S. cerevisiae to accept an orthogonal inhibitor. We used this tool to create a chemical epistasis miniarray profile (ChE-MAP) by measuring interactions between the chemically inhibited Tor2 kinase and a diverse library of deletion mutants. The ChE-MAP identified known TOR components and distinguished between TORC1- and TORC2-dependent functions. The results showed a TORC2-specific interaction with the pentose phosphate pathway, a previously unappreciated TORC2 function that suggests a role for the complex in balancing the high energy demand required for ribosome biogenesis. </div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24360963</PMID>
<DateCompleted><Year>2014</Year>
<Month>08</Month>
<Day>11</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>12</Month>
<Day>10</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2211-1247</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>5</Volume>
<Issue>6</Issue>
<PubDate><Year>2013</Year>
<Month>Dec</Month>
<Day>26</Day>
</PubDate>
</JournalIssue>
<Title>Cell reports</Title>
<ISOAbbreviation>Cell Rep</ISOAbbreviation>
</Journal>
<ArticleTitle>Chemical genetics of rapamycin-insensitive TORC2 in S. cerevisiae.</ArticleTitle>
<Pagination><MedlinePgn>1725-36</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.celrep.2013.11.040</ELocationID>
<ELocationID EIdType="pii" ValidYN="Y">S2211-1247(13)00724-9</ELocationID>
<Abstract><AbstractText>Current approaches for identifying synergistic targets use cell culture models to see if the combined effect of clinically available drugs is better than predicted by their individual efficacy. New techniques are needed to systematically and rationally identify targets and pathways that may be synergistic targets. Here, we created a tool to screen and identify molecular targets that may synergize with new inhibitors of target of rapamycin (TOR), a conserved protein that is a major integrator of cell proliferation signals in the nutrient-signaling pathway. Although clinical results from TOR complex 1 (TORC1)-specific inhibition using rapamycin analogs have been disappointing, trials using inhibitors that also target TORC2 have been promising. To understand this increased therapeutic efficacy and to discover secondary targets for combination therapy, we engineered Tor2 in S. cerevisiae to accept an orthogonal inhibitor. We used this tool to create a chemical epistasis miniarray profile (ChE-MAP) by measuring interactions between the chemically inhibited Tor2 kinase and a diverse library of deletion mutants. The ChE-MAP identified known TOR components and distinguished between TORC1- and TORC2-dependent functions. The results showed a TORC2-specific interaction with the pentose phosphate pathway, a previously unappreciated TORC2 function that suggests a role for the complex in balancing the high energy demand required for ribosome biogenesis. </AbstractText>
<CopyrightInformation>Copyright © 2013 The Authors. Published by Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kliegman</LastName>
<ForeName>Joseph I</ForeName>
<Initials>JI</Initials>
<AffiliationInfo><Affiliation>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, San Francisco, CA 94158, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fiedler</LastName>
<ForeName>Dorothea</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Department of Chemistry, Princeton University, Princeton, NJ 08540, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ryan</LastName>
<ForeName>Colm J</ForeName>
<Initials>CJ</Initials>
<AffiliationInfo><Affiliation>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158, USA; School of Computer Science and Informatics, University College Dublin, Dublin 4, Ireland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Yi-Fan</ForeName>
<Initials>YF</Initials>
<AffiliationInfo><Affiliation>Department of Chemistry, Princeton University, Princeton, NJ 08540, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Su</LastName>
<ForeName>Xiao-Yang</ForeName>
<Initials>XY</Initials>
<AffiliationInfo><Affiliation>Department of Chemistry, Princeton University, Princeton, NJ 08540, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Thomas</LastName>
<ForeName>David</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Department of Chemistry, Princeton University, Princeton, NJ 08540, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Caccese</LastName>
<ForeName>Max C</ForeName>
<Initials>MC</Initials>
<AffiliationInfo><Affiliation>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, San Francisco, CA 94158, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cheng</LastName>
<ForeName>Ada</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shales</LastName>
<ForeName>Michael</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rabinowitz</LastName>
<ForeName>Joshua D</ForeName>
<Initials>JD</Initials>
<AffiliationInfo><Affiliation>Department of Chemistry, Princeton University, Princeton, NJ 08540, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Krogan</LastName>
<ForeName>Nevan J</ForeName>
<Initials>NJ</Initials>
<AffiliationInfo><Affiliation>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158, USA; J. David Gladstone Institutes, San Francisco, CA 94158, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shokat</LastName>
<ForeName>Kevan M</ForeName>
<Initials>KM</Initials>
<AffiliationInfo><Affiliation>Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biosciences, QB3, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, San Francisco, CA 94158, USA. Electronic address: kevan.shokat@ucsf.edu.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>GM081879</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>GM084279</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>P50 GM081879</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>GM084448</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 GM098101</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 CA163591</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>GM098101</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><Agency>Howard Hughes Medical Institute</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 GM084448</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 GM084279</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
<PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2013</Year>
<Month>12</Month>
<Day>19</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Cell Rep</MedlineTA>
<NlmUniqueID>101573691</NlmUniqueID>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D018797">Cell Cycle Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000081082">Phosphoinositide-3 Kinase Inhibitors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D029701">Saccharomyces cerevisiae Proteins</NameOfSubstance>
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<Chemical><RegistryNumber>EC 2.7.1.137</RegistryNumber>
<NameOfSubstance UI="C083324">TOR1 protein, S cerevisiae</NameOfSubstance>
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<Chemical><RegistryNumber>EC 2.7.1.137</RegistryNumber>
<NameOfSubstance UI="C081135">TOR2 protein, S cerevisiae</NameOfSubstance>
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<Chemical><RegistryNumber>W36ZG6FT64</RegistryNumber>
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<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D018797" MajorTopicYN="N">Cell Cycle Proteins</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004843" MajorTopicYN="Y">Epistasis, Genetic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017353" MajorTopicYN="N">Gene Deletion</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D057166" MajorTopicYN="N">High-Throughput Screening Assays</DescriptorName>
<QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010427" MajorTopicYN="N">Pentose Phosphate Pathway</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019869" MajorTopicYN="N">Phosphatidylinositol 3-Kinases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000081082" MajorTopicYN="Y">Phosphoinositide-3 Kinase Inhibitors</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D029701" MajorTopicYN="N">Saccharomyces cerevisiae Proteins</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName>
<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="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
</MeshHeadingList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year>
<Month>01</Month>
<Day>24</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2013</Year>
<Month>07</Month>
<Day>10</Day>
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<PubMedPubDate PubStatus="accepted"><Year>2013</Year>
<Month>11</Month>
<Day>22</Day>
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<PubMedPubDate PubStatus="entrez"><Year>2013</Year>
<Month>12</Month>
<Day>24</Day>
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	Serveur d'exploration sur la rapamycine et les champignons
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Chemical genetics of rapamycin-insensitive TORC2 in S. cerevisiae.

Chemical genetics of rapamycin-insensitive TORC2 in S. cerevisiae.

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