TORC2 signaling pathway guarantees genome stability in the face of DNA strand breaks.
Identifieur interne : 000F67 ( Main/Exploration ); précédent : 000F66; suivant : 000F68TORC2 signaling pathway guarantees genome stability in the face of DNA strand breaks.
Auteurs : Kenji Shimada [Suisse] ; Ireos Filipuzzi ; Michael Stahl ; Stephen B. Helliwell ; Christian Studer ; Dominic Hoepfner ; Andrew Seeber ; Robbie Loewith ; N Rao Movva ; Susan M. GasserSource :
- Molecular cell [ 1097-4164 ] ; 2013.
Descripteurs français
- KwdFr :
- Actines (antagonistes et inhibiteurs), Actines (métabolisme), Altération de l'ADN (génétique), Bléomycine (pharmacologie), Chromosomes (effets des médicaments et des substances chimiques), Chromosomes (effets des radiations), Chromosomes (génétique), Complexe-2 cible mécanistique de la rapamycine (MeSH), Complexes multiprotéiques (antagonistes et inhibiteurs), Complexes multiprotéiques (génétique), Complexes multiprotéiques (métabolisme), Composés hétérocycliques bicycliques (pharmacologie), Facteurs de transcription (antagonistes et inhibiteurs), Facteurs de transcription (génétique), Facteurs de transcription (métabolisme), Glycogen Synthase Kinase 3 (métabolisme), Instabilité du génome (effets des médicaments et des substances chimiques), Instabilité du génome (effets des radiations), Protéines de Saccharomyces cerevisiae (antagonistes et inhibiteurs), Protéines de Saccharomyces cerevisiae (génétique), Protéines de Saccharomyces cerevisiae (métabolisme), Rayonnement ionisant (MeSH), Réplication de l'ADN (effets des médicaments et des substances chimiques), Réplication de l'ADN (effets des radiations), Saccharomyces cerevisiae (génétique), Sérine-thréonine kinases TOR (antagonistes et inhibiteurs), Sérine-thréonine kinases TOR (génétique), Sérine-thréonine kinases TOR (métabolisme), Thiazolidines (pharmacologie), Transduction du signal (effets des médicaments et des substances chimiques), Transduction du signal (effets des radiations).
- MESH :
- antagonistes et inhibiteurs : Actines, Complexes multiprotéiques, Facteurs de transcription, Protéines de Saccharomyces cerevisiae, Sérine-thréonine kinases TOR.
- effets des médicaments et des substances chimiques : Chromosomes, Instabilité du génome, Réplication de l'ADN, Transduction du signal.
- effets des radiations : Chromosomes, Instabilité du génome, Réplication de l'ADN, Transduction du signal.
- génétique : Altération de l'ADN, Chromosomes, Complexes multiprotéiques, Facteurs de transcription, Protéines de Saccharomyces cerevisiae, Saccharomyces cerevisiae, Sérine-thréonine kinases TOR.
- métabolisme : Actines, Complexes multiprotéiques, Facteurs de transcription, Glycogen Synthase Kinase 3, Protéines de Saccharomyces cerevisiae, Sérine-thréonine kinases TOR.
- pharmacologie : Bléomycine, Composés hétérocycliques bicycliques, Thiazolidines.
- Complexe-2 cible mécanistique de la rapamycine, Rayonnement ionisant.
English descriptors
- KwdEn :
- Actins (antagonists & inhibitors), Actins (metabolism), Bleomycin (pharmacology), Bridged Bicyclo Compounds, Heterocyclic (pharmacology), Chromosomes (drug effects), Chromosomes (genetics), Chromosomes (radiation effects), DNA Damage (genetics), DNA Replication (drug effects), DNA Replication (radiation effects), Genomic Instability (drug effects), Genomic Instability (radiation effects), Glycogen Synthase Kinase 3 (metabolism), Mechanistic Target of Rapamycin Complex 2 (MeSH), Multiprotein Complexes (antagonists & inhibitors), Multiprotein Complexes (genetics), Multiprotein Complexes (metabolism), Radiation, Ionizing (MeSH), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae Proteins (antagonists & inhibitors), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (drug effects), Signal Transduction (radiation effects), TOR Serine-Threonine Kinases (antagonists & inhibitors), TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (metabolism), Thiazolidines (pharmacology), Transcription Factors (antagonists & inhibitors), Transcription Factors (genetics), Transcription Factors (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Actins, Multiprotein Complexes, Saccharomyces cerevisiae Proteins, TOR Serine-Threonine Kinases, Transcription Factors.
- chemical , genetics : Multiprotein Complexes, Saccharomyces cerevisiae Proteins, TOR Serine-Threonine Kinases, Transcription Factors.
- chemical , metabolism : Actins, Glycogen Synthase Kinase 3, Multiprotein Complexes, Saccharomyces cerevisiae Proteins, TOR Serine-Threonine Kinases, Transcription Factors.
- chemical , pharmacology : Bleomycin, Bridged Bicyclo Compounds, Heterocyclic, Thiazolidines.
- drug effects : Chromosomes, DNA Replication, Genomic Instability, Signal Transduction.
- genetics : Chromosomes, DNA Damage, Saccharomyces cerevisiae.
- radiation effects : Chromosomes, DNA Replication, Genomic Instability, Signal Transduction.
- chemical : Mechanistic Target of Rapamycin Complex 2, Radiation, Ionizing.
Abstract
A chemicogenetic screen was performed in budding yeast mutants that have a weakened replication stress response. This identified an inhibitor of target of rapamycin (TOR) complexes 1 and 2 that selectively enhances the sensitivity of sgs1Δ cells to hydroxyurea and camptothecin. More importantly, the inhibitor has strong synthetic lethality in combination with either the break-inducing antibiotic Zeocin or ionizing radiation, independent of the strain background. Lethality correlates with a rapid fragmentation of chromosomes that occurs only when TORC2, but not TORC1, is repressed. Genetic inhibition of Tor2 kinase, or its downstream effector kinases Ypk1/Ypk2, conferred similar synergistic effects in the presence of Zeocin. Given that Ypk1/Ypk2 controls the actin cytoskeleton, we tested the effects of actin modulators latrunculin A and jasplakinolide. These phenocopy TORC2 inhibition on Zeocin, although modulation of calcineurin-sensitive transcription does not. These results implicate TORC2-mediated actin filament regulation in the survival of low levels of DNA damage.
DOI: 10.1016/j.molcel.2013.08.019
PubMed: 24035500
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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inhibitors)</term><term>Multiprotein Complexes (genetics)</term><term>Multiprotein Complexes (metabolism)</term><term>Radiation, Ionizing (MeSH)</term><term>Saccharomyces cerevisiae (genetics)</term><term>Saccharomyces cerevisiae Proteins (antagonists & inhibitors)</term><term>Saccharomyces cerevisiae Proteins (genetics)</term><term>Saccharomyces cerevisiae Proteins (metabolism)</term><term>Signal Transduction (drug effects)</term><term>Signal Transduction (radiation effects)</term><term>TOR Serine-Threonine Kinases (antagonists & inhibitors)</term><term>TOR Serine-Threonine Kinases (genetics)</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>Thiazolidines (pharmacology)</term><term>Transcription Factors (antagonists & inhibitors)</term><term>Transcription Factors (genetics)</term><term>Transcription Factors (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Actines (antagonistes et inhibiteurs)</term><term>Actines (métabolisme)</term><term>Altération de l'ADN (génétique)</term><term>Bléomycine (pharmacologie)</term><term>Chromosomes (effets des médicaments et des substances chimiques)</term><term>Chromosomes (effets des radiations)</term><term>Chromosomes (génétique)</term><term>Complexe-2 cible mécanistique de la rapamycine (MeSH)</term><term>Complexes multiprotéiques (antagonistes et inhibiteurs)</term><term>Complexes multiprotéiques (génétique)</term><term>Complexes multiprotéiques (métabolisme)</term><term>Composés hétérocycliques bicycliques (pharmacologie)</term><term>Facteurs de transcription (antagonistes et inhibiteurs)</term><term>Facteurs de transcription (génétique)</term><term>Facteurs de transcription (métabolisme)</term><term>Glycogen Synthase Kinase 3 (métabolisme)</term><term>Instabilité du génome (effets des médicaments et des substances chimiques)</term><term>Instabilité du génome (effets des radiations)</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>Rayonnement ionisant (MeSH)</term><term>Réplication de l'ADN (effets des médicaments et des substances chimiques)</term><term>Réplication de l'ADN (effets des radiations)</term><term>Saccharomyces cerevisiae (génétique)</term><term>Sérine-thréonine kinases TOR (antagonistes et inhibiteurs)</term><term>Sérine-thréonine kinases TOR (génétique)</term><term>Sérine-thréonine kinases TOR (métabolisme)</term><term>Thiazolidines (pharmacologie)</term><term>Transduction du signal (effets des médicaments et des substances chimiques)</term><term>Transduction du signal (effets des radiations)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Actins</term><term>Multiprotein Complexes</term><term>Saccharomyces cerevisiae Proteins</term><term>TOR Serine-Threonine 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cerevisiae</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Chromosomes</term><term>DNA Replication</term><term>Genomic Instability</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Chromosomes</term><term>Instabilité du génome</term><term>Réplication de l'ADN</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="effets des radiations" xml:lang="fr"><term>Chromosomes</term><term>Instabilité du génome</term><term>Réplication de l'ADN</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Chromosomes</term><term>DNA Damage</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Altération de l'ADN</term><term>Chromosomes</term><term>Complexes multiprotéiques</term><term>Facteurs de transcription</term><term>Protéines de Saccharomyces cerevisiae</term><term>Saccharomyces cerevisiae</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Actines</term><term>Complexes multiprotéiques</term><term>Facteurs de transcription</term><term>Glycogen Synthase Kinase 3</term><term>Protéines de Saccharomyces cerevisiae</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Bléomycine</term><term>Composés hétérocycliques bicycliques</term><term>Thiazolidines</term></keywords><keywords scheme="MESH" qualifier="radiation effects" xml:lang="en"><term>Chromosomes</term><term>DNA Replication</term><term>Genomic Instability</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Mechanistic Target of Rapamycin Complex 2</term><term>Radiation, Ionizing</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Complexe-2 cible mécanistique de la rapamycine</term><term>Rayonnement ionisant</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A chemicogenetic screen was performed in budding yeast mutants that have a weakened replication stress response. This identified an inhibitor of target of rapamycin (TOR) complexes 1 and 2 that selectively enhances the sensitivity of sgs1Δ cells to hydroxyurea and camptothecin. More importantly, the inhibitor has strong synthetic lethality in combination with either the break-inducing antibiotic Zeocin or ionizing radiation, independent of the strain background. Lethality correlates with a rapid fragmentation of chromosomes that occurs only when TORC2, but not TORC1, is repressed. Genetic inhibition of Tor2 kinase, or its downstream effector kinases Ypk1/Ypk2, conferred similar synergistic effects in the presence of Zeocin. Given that Ypk1/Ypk2 controls the actin cytoskeleton, we tested the effects of actin modulators latrunculin A and jasplakinolide. These phenocopy TORC2 inhibition on Zeocin, although modulation of calcineurin-sensitive transcription does not. These results implicate TORC2-mediated actin filament regulation in the survival of low levels of DNA damage.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24035500</PMID><DateCompleted><Year>2013</Year><Month>12</Month><Day>09</Day></DateCompleted><DateRevised><Year>2017</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1097-4164</ISSN><JournalIssue CitedMedium="Internet"><Volume>51</Volume><Issue>6</Issue><PubDate><Year>2013</Year><Month>Sep</Month><Day>26</Day></PubDate></JournalIssue><Title>Molecular cell</Title><ISOAbbreviation>Mol Cell</ISOAbbreviation></Journal><ArticleTitle>TORC2 signaling pathway guarantees genome stability in the face of DNA strand breaks.</ArticleTitle><Pagination><MedlinePgn>829-39</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.molcel.2013.08.019</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1097-2765(13)00592-3</ELocationID><Abstract><AbstractText>A chemicogenetic screen was performed in budding yeast mutants that have a weakened replication stress response. This identified an inhibitor of target of rapamycin (TOR) complexes 1 and 2 that selectively enhances the sensitivity of sgs1Δ cells to hydroxyurea and camptothecin. More importantly, the inhibitor has strong synthetic lethality in combination with either the break-inducing antibiotic Zeocin or ionizing radiation, independent of the strain background. Lethality correlates with a rapid fragmentation of chromosomes that occurs only when TORC2, but not TORC1, is repressed. Genetic inhibition of Tor2 kinase, or its downstream effector kinases Ypk1/Ypk2, conferred similar synergistic effects in the presence of Zeocin. Given that Ypk1/Ypk2 controls the actin cytoskeleton, we tested the effects of actin modulators latrunculin A and jasplakinolide. These phenocopy TORC2 inhibition on Zeocin, although modulation of calcineurin-sensitive transcription does not. These results implicate TORC2-mediated actin filament regulation in the survival of low levels of DNA damage.</AbstractText><CopyrightInformation>Copyright © 2013 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shimada</LastName><ForeName>Kenji</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, 4058 Basel, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Filipuzzi</LastName><ForeName>Ireos</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Stahl</LastName><ForeName>Michael</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Helliwell</LastName><ForeName>Stephen B</ForeName><Initials>SB</Initials></Author><Author ValidYN="Y"><LastName>Studer</LastName><ForeName>Christian</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Hoepfner</LastName><ForeName>Dominic</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Seeber</LastName><ForeName>Andrew</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Loewith</LastName><ForeName>Robbie</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Movva</LastName><ForeName>N Rao</ForeName><Initials>NR</Initials></Author><Author ValidYN="Y"><LastName>Gasser</LastName><ForeName>Susan M</ForeName><Initials>SM</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>2013</Year><Month>09</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mol Cell</MedlineTA><NlmUniqueID>9802571</NlmUniqueID><ISSNLinking>1097-2765</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000199">Actins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019086">Bridged Bicyclo Compounds, Heterocyclic</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D046912">Multiprotein Complexes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029701">Saccharomyces cerevisiae Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C561842">TORC1 protein complex, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053778">Thiazolidines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>11056-06-7</RegistryNumber><NameOfSubstance UI="D001761">Bleomycin</NameOfSubstance></Chemical><Chemical><RegistryNumber>181494-14-4</RegistryNumber><NameOfSubstance UI="C105427">Zeocin</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D000076225">Mechanistic Target of Rapamycin Complex 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.26</RegistryNumber><NameOfSubstance UI="D038362">Glycogen Synthase Kinase 3</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.12.1</RegistryNumber><NameOfSubstance UI="C068124">MCK1 protein, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>SRQ9WWM084</RegistryNumber><NameOfSubstance UI="C037067">latrunculin A</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000199" MajorTopicYN="N">Actins</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001761" MajorTopicYN="N">Bleomycin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019086" MajorTopicYN="N">Bridged Bicyclo Compounds, Heterocyclic</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002875" MajorTopicYN="N">Chromosomes</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004249" MajorTopicYN="N">DNA Damage</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004261" MajorTopicYN="N">DNA Replication</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042822" MajorTopicYN="Y">Genomic Instability</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D038362" MajorTopicYN="N">Glycogen Synthase Kinase 3</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000076225" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D046912" MajorTopicYN="N">Multiprotein Complexes</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000235" 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effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053778" MajorTopicYN="N">Thiazolidines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>03</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2013</Year><Month>07</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>08</Month><Day>08</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>9</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>9</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>12</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24035500</ArticleId><ArticleId IdType="pii">S1097-2765(13)00592-3</ArticleId><ArticleId IdType="doi">10.1016/j.molcel.2013.08.019</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Suisse</li></country></list><tree><noCountry><name sortKey="Filipuzzi, Ireos" sort="Filipuzzi, Ireos" uniqKey="Filipuzzi I" first="Ireos" last="Filipuzzi">Ireos Filipuzzi</name><name sortKey="Gasser, Susan M" sort="Gasser, Susan M" uniqKey="Gasser S" first="Susan M" last="Gasser">Susan M. Gasser</name><name sortKey="Helliwell, Stephen B" sort="Helliwell, Stephen B" uniqKey="Helliwell S" first="Stephen B" last="Helliwell">Stephen B. Helliwell</name><name sortKey="Hoepfner, Dominic" sort="Hoepfner, Dominic" uniqKey="Hoepfner D" first="Dominic" last="Hoepfner">Dominic Hoepfner</name><name sortKey="Loewith, Robbie" sort="Loewith, Robbie" uniqKey="Loewith R" first="Robbie" last="Loewith">Robbie Loewith</name><name sortKey="Movva, N Rao" sort="Movva, N Rao" uniqKey="Movva N" first="N Rao" last="Movva">N Rao Movva</name><name sortKey="Seeber, Andrew" sort="Seeber, Andrew" uniqKey="Seeber A" first="Andrew" last="Seeber">Andrew Seeber</name><name sortKey="Stahl, Michael" sort="Stahl, Michael" uniqKey="Stahl M" first="Michael" last="Stahl">Michael Stahl</name><name sortKey="Studer, Christian" sort="Studer, Christian" uniqKey="Studer C" first="Christian" last="Studer">Christian Studer</name></noCountry><country name="Suisse"><noRegion><name sortKey="Shimada, Kenji" sort="Shimada, Kenji" uniqKey="Shimada K" first="Kenji" last="Shimada">Kenji Shimada</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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{{Explor lien
|wiki= Bois
|area= RapamycinFungusV1
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|clé= pubmed:24035500
|texte= TORC2 signaling pathway guarantees genome stability in the face of DNA strand breaks.
}}
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