mTORC1 restricts hepatitis C virus RNA replication through ULK1-mediated suppression of miR-122 and facilitates post-replication events.
Identifieur interne : 000006 ( Main/Exploration ); précédent : 000005; suivant : 000007mTORC1 restricts hepatitis C virus RNA replication through ULK1-mediated suppression of miR-122 and facilitates post-replication events.
Auteurs : Manish Kumar Johri [Inde] ; Hiren Vasantrai Lashkari [Inde] ; Divya Gupta [Inde] ; Dhiviya Vedagiri [Inde] ; Krishnan Harinivas Harshan [Inde]Source :
- The Journal of general virology [ 1465-2099 ] ; 2020.
Descripteurs français
- KwdFr :
- Autophagie (génétique), Hepacivirus (génétique), Homologue de la protéine-1 associée à l'autophagie (génétique), Humains (MeSH), Hépatite C (génétique), Hépatite C (virologie), Lignée cellulaire tumorale (MeSH), Protéines et peptides de signalisation intracellulaire (génétique), Réplication virale (génétique), Sérine-thréonine kinases TOR (génétique), Transduction du signal (génétique), microARN (génétique).
- MESH :
- génétique : Autophagie, Hepacivirus, Homologue de la protéine-1 associée à l'autophagie, Hépatite C, Protéines et peptides de signalisation intracellulaire, Réplication virale, Sérine-thréonine kinases TOR, Transduction du signal, microARN.
- virologie : Hépatite C.
- Humains, Lignée cellulaire tumorale.
English descriptors
- KwdEn :
- Autophagy (genetics), Autophagy-Related Protein-1 Homolog (genetics), Cell Line, Tumor (MeSH), Hepacivirus (genetics), Hepatitis C (genetics), Hepatitis C (virology), Humans (MeSH), Intracellular Signaling Peptides and Proteins (genetics), MicroRNAs (genetics), Signal Transduction (genetics), TOR Serine-Threonine Kinases (genetics), Virus Replication (genetics).
- MESH :
- chemical , genetics : Autophagy-Related Protein-1 Homolog, Intracellular Signaling Peptides and Proteins, MicroRNAs, TOR Serine-Threonine Kinases.
- genetics : Autophagy, Hepacivirus, Hepatitis C, Signal Transduction, Virus Replication.
- virology : Hepatitis C.
- Cell Line, Tumor, Humans.
Abstract
The mechanistic target of rapamycin (mTOR), an important kinase that assimilates several upstream signals, associates into two functional complexes, mTORC1 and mTORC2. In this study, we demonstrate that HCV infection activates mTORC1 that functions in important antiviral response. Pharmacological inhibition of mTOR complexes augmented cellular HCV RNA levels, the observation confirmed further by Raptor depletion, indicating antiviral roles of mTORC1. ULK1 depletion phenocopied mTOR inhibition and thus suggested that mTORC1 restricts HCV replication through ULK1. We reveal that ULK1 depletion augmented the levels of miR-122, a critical host factor for HCV replication, thus possibly regulating HCV replication. The increase in HCV RNA levels, however, failed to augment intracellular infectious virion production, reflecting a lower rate of virion assembly. Higher intracellular HCV RNA levels, however, did not result in a corresponding increase in HCV RNA and infectious titres in mTOR inhibited supernatants, but in contrast showed a consistent drop, confirming defective viral assembly caused by the inhibition. Consistent with this, the mTOR activator caused a significant drop in HCV RNA levels both in infected cells and in the supernatant. Our results demonstrate that ULK1 depletion did not affect autophagy, suggesting that ULK1-mediated HCV regulation is autophagy independent. Together, our data demonstrate that mTORC1 functions to suppress HCV RNA replication, but facilitates the virion packaging and release. Our studies reveal that the activation of mTOR by HCV infection is an antiviral measure by the cells.
DOI: 10.1099/jgv.0.001356
PubMed: 31821132
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Kumar Johri</name><affiliation wicri:level="1"><nlm:affiliation>Academy of Scientific and Innovative Research (AcSIR), CSIR-CCMB Campus, Hyderabad, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Academy of Scientific and Innovative Research (AcSIR), CSIR-CCMB Campus, Hyderabad</wicri:regionArea><wicri:noRegion>Hyderabad</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-500007, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-500007</wicri:regionArea><wicri:noRegion>Hyderabad-500007</wicri:noRegion></affiliation></author><author><name sortKey="Lashkari, Hiren Vasantrai" sort="Lashkari, Hiren Vasantrai" uniqKey="Lashkari H" first="Hiren Vasantrai" last="Lashkari">Hiren Vasantrai Lashkari</name><affiliation wicri:level="1"><nlm:affiliation>CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-500007, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-500007</wicri:regionArea><wicri:noRegion>Hyderabad-500007</wicri:noRegion></affiliation></author><author><name sortKey="Gupta, Divya" sort="Gupta, Divya" uniqKey="Gupta D" first="Divya" last="Gupta">Divya Gupta</name><affiliation wicri:level="1"><nlm:affiliation>CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-500007, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-500007</wicri:regionArea><wicri:noRegion>Hyderabad-500007</wicri:noRegion></affiliation></author><author><name sortKey="Vedagiri, Dhiviya" sort="Vedagiri, Dhiviya" uniqKey="Vedagiri D" first="Dhiviya" last="Vedagiri">Dhiviya Vedagiri</name><affiliation wicri:level="1"><nlm:affiliation>Academy of Scientific and Innovative Research (AcSIR), CSIR-CCMB Campus, Hyderabad, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Academy of Scientific and Innovative Research (AcSIR), CSIR-CCMB Campus, Hyderabad</wicri:regionArea><wicri:noRegion>Hyderabad</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-500007, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-500007</wicri:regionArea><wicri:noRegion>Hyderabad-500007</wicri:noRegion></affiliation></author><author><name sortKey="Harshan, Krishnan Harinivas" sort="Harshan, Krishnan Harinivas" uniqKey="Harshan K" first="Krishnan Harinivas" last="Harshan">Krishnan Harinivas Harshan</name><affiliation wicri:level="1"><nlm:affiliation>CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-500007, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-500007</wicri:regionArea><wicri:noRegion>Hyderabad-500007</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Academy of Scientific and Innovative Research (AcSIR), CSIR-CCMB Campus, Hyderabad, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Academy of Scientific and Innovative Research (AcSIR), CSIR-CCMB Campus, Hyderabad</wicri:regionArea><wicri:noRegion>Hyderabad</wicri:noRegion></affiliation></author></analytic><series><title level="j">The Journal of general virology</title><idno type="eISSN">1465-2099</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Autophagy (genetics)</term><term>Autophagy-Related Protein-1 Homolog (genetics)</term><term>Cell Line, Tumor (MeSH)</term><term>Hepacivirus (genetics)</term><term>Hepatitis C (genetics)</term><term>Hepatitis C (virology)</term><term>Humans (MeSH)</term><term>Intracellular Signaling Peptides and Proteins (genetics)</term><term>MicroRNAs (genetics)</term><term>Signal Transduction (genetics)</term><term>TOR Serine-Threonine Kinases (genetics)</term><term>Virus Replication (genetics)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Autophagie (génétique)</term><term>Hepacivirus (génétique)</term><term>Homologue de la protéine-1 associée à l'autophagie (génétique)</term><term>Humains (MeSH)</term><term>Hépatite C (génétique)</term><term>Hépatite C (virologie)</term><term>Lignée cellulaire tumorale (MeSH)</term><term>Protéines et peptides de signalisation intracellulaire (génétique)</term><term>Réplication virale (génétique)</term><term>Sérine-thréonine kinases TOR (génétique)</term><term>Transduction du signal (génétique)</term><term>microARN (génétique)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Autophagy-Related Protein-1 Homolog</term><term>Intracellular Signaling Peptides and Proteins</term><term>MicroRNAs</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Autophagy</term><term>Hepacivirus</term><term>Hepatitis C</term><term>Signal Transduction</term><term>Virus Replication</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Autophagie</term><term>Hepacivirus</term><term>Homologue de la protéine-1 associée à l'autophagie</term><term>Hépatite C</term><term>Protéines et peptides de signalisation intracellulaire</term><term>Réplication virale</term><term>Sérine-thréonine kinases TOR</term><term>Transduction du signal</term><term>microARN</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Hépatite C</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Hepatitis C</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Humains</term><term>Lignée cellulaire tumorale</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The mechanistic target of rapamycin (mTOR), an important kinase that assimilates several upstream signals, associates into two functional complexes, mTORC1 and mTORC2. In this study, we demonstrate that HCV infection activates mTORC1 that functions in important antiviral response. Pharmacological inhibition of mTOR complexes augmented cellular HCV RNA levels, the observation confirmed further by Raptor depletion, indicating antiviral roles of mTORC1. ULK1 depletion phenocopied mTOR inhibition and thus suggested that mTORC1 restricts HCV replication through ULK1. We reveal that ULK1 depletion augmented the levels of miR-122, a critical host factor for HCV replication, thus possibly regulating HCV replication. The increase in HCV RNA levels, however, failed to augment intracellular infectious virion production, reflecting a lower rate of virion assembly. Higher intracellular HCV RNA levels, however, did not result in a corresponding increase in HCV RNA and infectious titres in mTOR inhibited supernatants, but in contrast showed a consistent drop, confirming defective viral assembly caused by the inhibition. Consistent with this, the mTOR activator caused a significant drop in HCV RNA levels both in infected cells and in the supernatant. Our results demonstrate that ULK1 depletion did not affect autophagy, suggesting that ULK1-mediated HCV regulation is autophagy independent. Together, our data demonstrate that mTORC1 functions to suppress HCV RNA replication, but facilitates the virion packaging and release. Our studies reveal that the activation of mTOR by HCV infection is an antiviral measure by the cells.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31821132</PMID><DateCompleted><Year>2020</Year><Month>08</Month><Day>05</Day></DateCompleted><DateRevised><Year>2020</Year><Month>08</Month><Day>05</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1465-2099</ISSN><JournalIssue CitedMedium="Internet"><Volume>101</Volume><Issue>1</Issue><PubDate><Year>2020</Year><Month>01</Month></PubDate></JournalIssue><Title>The Journal of general virology</Title><ISOAbbreviation>J Gen Virol</ISOAbbreviation></Journal><ArticleTitle>mTORC1 restricts hepatitis C virus RNA replication through ULK1-mediated suppression of miR-122 and facilitates post-replication events.</ArticleTitle><Pagination><MedlinePgn>86-95</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1099/jgv.0.001356</ELocationID><Abstract><AbstractText>The mechanistic target of rapamycin (mTOR), an important kinase that assimilates several upstream signals, associates into two functional complexes, mTORC1 and mTORC2. In this study, we demonstrate that HCV infection activates mTORC1 that functions in important antiviral response. Pharmacological inhibition of mTOR complexes augmented cellular HCV RNA levels, the observation confirmed further by Raptor depletion, indicating antiviral roles of mTORC1. ULK1 depletion phenocopied mTOR inhibition and thus suggested that mTORC1 restricts HCV replication through ULK1. We reveal that ULK1 depletion augmented the levels of miR-122, a critical host factor for HCV replication, thus possibly regulating HCV replication. The increase in HCV RNA levels, however, failed to augment intracellular infectious virion production, reflecting a lower rate of virion assembly. Higher intracellular HCV RNA levels, however, did not result in a corresponding increase in HCV RNA and infectious titres in mTOR inhibited supernatants, but in contrast showed a consistent drop, confirming defective viral assembly caused by the inhibition. Consistent with this, the mTOR activator caused a significant drop in HCV RNA levels both in infected cells and in the supernatant. Our results demonstrate that ULK1 depletion did not affect autophagy, suggesting that ULK1-mediated HCV regulation is autophagy independent. Together, our data demonstrate that mTORC1 functions to suppress HCV RNA replication, but facilitates the virion packaging and release. Our studies reveal that the activation of mTOR by HCV infection is an antiviral measure by the cells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Johri</LastName><ForeName>Manish Kumar</ForeName><Initials>MK</Initials><AffiliationInfo><Affiliation>Academy of Scientific and Innovative Research (AcSIR), CSIR-CCMB Campus, Hyderabad, India.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-500007, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lashkari</LastName><ForeName>Hiren Vasantrai</ForeName><Initials>HV</Initials><AffiliationInfo><Affiliation>CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-500007, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gupta</LastName><ForeName>Divya</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-500007, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vedagiri</LastName><ForeName>Dhiviya</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Academy of Scientific and Innovative Research (AcSIR), CSIR-CCMB Campus, Hyderabad, India.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-500007, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Harshan</LastName><ForeName>Krishnan Harinivas</ForeName><Initials>KH</Initials><AffiliationInfo><Affiliation>CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-500007, India.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Academy of Scientific and Innovative Research (AcSIR), CSIR-CCMB Campus, Hyderabad, India.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Gen Virol</MedlineTA><NlmUniqueID>0077340</NlmUniqueID><ISSNLinking>0022-1317</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D047908">Intracellular Signaling Peptides and Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C531907">MIRN122 microRNA, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D035683">MicroRNAs</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>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D000071189">Autophagy-Related Protein-1 Homolog</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="C484754">ULK1 protein, human</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000071189" MajorTopicYN="N">Autophagy-Related Protein-1 Homolog</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016174" MajorTopicYN="N">Hepacivirus</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006526" MajorTopicYN="N">Hepatitis C</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D047908" MajorTopicYN="N">Intracellular Signaling Peptides and Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D035683" MajorTopicYN="N">MicroRNAs</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Autophagy</Keyword><Keyword MajorTopicYN="Y">Hepatitis C virus</Keyword><Keyword MajorTopicYN="Y">Replication</Keyword><Keyword MajorTopicYN="Y">ULK1</Keyword><Keyword MajorTopicYN="Y">mTOR</Keyword><Keyword MajorTopicYN="Y">miR-122</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>12</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>8</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>12</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31821132</ArticleId><ArticleId IdType="doi">10.1099/jgv.0.001356</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Inde</li></country></list><tree><country name="Inde"><noRegion><name sortKey="Johri, Manish Kumar" sort="Johri, Manish Kumar" uniqKey="Johri M" first="Manish Kumar" last="Johri">Manish Kumar Johri</name></noRegion><name sortKey="Gupta, Divya" sort="Gupta, Divya" uniqKey="Gupta D" first="Divya" last="Gupta">Divya Gupta</name><name sortKey="Harshan, Krishnan Harinivas" sort="Harshan, Krishnan Harinivas" uniqKey="Harshan K" first="Krishnan Harinivas" last="Harshan">Krishnan Harinivas Harshan</name><name sortKey="Harshan, Krishnan Harinivas" sort="Harshan, Krishnan Harinivas" uniqKey="Harshan K" first="Krishnan Harinivas" last="Harshan">Krishnan Harinivas Harshan</name><name sortKey="Johri, Manish Kumar" sort="Johri, Manish Kumar" uniqKey="Johri M" first="Manish Kumar" last="Johri">Manish Kumar Johri</name><name sortKey="Lashkari, Hiren Vasantrai" sort="Lashkari, Hiren Vasantrai" uniqKey="Lashkari H" first="Hiren Vasantrai" last="Lashkari">Hiren Vasantrai Lashkari</name><name sortKey="Vedagiri, Dhiviya" sort="Vedagiri, Dhiviya" uniqKey="Vedagiri D" first="Dhiviya" last="Vedagiri">Dhiviya Vedagiri</name><name sortKey="Vedagiri, Dhiviya" sort="Vedagiri, Dhiviya" uniqKey="Vedagiri D" first="Dhiviya" last="Vedagiri">Dhiviya Vedagiri</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:31821132" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a RapamycinFungusV1
| This area was generated with Dilib version V0.6.38. |  |