ESAT6 inhibits autophagy flux and promotes BCG proliferation through MTOR.
Identifieur interne : 000B16 ( Main/Exploration ); précédent : 000B15; suivant : 000B17ESAT6 inhibits autophagy flux and promotes BCG proliferation through MTOR.
Auteurs : Hu Dong [République populaire de Chine] ; Wu Jing [République populaire de Chine] ; Zhao Runpeng [République populaire de Chine] ; Xu Xuewei [République populaire de Chine] ; Mu Min [République populaire de Chine] ; Cai Ru [République populaire de Chine] ; Xing Yingru [République populaire de Chine] ; Ni Shengfa [République populaire de Chine] ; Zhang Rongbo [République populaire de Chine]Source :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2016.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Antigènes bactériens (métabolisme), Autophagie (MeSH), Cellules RAW 264.7 (MeSH), Cellules cultivées (MeSH), Charge bactérienne (physiologie), Macrophages (cytologie), Macrophages (microbiologie), Macrophages (physiologie), Mycobacterium bovis (physiologie), Prolifération cellulaire (physiologie), Protéines bactériennes (métabolisme), Souris (MeSH), Survie cellulaire (physiologie), Sérine-thréonine kinases TOR (métabolisme).
- MESH :
- cytologie : Macrophages.
- microbiologie : Macrophages.
- métabolisme : Antigènes bactériens, Protéines bactériennes, Sérine-thréonine kinases TOR.
- physiologie : Charge bactérienne, Macrophages, Mycobacterium bovis, Prolifération cellulaire, Survie cellulaire.
- Animaux, Autophagie, Cellules RAW 264.7, Cellules cultivées, Souris.
English descriptors
- KwdEn :
- Animals (MeSH), Antigens, Bacterial (metabolism), Autophagy (MeSH), Bacterial Load (physiology), Bacterial Proteins (metabolism), Cell Proliferation (physiology), Cell Survival (physiology), Cells, Cultured (MeSH), Macrophages (cytology), Macrophages (microbiology), Macrophages (physiology), Mice (MeSH), Mycobacterium bovis (physiology), RAW 264.7 Cells (MeSH), TOR Serine-Threonine Kinases (metabolism).
- MESH :
- chemical , metabolism : Antigens, Bacterial, Bacterial Proteins, TOR Serine-Threonine Kinases.
- cytology : Macrophages.
- microbiology : Macrophages.
- physiology : Bacterial Load, Cell Proliferation, Cell Survival, Macrophages, Mycobacterium bovis.
- Animals, Autophagy, Cells, Cultured, Mice, RAW 264.7 Cells.
Abstract
In recent years, increasing studies have found that pathogenic Mycobacterium tuberculosis (Mtb) inhibits autophagy, which mediates the anti-mycobacterial response, but the mechanism is not clear. We previously reported that secretory acid phosphatase (SapM) of Mtb can negatively regulate autophagy flux. Recently, another virulence factor of Mtb, early secretory antigenic target 6 (ESAT6), has been found to be involved in inhibiting autophagy, but the mechanism remains unclear. In this study, we show that ESAT6 hampers autophagy flux to boost bacillus Calmette-Guerin (BCG) proliferation and reveals a mechanism by which ESAT6 blocks autophagosome-lysosome fusion in a mammalian target of rapamycin (MTOR)-dependent manner. In both Raw264.7 cells and primary macrophages derived from the murine abdominal cavity (ACM), ESAT6 repressed autophagy flux by interfering with the autophagosome-lysosome fusion, which resulted in an increased load of BCG. Impaired degradation of LC3Ⅱ and SQSTM1 by ESAT6 was related to the upregulated activity of MTOR. Contrarily, inhibiting MTOR with Torin1 removed the ESAT6-induced autophagy block and lysosome dysfunction. Furthermore, in both Raw264.7 and ACM cells, MTOR inhibition significantly suppressed the survival of BCG. In conclusion, our study highlights how ESAT6 blocks autophagy and promotes BCG survival in a way that activates MTOR.
DOI: 10.1016/j.bbrc.2016.06.042
PubMed: 27317487
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Medical Inspection Center, Anhui University of Science and Technology, Huainan, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China; Medical Inspection Center, Anhui University of Science and Technology, Huainan</wicri:regionArea><wicri:noRegion>Huainan</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27317487</idno><idno type="pmid">27317487</idno><idno type="doi">10.1016/j.bbrc.2016.06.042</idno><idno type="wicri:Area/Main/Corpus">000A27</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000A27</idno><idno type="wicri:Area/Main/Curation">000A27</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000A27</idno><idno type="wicri:Area/Main/Exploration">000A27</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">ESAT6 inhibits autophagy flux and promotes BCG proliferation through MTOR.</title><author><name sortKey="Dong, Hu" sort="Dong, Hu" uniqKey="Dong H" first="Hu" last="Dong">Hu Dong</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China; Medical Inspection Center, Anhui University of Science and Technology, Huainan, China. 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Electronic address: wujing8008@126.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China; Medical Inspection Center, Anhui University of Science and Technology, Huainan</wicri:regionArea><wicri:noRegion>Huainan</wicri:noRegion></affiliation></author><author><name sortKey="Runpeng, Zhao" sort="Runpeng, Zhao" uniqKey="Runpeng Z" first="Zhao" last="Runpeng">Zhao Runpeng</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medical Immunology, Medical School, Anhui University of Science and Technology</wicri:regionArea><wicri:noRegion>Anhui University of Science and Technology</wicri:noRegion></affiliation></author><author><name sortKey="Xuewei, Xu" sort="Xuewei, Xu" uniqKey="Xuewei X" first="Xu" last="Xuewei">Xu Xuewei</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medical Immunology, Medical School, Anhui University of Science and Technology</wicri:regionArea><wicri:noRegion>Anhui University of Science and Technology</wicri:noRegion></affiliation></author><author><name sortKey="Min, Mu" sort="Min, Mu" uniqKey="Min M" first="Mu" last="Min">Mu Min</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medical Immunology, Medical School, Anhui University of Science and Technology</wicri:regionArea><wicri:noRegion>Anhui University of Science and Technology</wicri:noRegion></affiliation></author><author><name sortKey="Ru, Cai" sort="Ru, Cai" uniqKey="Ru C" first="Cai" last="Ru">Cai Ru</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medical Immunology, Medical School, Anhui University of Science and Technology</wicri:regionArea><wicri:noRegion>Anhui University of Science and Technology</wicri:noRegion></affiliation></author><author><name sortKey="Yingru, Xing" sort="Yingru, Xing" uniqKey="Yingru X" first="Xing" last="Yingru">Xing Yingru</name><affiliation wicri:level="1"><nlm:affiliation>Affiliated Cancer Hospital, Anhui University of Science and Technology, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Affiliated Cancer Hospital, Anhui University of Science and Technology</wicri:regionArea><wicri:noRegion>Anhui University of Science and Technology</wicri:noRegion></affiliation></author><author><name sortKey="Shengfa, Ni" sort="Shengfa, Ni" uniqKey="Shengfa N" first="Ni" last="Shengfa">Ni Shengfa</name><affiliation wicri:level="1"><nlm:affiliation>Affiliated Cancer Hospital, Anhui University of Science and Technology, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Affiliated Cancer Hospital, Anhui University of Science and Technology</wicri:regionArea><wicri:noRegion>Anhui University of Science and Technology</wicri:noRegion></affiliation></author><author><name sortKey="Rongbo, Zhang" sort="Rongbo, Zhang" uniqKey="Rongbo Z" first="Zhang" last="Rongbo">Zhang Rongbo</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China; Medical Inspection Center, Anhui University of Science and Technology, Huainan, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China; Medical Inspection Center, Anhui University of Science and Technology, Huainan</wicri:regionArea><wicri:noRegion>Huainan</wicri:noRegion></affiliation></author></analytic><series><title level="j">Biochemical and biophysical research communications</title><idno type="eISSN">1090-2104</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>Antigens, Bacterial (metabolism)</term><term>Autophagy (MeSH)</term><term>Bacterial Load (physiology)</term><term>Bacterial Proteins (metabolism)</term><term>Cell Proliferation (physiology)</term><term>Cell Survival (physiology)</term><term>Cells, Cultured (MeSH)</term><term>Macrophages (cytology)</term><term>Macrophages (microbiology)</term><term>Macrophages (physiology)</term><term>Mice (MeSH)</term><term>Mycobacterium bovis (physiology)</term><term>RAW 264.7 Cells (MeSH)</term><term>TOR Serine-Threonine Kinases (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Antigènes bactériens (métabolisme)</term><term>Autophagie (MeSH)</term><term>Cellules RAW 264.7 (MeSH)</term><term>Cellules cultivées (MeSH)</term><term>Charge bactérienne (physiologie)</term><term>Macrophages (cytologie)</term><term>Macrophages (microbiologie)</term><term>Macrophages (physiologie)</term><term>Mycobacterium bovis (physiologie)</term><term>Prolifération cellulaire (physiologie)</term><term>Protéines bactériennes (métabolisme)</term><term>Souris (MeSH)</term><term>Survie cellulaire (physiologie)</term><term>Sérine-thréonine kinases TOR (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antigens, Bacterial</term><term>Bacterial Proteins</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antigènes bactériens</term><term>Protéines bactériennes</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Charge bactérienne</term><term>Macrophages</term><term>Mycobacterium bovis</term><term>Prolifération cellulaire</term><term>Survie cellulaire</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Bacterial Load</term><term>Cell Proliferation</term><term>Cell Survival</term><term>Macrophages</term><term>Mycobacterium bovis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Autophagy</term><term>Cells, Cultured</term><term>Mice</term><term>RAW 264.7 Cells</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Autophagie</term><term>Cellules RAW 264.7</term><term>Cellules cultivées</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In recent years, increasing studies have found that pathogenic Mycobacterium tuberculosis (Mtb) inhibits autophagy, which mediates the anti-mycobacterial response, but the mechanism is not clear. We previously reported that secretory acid phosphatase (SapM) of Mtb can negatively regulate autophagy flux. Recently, another virulence factor of Mtb, early secretory antigenic target 6 (ESAT6), has been found to be involved in inhibiting autophagy, but the mechanism remains unclear. In this study, we show that ESAT6 hampers autophagy flux to boost bacillus Calmette-Guerin (BCG) proliferation and reveals a mechanism by which ESAT6 blocks autophagosome-lysosome fusion in a mammalian target of rapamycin (MTOR)-dependent manner. In both Raw264.7 cells and primary macrophages derived from the murine abdominal cavity (ACM), ESAT6 repressed autophagy flux by interfering with the autophagosome-lysosome fusion, which resulted in an increased load of BCG. Impaired degradation of LC3Ⅱ and SQSTM1 by ESAT6 was related to the upregulated activity of MTOR. Contrarily, inhibiting MTOR with Torin1 removed the ESAT6-induced autophagy block and lysosome dysfunction. Furthermore, in both Raw264.7 and ACM cells, MTOR inhibition significantly suppressed the survival of BCG. In conclusion, our study highlights how ESAT6 blocks autophagy and promotes BCG survival in a way that activates MTOR.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27317487</PMID><DateCompleted><Year>2017</Year><Month>06</Month><Day>19</Day></DateCompleted><DateRevised><Year>2017</Year><Month>11</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2104</ISSN><JournalIssue CitedMedium="Internet"><Volume>477</Volume><Issue>2</Issue><PubDate><Year>2016</Year><Month>08</Month><Day>19</Day></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem Biophys Res Commun</ISOAbbreviation></Journal><ArticleTitle>ESAT6 inhibits autophagy flux and promotes BCG proliferation through MTOR.</ArticleTitle><Pagination><MedlinePgn>195-201</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbrc.2016.06.042</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0006-291X(16)30960-3</ELocationID><Abstract><AbstractText>In recent years, increasing studies have found that pathogenic Mycobacterium tuberculosis (Mtb) inhibits autophagy, which mediates the anti-mycobacterial response, but the mechanism is not clear. We previously reported that secretory acid phosphatase (SapM) of Mtb can negatively regulate autophagy flux. Recently, another virulence factor of Mtb, early secretory antigenic target 6 (ESAT6), has been found to be involved in inhibiting autophagy, but the mechanism remains unclear. In this study, we show that ESAT6 hampers autophagy flux to boost bacillus Calmette-Guerin (BCG) proliferation and reveals a mechanism by which ESAT6 blocks autophagosome-lysosome fusion in a mammalian target of rapamycin (MTOR)-dependent manner. In both Raw264.7 cells and primary macrophages derived from the murine abdominal cavity (ACM), ESAT6 repressed autophagy flux by interfering with the autophagosome-lysosome fusion, which resulted in an increased load of BCG. Impaired degradation of LC3Ⅱ and SQSTM1 by ESAT6 was related to the upregulated activity of MTOR. Contrarily, inhibiting MTOR with Torin1 removed the ESAT6-induced autophagy block and lysosome dysfunction. Furthermore, in both Raw264.7 and ACM cells, MTOR inhibition significantly suppressed the survival of BCG. In conclusion, our study highlights how ESAT6 blocks autophagy and promotes BCG survival in a way that activates MTOR.</AbstractText><CopyrightInformation>Copyright © 2016 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dong</LastName><ForeName>Hu</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China; Medical Inspection Center, Anhui University of Science and Technology, Huainan, China. Electronic address: austhudong@126.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jing</LastName><ForeName>Wu</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China; Medical Inspection Center, Anhui University of Science and Technology, Huainan, China. Electronic address: wujing8008@126.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Runpeng</LastName><ForeName>Zhao</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xuewei</LastName><ForeName>Xu</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Min</LastName><ForeName>Mu</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ru</LastName><ForeName>Cai</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yingru</LastName><ForeName>Xing</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Affiliated Cancer Hospital, Anhui University of Science and Technology, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shengfa</LastName><ForeName>Ni</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Affiliated Cancer Hospital, Anhui University of Science and Technology, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rongbo</LastName><ForeName>Zhang</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Medical Immunology, Medical School, Anhui University of Science and Technology, China; Medical Inspection Center, Anhui University of Science and Technology, Huainan, China.</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><ArticleDate DateType="Electronic"><Year>2016</Year><Month>06</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Biochem Biophys Res Commun</MedlineTA><NlmUniqueID>0372516</NlmUniqueID><ISSNLinking>0006-291X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000942">Antigens, Bacterial</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001426">Bacterial Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C093276">ESAT-6 protein, Mycobacterium tuberculosis</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000942" MajorTopicYN="N">Antigens, Bacterial</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058491" MajorTopicYN="N">Bacterial Load</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001426" MajorTopicYN="N">Bacterial Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009163" MajorTopicYN="N">Mycobacterium bovis</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000067996" MajorTopicYN="N">RAW 264.7 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Autophagy</Keyword><Keyword MajorTopicYN="Y">Early secretory antigenic target 6</Keyword><Keyword MajorTopicYN="Y">Lysosome</Keyword><Keyword MajorTopicYN="Y">Macrophage</Keyword><Keyword MajorTopicYN="Y">Mammalian target of rapamycin</Keyword><Keyword MajorTopicYN="Y">Mycobacterium tuberculosis</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>06</Month><Day>03</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>06</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>6</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>6</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>6</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27317487</ArticleId><ArticleId IdType="pii">S0006-291X(16)30960-3</ArticleId><ArticleId IdType="doi">10.1016/j.bbrc.2016.06.042</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Dong, Hu" sort="Dong, Hu" uniqKey="Dong H" first="Hu" last="Dong">Hu Dong</name></noRegion><name sortKey="Jing, Wu" sort="Jing, Wu" uniqKey="Jing W" first="Wu" last="Jing">Wu Jing</name><name sortKey="Min, Mu" sort="Min, Mu" uniqKey="Min M" first="Mu" last="Min">Mu Min</name><name sortKey="Rongbo, Zhang" sort="Rongbo, Zhang" uniqKey="Rongbo Z" first="Zhang" last="Rongbo">Zhang Rongbo</name><name sortKey="Ru, Cai" sort="Ru, Cai" uniqKey="Ru C" first="Cai" last="Ru">Cai Ru</name><name sortKey="Runpeng, Zhao" sort="Runpeng, Zhao" uniqKey="Runpeng Z" first="Zhao" last="Runpeng">Zhao Runpeng</name><name sortKey="Shengfa, Ni" sort="Shengfa, Ni" uniqKey="Shengfa N" first="Ni" last="Shengfa">Ni Shengfa</name><name sortKey="Xuewei, Xu" sort="Xuewei, Xu" uniqKey="Xuewei X" first="Xu" last="Xuewei">Xu Xuewei</name><name sortKey="Yingru, Xing" sort="Yingru, Xing" uniqKey="Yingru X" first="Xing" last="Yingru">Xing Yingru</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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