Inhibition of autophagy ameliorates acute lung injury caused by avian influenza A H5N1 infection.
Identifieur interne : 001185 ( Main/Corpus ); précédent : 001184; suivant : 001186Inhibition of autophagy ameliorates acute lung injury caused by avian influenza A H5N1 infection.
Auteurs : Yang Sun ; Chenggang Li ; Yuelong Shu ; Xiangwu Ju ; Zhen Zou ; Hongliang Wang ; Shuan Rao ; Feng Guo ; Haolin Liu ; Wenlong Nan ; Yan Zhao ; Yiwu Yan ; Jun Tang ; Chen Zhao ; Peng Yang ; Kangtai Liu ; Shunxin Wang ; Huijun Lu ; Xiao Li ; Lei Tan ; Rongbao Gao ; Jingdong Song ; Xiang Gao ; Xinlun Tian ; Yingzhi Qin ; Kai-Feng Xu ; Dangsheng Li ; Ningyi Jin ; Chengyu JiangSource :
- Science signaling [ 1937-9145 ] ; 2012.
English descriptors
- KwdEn :
- Analysis of Variance (MeSH), Animals (MeSH), Autophagy (drug effects), Autophagy (physiology), Autophagy-Related Protein 5 (MeSH), Blotting, Western (MeSH), Cell Line (MeSH), DNA Primers (genetics), Epithelial Cells (physiology), Gene Knockdown Techniques (MeSH), Hemagglutinin Glycoproteins, Influenza Virus (administration & dosage), Hemagglutinin Glycoproteins, Influenza Virus (pharmacology), Humans (MeSH), Influenza A Virus, H5N1 Subtype (MeSH), Influenza, Human (pathology), Lung (ultrastructure), Lung (virology), Mice (MeSH), Mice, Inbred BALB C (MeSH), Microscopy, Electron (MeSH), Microtubule-Associated Proteins (genetics), Oncogene Protein v-akt (metabolism), Phagosomes (pathology), Real-Time Polymerase Chain Reaction (MeSH), Signal Transduction (physiology), TOR Serine-Threonine Kinases (metabolism), Tuberous Sclerosis Complex 2 Protein (MeSH), Tumor Suppressor Proteins (metabolism).
- MESH :
- chemical , administration & dosage : Hemagglutinin Glycoproteins, Influenza Virus.
- chemical , genetics : DNA Primers, Microtubule-Associated Proteins.
- chemical , metabolism : Oncogene Protein v-akt, TOR Serine-Threonine Kinases, Tumor Suppressor Proteins.
- chemical , pharmacology : Hemagglutinin Glycoproteins, Influenza Virus.
- chemical : Autophagy-Related Protein 5, Tuberous Sclerosis Complex 2 Protein.
- drug effects : Autophagy.
- pathology : Influenza, Human, Phagosomes.
- physiology : Autophagy, Epithelial Cells, Signal Transduction.
- ultrastructure : Lung.
- virology : Lung.
- Analysis of Variance, Animals, Blotting, Western, Cell Line, Gene Knockdown Techniques, Humans, Influenza A Virus, H5N1 Subtype, Mice, Mice, Inbred BALB C, Microscopy, Electron, Real-Time Polymerase Chain Reaction.
Abstract
The threat of a new influenza pandemic has existed since 1997, when the highly pathogenic H5N1 strain of avian influenza A virus infected humans in Hong Kong and spread across Asia, where it continued to infect poultry and people. The human mortality rate of H5N1 infection is about 60%, whereas that of seasonal H1N1 infection is less than 0.1%. The high mortality rate associated with H5N1 infection is predominantly a result of respiratory failure caused by acute lung injury; however, how viral infection contributes to this disease pathology is unclear. Here, we used electron microscopy to show the accumulation of autophagosomes in H5N1-infected lungs from a human cadaver and mice, as well as in infected A549 human epithelial lung cells. We also showed that H5N1, but not seasonal H1N1, induced autophagic cell death in alveolar epithelial cells through a pathway involving the kinase Akt, the tumor suppressor protein TSC2, and the mammalian target of rapamycin. Additionally, we suggest that the hemagglutinin protein of H5N1 may be responsible for stimulating autophagy. When applied prophylactically, reagents that blocked virus-induced autophagic signaling substantially increased the survival rate of mice and substantially ameliorated the acute lung injury and mortality caused by H5N1 infection. We conclude that the autophagic cell death of alveolar epithelial cells likely plays a crucial role in the high mortality rate of H5N1 infection, and we suggest that autophagy-blocking agents might be useful as prophylactics and therapeutics against infection of humans by the H5N1 virus.
DOI: 10.1126/scisignal.2001931
PubMed: 22355189
Links to Exploration step
pubmed:22355189Le document en format XML
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China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Chenggang" sort="Li, Chenggang" uniqKey="Li C" first="Chenggang" last="Li">Chenggang Li</name></author><author><name sortKey="Shu, Yuelong" sort="Shu, Yuelong" uniqKey="Shu Y" first="Yuelong" last="Shu">Yuelong Shu</name></author><author><name sortKey="Ju, Xiangwu" sort="Ju, Xiangwu" uniqKey="Ju X" first="Xiangwu" last="Ju">Xiangwu Ju</name></author><author><name sortKey="Zou, Zhen" sort="Zou, Zhen" uniqKey="Zou Z" first="Zhen" last="Zou">Zhen Zou</name></author><author><name sortKey="Wang, Hongliang" sort="Wang, Hongliang" uniqKey="Wang H" first="Hongliang" last="Wang">Hongliang Wang</name></author><author><name sortKey="Rao, Shuan" sort="Rao, Shuan" uniqKey="Rao S" first="Shuan" last="Rao">Shuan Rao</name></author><author><name sortKey="Guo, Feng" sort="Guo, Feng" uniqKey="Guo F" first="Feng" last="Guo">Feng Guo</name></author><author><name sortKey="Liu, Haolin" sort="Liu, Haolin" uniqKey="Liu H" first="Haolin" last="Liu">Haolin Liu</name></author><author><name sortKey="Nan, Wenlong" sort="Nan, Wenlong" uniqKey="Nan W" first="Wenlong" last="Nan">Wenlong Nan</name></author><author><name sortKey="Zhao, Yan" sort="Zhao, Yan" uniqKey="Zhao Y" first="Yan" last="Zhao">Yan Zhao</name></author><author><name sortKey="Yan, Yiwu" sort="Yan, Yiwu" uniqKey="Yan Y" first="Yiwu" last="Yan">Yiwu Yan</name></author><author><name sortKey="Tang, Jun" sort="Tang, Jun" uniqKey="Tang J" first="Jun" last="Tang">Jun Tang</name></author><author><name sortKey="Zhao, Chen" sort="Zhao, Chen" uniqKey="Zhao C" first="Chen" last="Zhao">Chen Zhao</name></author><author><name sortKey="Yang, Peng" sort="Yang, Peng" uniqKey="Yang P" first="Peng" last="Yang">Peng Yang</name></author><author><name sortKey="Liu, Kangtai" sort="Liu, Kangtai" uniqKey="Liu K" first="Kangtai" last="Liu">Kangtai Liu</name></author><author><name sortKey="Wang, Shunxin" sort="Wang, Shunxin" uniqKey="Wang S" first="Shunxin" last="Wang">Shunxin Wang</name></author><author><name sortKey="Lu, Huijun" sort="Lu, Huijun" uniqKey="Lu H" first="Huijun" last="Lu">Huijun Lu</name></author><author><name sortKey="Li, Xiao" sort="Li, Xiao" uniqKey="Li X" first="Xiao" last="Li">Xiao Li</name></author><author><name sortKey="Tan, Lei" sort="Tan, Lei" uniqKey="Tan L" first="Lei" last="Tan">Lei Tan</name></author><author><name sortKey="Gao, Rongbao" sort="Gao, Rongbao" uniqKey="Gao R" first="Rongbao" last="Gao">Rongbao Gao</name></author><author><name sortKey="Song, Jingdong" sort="Song, Jingdong" uniqKey="Song J" first="Jingdong" last="Song">Jingdong Song</name></author><author><name sortKey="Gao, Xiang" sort="Gao, Xiang" uniqKey="Gao X" first="Xiang" last="Gao">Xiang Gao</name></author><author><name sortKey="Tian, Xinlun" sort="Tian, Xinlun" uniqKey="Tian X" first="Xinlun" last="Tian">Xinlun Tian</name></author><author><name sortKey="Qin, Yingzhi" sort="Qin, Yingzhi" uniqKey="Qin Y" first="Yingzhi" last="Qin">Yingzhi Qin</name></author><author><name sortKey="Xu, Kai Feng" sort="Xu, Kai Feng" uniqKey="Xu K" first="Kai-Feng" last="Xu">Kai-Feng Xu</name></author><author><name sortKey="Li, Dangsheng" sort="Li, Dangsheng" uniqKey="Li D" first="Dangsheng" last="Li">Dangsheng Li</name></author><author><name sortKey="Jin, Ningyi" sort="Jin, Ningyi" uniqKey="Jin N" first="Ningyi" last="Jin">Ningyi Jin</name></author><author><name sortKey="Jiang, Chengyu" sort="Jiang, Chengyu" uniqKey="Jiang C" first="Chengyu" last="Jiang">Chengyu Jiang</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="RBID">pubmed:22355189</idno><idno type="pmid">22355189</idno><idno type="doi">10.1126/scisignal.2001931</idno><idno type="wicri:Area/Main/Corpus">001185</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">001185</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Inhibition of autophagy ameliorates acute lung injury caused by avian influenza A H5N1 infection.</title><author><name sortKey="Sun, Yang" sort="Sun, Yang" uniqKey="Sun Y" first="Yang" last="Sun">Yang Sun</name><affiliation><nlm:affiliation>State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Tsinghua University, Beijing 100005, P. R. China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Chenggang" sort="Li, Chenggang" uniqKey="Li C" first="Chenggang" last="Li">Chenggang Li</name></author><author><name sortKey="Shu, Yuelong" sort="Shu, Yuelong" uniqKey="Shu Y" first="Yuelong" last="Shu">Yuelong Shu</name></author><author><name sortKey="Ju, Xiangwu" sort="Ju, Xiangwu" uniqKey="Ju X" first="Xiangwu" last="Ju">Xiangwu Ju</name></author><author><name sortKey="Zou, Zhen" sort="Zou, Zhen" uniqKey="Zou Z" first="Zhen" last="Zou">Zhen Zou</name></author><author><name sortKey="Wang, Hongliang" sort="Wang, Hongliang" uniqKey="Wang H" first="Hongliang" last="Wang">Hongliang Wang</name></author><author><name sortKey="Rao, Shuan" sort="Rao, Shuan" uniqKey="Rao S" first="Shuan" last="Rao">Shuan Rao</name></author><author><name sortKey="Guo, Feng" sort="Guo, Feng" uniqKey="Guo F" first="Feng" last="Guo">Feng Guo</name></author><author><name sortKey="Liu, Haolin" sort="Liu, Haolin" uniqKey="Liu H" first="Haolin" last="Liu">Haolin Liu</name></author><author><name sortKey="Nan, Wenlong" sort="Nan, Wenlong" uniqKey="Nan W" first="Wenlong" last="Nan">Wenlong Nan</name></author><author><name sortKey="Zhao, Yan" sort="Zhao, Yan" uniqKey="Zhao Y" first="Yan" last="Zhao">Yan Zhao</name></author><author><name sortKey="Yan, Yiwu" sort="Yan, Yiwu" uniqKey="Yan Y" first="Yiwu" last="Yan">Yiwu Yan</name></author><author><name sortKey="Tang, Jun" sort="Tang, Jun" uniqKey="Tang J" first="Jun" last="Tang">Jun Tang</name></author><author><name sortKey="Zhao, Chen" sort="Zhao, Chen" uniqKey="Zhao C" first="Chen" last="Zhao">Chen Zhao</name></author><author><name sortKey="Yang, Peng" sort="Yang, Peng" uniqKey="Yang P" first="Peng" last="Yang">Peng Yang</name></author><author><name sortKey="Liu, Kangtai" sort="Liu, Kangtai" uniqKey="Liu K" first="Kangtai" last="Liu">Kangtai Liu</name></author><author><name sortKey="Wang, Shunxin" sort="Wang, Shunxin" uniqKey="Wang S" first="Shunxin" last="Wang">Shunxin Wang</name></author><author><name sortKey="Lu, Huijun" sort="Lu, Huijun" uniqKey="Lu H" first="Huijun" last="Lu">Huijun Lu</name></author><author><name sortKey="Li, Xiao" sort="Li, Xiao" uniqKey="Li X" first="Xiao" last="Li">Xiao Li</name></author><author><name sortKey="Tan, Lei" sort="Tan, Lei" uniqKey="Tan L" first="Lei" last="Tan">Lei Tan</name></author><author><name sortKey="Gao, Rongbao" sort="Gao, Rongbao" uniqKey="Gao R" first="Rongbao" last="Gao">Rongbao Gao</name></author><author><name sortKey="Song, Jingdong" sort="Song, Jingdong" uniqKey="Song J" first="Jingdong" last="Song">Jingdong Song</name></author><author><name sortKey="Gao, Xiang" sort="Gao, Xiang" uniqKey="Gao X" first="Xiang" last="Gao">Xiang Gao</name></author><author><name sortKey="Tian, Xinlun" sort="Tian, Xinlun" uniqKey="Tian X" first="Xinlun" last="Tian">Xinlun Tian</name></author><author><name sortKey="Qin, Yingzhi" sort="Qin, Yingzhi" uniqKey="Qin Y" first="Yingzhi" last="Qin">Yingzhi Qin</name></author><author><name sortKey="Xu, Kai Feng" sort="Xu, Kai Feng" uniqKey="Xu K" first="Kai-Feng" last="Xu">Kai-Feng Xu</name></author><author><name sortKey="Li, Dangsheng" sort="Li, Dangsheng" uniqKey="Li D" first="Dangsheng" last="Li">Dangsheng Li</name></author><author><name sortKey="Jin, Ningyi" sort="Jin, Ningyi" uniqKey="Jin N" first="Ningyi" last="Jin">Ningyi Jin</name></author><author><name sortKey="Jiang, Chengyu" sort="Jiang, Chengyu" uniqKey="Jiang C" first="Chengyu" last="Jiang">Chengyu Jiang</name></author></analytic><series><title level="j">Science signaling</title><idno type="eISSN">1937-9145</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Analysis of Variance (MeSH)</term><term>Animals (MeSH)</term><term>Autophagy (drug effects)</term><term>Autophagy (physiology)</term><term>Autophagy-Related Protein 5 (MeSH)</term><term>Blotting, Western (MeSH)</term><term>Cell Line (MeSH)</term><term>DNA Primers (genetics)</term><term>Epithelial Cells (physiology)</term><term>Gene Knockdown Techniques (MeSH)</term><term>Hemagglutinin Glycoproteins, Influenza Virus (administration & dosage)</term><term>Hemagglutinin Glycoproteins, Influenza Virus (pharmacology)</term><term>Humans (MeSH)</term><term>Influenza A Virus, H5N1 Subtype (MeSH)</term><term>Influenza, Human (pathology)</term><term>Lung (ultrastructure)</term><term>Lung (virology)</term><term>Mice (MeSH)</term><term>Mice, Inbred BALB C (MeSH)</term><term>Microscopy, Electron (MeSH)</term><term>Microtubule-Associated Proteins (genetics)</term><term>Oncogene Protein v-akt (metabolism)</term><term>Phagosomes (pathology)</term><term>Real-Time Polymerase Chain Reaction (MeSH)</term><term>Signal Transduction (physiology)</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>Tuberous Sclerosis Complex 2 Protein (MeSH)</term><term>Tumor Suppressor Proteins (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Hemagglutinin Glycoproteins, Influenza Virus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA Primers</term><term>Microtubule-Associated Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Oncogene Protein v-akt</term><term>TOR Serine-Threonine Kinases</term><term>Tumor Suppressor Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Hemagglutinin Glycoproteins, Influenza Virus</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Autophagy-Related Protein 5</term><term>Tuberous Sclerosis Complex 2 Protein</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Influenza, Human</term><term>Phagosomes</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Autophagy</term><term>Epithelial Cells</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Analysis of Variance</term><term>Animals</term><term>Blotting, Western</term><term>Cell Line</term><term>Gene Knockdown Techniques</term><term>Humans</term><term>Influenza A Virus, H5N1 Subtype</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Microscopy, Electron</term><term>Real-Time Polymerase Chain Reaction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The threat of a new influenza pandemic has existed since 1997, when the highly pathogenic H5N1 strain of avian influenza A virus infected humans in Hong Kong and spread across Asia, where it continued to infect poultry and people. The human mortality rate of H5N1 infection is about 60%, whereas that of seasonal H1N1 infection is less than 0.1%. The high mortality rate associated with H5N1 infection is predominantly a result of respiratory failure caused by acute lung injury; however, how viral infection contributes to this disease pathology is unclear. Here, we used electron microscopy to show the accumulation of autophagosomes in H5N1-infected lungs from a human cadaver and mice, as well as in infected A549 human epithelial lung cells. We also showed that H5N1, but not seasonal H1N1, induced autophagic cell death in alveolar epithelial cells through a pathway involving the kinase Akt, the tumor suppressor protein TSC2, and the mammalian target of rapamycin. Additionally, we suggest that the hemagglutinin protein of H5N1 may be responsible for stimulating autophagy. When applied prophylactically, reagents that blocked virus-induced autophagic signaling substantially increased the survival rate of mice and substantially ameliorated the acute lung injury and mortality caused by H5N1 infection. We conclude that the autophagic cell death of alveolar epithelial cells likely plays a crucial role in the high mortality rate of H5N1 infection, and we suggest that autophagy-blocking agents might be useful as prophylactics and therapeutics against infection of humans by the H5N1 virus.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22355189</PMID><DateCompleted><Year>2012</Year><Month>06</Month><Day>15</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>01</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1937-9145</ISSN><JournalIssue CitedMedium="Internet"><Volume>5</Volume><Issue>212</Issue><PubDate><Year>2012</Year><Month>Feb</Month><Day>21</Day></PubDate></JournalIssue><Title>Science signaling</Title><ISOAbbreviation>Sci Signal</ISOAbbreviation></Journal><ArticleTitle>Inhibition of autophagy ameliorates acute lung injury caused by avian influenza A H5N1 infection.</ArticleTitle><Pagination><MedlinePgn>ra16</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1126/scisignal.2001931</ELocationID><Abstract><AbstractText>The threat of a new influenza pandemic has existed since 1997, when the highly pathogenic H5N1 strain of avian influenza A virus infected humans in Hong Kong and spread across Asia, where it continued to infect poultry and people. The human mortality rate of H5N1 infection is about 60%, whereas that of seasonal H1N1 infection is less than 0.1%. The high mortality rate associated with H5N1 infection is predominantly a result of respiratory failure caused by acute lung injury; however, how viral infection contributes to this disease pathology is unclear. Here, we used electron microscopy to show the accumulation of autophagosomes in H5N1-infected lungs from a human cadaver and mice, as well as in infected A549 human epithelial lung cells. We also showed that H5N1, but not seasonal H1N1, induced autophagic cell death in alveolar epithelial cells through a pathway involving the kinase Akt, the tumor suppressor protein TSC2, and the mammalian target of rapamycin. Additionally, we suggest that the hemagglutinin protein of H5N1 may be responsible for stimulating autophagy. When applied prophylactically, reagents that blocked virus-induced autophagic signaling substantially increased the survival rate of mice and substantially ameliorated the acute lung injury and mortality caused by H5N1 infection. We conclude that the autophagic cell death of alveolar epithelial cells likely plays a crucial role in the high mortality rate of H5N1 infection, and we suggest that autophagy-blocking agents might be useful as prophylactics and therapeutics against infection of humans by the H5N1 virus.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Yang</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Tsinghua University, Beijing 100005, P. R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Chenggang</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Shu</LastName><ForeName>Yuelong</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Ju</LastName><ForeName>Xiangwu</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Zou</LastName><ForeName>Zhen</ForeName><Initials>Z</Initials></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Hongliang</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Rao</LastName><ForeName>Shuan</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Feng</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Haolin</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Nan</LastName><ForeName>Wenlong</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Yan</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Yiwu</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Tang</LastName><ForeName>Jun</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Chen</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Peng</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Kangtai</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Shunxin</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Huijun</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Xiao</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Tan</LastName><ForeName>Lei</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Gao</LastName><ForeName>Rongbao</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Jingdong</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Gao</LastName><ForeName>Xiang</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Tian</LastName><ForeName>Xinlun</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Qin</LastName><ForeName>Yingzhi</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Kai-Feng</ForeName><Initials>KF</Initials></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Dangsheng</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Jin</LastName><ForeName>Ningyi</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Chengyu</ForeName><Initials>C</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>2012</Year><Month>02</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Sci Signal</MedlineTA><NlmUniqueID>101465400</NlmUniqueID><ISSNLinking>1945-0877</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C495773">Atg5 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000071187">Autophagy-Related Protein 5</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017931">DNA 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Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D051058">Oncogene Protein v-akt</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000704" MajorTopicYN="N">Analysis of Variance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000071187" MajorTopicYN="N">Autophagy-Related Protein 5</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015153" MajorTopicYN="N">Blotting, Western</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell 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Subtype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007251" MajorTopicYN="N">Influenza, Human</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000648" MajorTopicYN="Y">ultrastructure</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008854" MajorTopicYN="N">Microscopy, Electron</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008869" MajorTopicYN="N">Microtubule-Associated Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051058" MajorTopicYN="N">Oncogene Protein v-akt</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010588" MajorTopicYN="N">Phagosomes</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D060888" MajorTopicYN="N">Real-Time Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000077005" MajorTopicYN="N">Tuberous Sclerosis Complex 2 Protein</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D025521" MajorTopicYN="N">Tumor Suppressor Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>2</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>2</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>6</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">22355189</ArticleId><ArticleId IdType="pii">5/212/ra16</ArticleId><ArticleId IdType="doi">10.1126/scisignal.2001931</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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|area= RapamycinFungusV1
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|texte= Inhibition of autophagy ameliorates acute lung injury caused by avian influenza A H5N1 infection.
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