Syncytia generated by hemagglutinin-neuraminidase and fusion proteins of virulent Newcastle disease virus induce complete autophagy by activating AMPK-mTORC1-ULK1 signaling>.
Identifieur interne : 000224 ( Main/Exploration ); précédent : 000223; suivant : 000225Syncytia generated by hemagglutinin-neuraminidase and fusion proteins of virulent Newcastle disease virus induce complete autophagy by activating AMPK-mTORC1-ULK1 signaling>.
Auteurs : Shanhui Ren [République populaire de Chine] ; Zaib Ur Rehman [République populaire de Chine] ; Mengyu Shi [République populaire de Chine] ; Bin Yang [République populaire de Chine] ; Yurong Qu [République populaire de Chine] ; Xiao Feng Yang [République populaire de Chine] ; Qi Shao [République populaire de Chine] ; Chunchun Meng [République populaire de Chine] ; Zengqi Yang [République populaire de Chine] ; Xiaolong Gao [République populaire de Chine] ; Yingjie Sun [République populaire de Chine] ; Chan Ding [République populaire de Chine]Source :
- Veterinary microbiology [ 1873-2542 ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Autophagie (MeSH), Autophagosomes (métabolisme), Autophagosomes (virologie), Cellules A549 (MeSH), Cellules géantes (métabolisme), Cellules géantes (virologie), Complexe-1 cible mécanistique de la rapamycine (métabolisme), Fibroblastes (virologie), Humains (MeSH), Hémagglutinines virales (génétique), Lignée cellulaire (MeSH), Lysosomes (métabolisme), Lysosomes (virologie), Maladie de Newcastle (anatomopathologie), Mutation (MeSH), Petit ARN interférent (MeSH), Plasmides (génétique), Poulets (MeSH), Protein kinases (métabolisme), Protéines de fusion virale (génétique), Protéines et peptides de signalisation intracellulaire (MeSH), Sialidase (génétique), Transduction du signal (MeSH), Transfection (MeSH), Virus de la maladie de Newcastle (génétique), Virus de la maladie de Newcastle (pathogénicité).
- MESH :
- anatomopathologie : Maladie de Newcastle.
- génétique : Hémagglutinines virales, Plasmides, Protéines de fusion virale, Sialidase, Virus de la maladie de Newcastle.
- métabolisme : Autophagosomes, Cellules géantes, Complexe-1 cible mécanistique de la rapamycine, Lysosomes, Protein kinases.
- pathogénicité : Virus de la maladie de Newcastle.
- virologie : Autophagosomes, Cellules géantes, Fibroblastes, Lysosomes.
- Animaux, Autophagie, Cellules A549, Humains, Lignée cellulaire, Mutation, Petit ARN interférent, Poulets, Protéines et peptides de signalisation intracellulaire, Transduction du signal, Transfection.
English descriptors
- KwdEn :
- A549 Cells (MeSH), Animals (MeSH), Autophagosomes (metabolism), Autophagosomes (virology), Autophagy (MeSH), Cell Line (MeSH), Chickens (MeSH), Fibroblasts (virology), Giant Cells (metabolism), Giant Cells (virology), Hemagglutinins, Viral (genetics), Humans (MeSH), Intracellular Signaling Peptides and Proteins (MeSH), Lysosomes (metabolism), Lysosomes (virology), Mechanistic Target of Rapamycin Complex 1 (metabolism), Mutation (MeSH), Neuraminidase (genetics), Newcastle Disease (pathology), Newcastle disease virus (genetics), Newcastle disease virus (pathogenicity), Plasmids (genetics), Protein Kinases (metabolism), RNA, Small Interfering (MeSH), Signal Transduction (MeSH), Transfection (MeSH), Viral Fusion Proteins (genetics).
- MESH :
- chemical , genetics : Hemagglutinins, Viral, Neuraminidase, Viral Fusion Proteins.
- genetics : Newcastle disease virus, Plasmids.
- metabolism : Autophagosomes, Giant Cells, Lysosomes, Mechanistic Target of Rapamycin Complex 1, Protein Kinases.
- pathogenicity : Newcastle disease virus.
- pathology : Newcastle Disease.
- virology : Autophagosomes, Fibroblasts, Giant Cells, Lysosomes.
- A549 Cells, Animals, Autophagy, Cell Line, Chickens, Humans, Intracellular Signaling Peptides and Proteins, Mutation, RNA, Small Interfering, Signal Transduction, Transfection.
Abstract
Autophagy triggered by glycoprotein-mediated membrane fusion has been reported for several paramyxoviruses. However, the function of HN and F glycoproteins of NDV and their role in autophagy induction have not been studied. Here, we found that co-transfection of HN and F of virulent NDV rapidly induced syncytium formation and triggered a steady state autophagy flux in adenocarcinomic human alveolar basal epithelial (A549) cells and chicken embryo fibroblast (DF-1) cells. Furthermore, we clearly identified that F and HN synergistically induced autophagosome fusion with lysosomes for subsequent degradation. The seven cleavage site mutations of F significantly decreased the autophagy induction, compared with those of wildtype virulent F. RNAi and pharmacological experiments suggested that autophagy benefitted membrane fusion and syncytium formation induced by F and HN of NDV. Activated F1 co-operated with HN to stimulate AMPK kinase and downstream ULK1 activation to suppress mTORC1 signaling. Our data described the synergistic role of HN and F in the induction of completed autophagic flux through the activation of AMPK- mTORC1- ULK1 pathway.
DOI: 10.1016/j.vetmic.2019.01.002
PubMed: 30658866
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<author><name sortKey="Ren, Shanhui" sort="Ren, Shanhui" uniqKey="Ren S" first="Shanhui" last="Ren">Shanhui Ren</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, 200241, PR China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Rehman, Zaib Ur" sort="Rehman, Zaib Ur" uniqKey="Rehman Z" first="Zaib Ur" last="Rehman">Zaib Ur Rehman</name>
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<author><name sortKey="Shi, Mengyu" sort="Shi, Mengyu" uniqKey="Shi M" first="Mengyu" last="Shi">Mengyu Shi</name>
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<author><name sortKey="Yang, Bin" sort="Yang, Bin" uniqKey="Yang B" first="Bin" last="Yang">Bin Yang</name>
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<author><name sortKey="Qu, Yurong" sort="Qu, Yurong" uniqKey="Qu Y" first="Yurong" last="Qu">Yurong Qu</name>
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<author><name sortKey="Yang, Xiao Feng" sort="Yang, Xiao Feng" uniqKey="Yang X" first="Xiao Feng" last="Yang">Xiao Feng Yang</name>
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<author><name sortKey="Shao, Qi" sort="Shao, Qi" uniqKey="Shao Q" first="Qi" last="Shao">Qi Shao</name>
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<author><name sortKey="Meng, Chunchun" sort="Meng, Chunchun" uniqKey="Meng C" first="Chunchun" last="Meng">Chunchun Meng</name>
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<author><name sortKey="Yang, Zengqi" sort="Yang, Zengqi" uniqKey="Yang Z" first="Zengqi" last="Yang">Zengqi Yang</name>
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<author><name sortKey="Gao, Xiaolong" sort="Gao, Xiaolong" uniqKey="Gao X" first="Xiaolong" last="Gao">Xiaolong Gao</name>
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<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Ding, Chan" sort="Ding, Chan" uniqKey="Ding C" first="Chan" last="Ding">Chan Ding</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, 200241, PR China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Disease and Zoonoses, Yang Zhou, 225009</wicri:regionArea>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Syncytia generated by hemagglutinin-neuraminidase and fusion proteins of virulent Newcastle disease virus induce complete autophagy by activating AMPK-mTORC1-ULK1 signaling>.</title>
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<author><name sortKey="Rehman, Zaib Ur" sort="Rehman, Zaib Ur" uniqKey="Rehman Z" first="Zaib Ur" last="Rehman">Zaib Ur Rehman</name>
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<author><name sortKey="Yang, Bin" sort="Yang, Bin" uniqKey="Yang B" first="Bin" last="Yang">Bin Yang</name>
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<author><name sortKey="Qu, Yurong" sort="Qu, Yurong" uniqKey="Qu Y" first="Yurong" last="Qu">Yurong Qu</name>
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<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Yang, Xiao Feng" sort="Yang, Xiao Feng" uniqKey="Yang X" first="Xiao Feng" last="Yang">Xiao Feng Yang</name>
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<author><name sortKey="Shao, Qi" sort="Shao, Qi" uniqKey="Shao Q" first="Qi" last="Shao">Qi Shao</name>
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<country xml:lang="fr">République populaire de Chine</country>
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<wicri:noRegion>200241</wicri:noRegion>
</affiliation>
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<author><name sortKey="Meng, Chunchun" sort="Meng, Chunchun" uniqKey="Meng C" first="Chunchun" last="Meng">Chunchun Meng</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, 200241, PR China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, 200241</wicri:regionArea>
<wicri:noRegion>200241</wicri:noRegion>
</affiliation>
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<author><name sortKey="Yang, Zengqi" sort="Yang, Zengqi" uniqKey="Yang Z" first="Zengqi" last="Yang">Zengqi Yang</name>
<affiliation wicri:level="1"><nlm:affiliation>College of Veterinary Medicine, Northwest A&F University, Yangling, 712100, Shaanxi, PR China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>College of Veterinary Medicine, Northwest A&F University, Yangling, 712100, Shaanxi</wicri:regionArea>
<wicri:noRegion>Shaanxi</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Gao, Xiaolong" sort="Gao, Xiaolong" uniqKey="Gao X" first="Xiaolong" last="Gao">Xiaolong Gao</name>
<affiliation wicri:level="1"><nlm:affiliation>College of Agriculture and Animal Husbandary, Qinghai University, Xining, Qinghai 810016, PR China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>College of Agriculture and Animal Husbandary, Qinghai University, Xining, Qinghai 810016</wicri:regionArea>
<wicri:noRegion>Qinghai 810016</wicri:noRegion>
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<author><name sortKey="Sun, Yingjie" sort="Sun, Yingjie" uniqKey="Sun Y" first="Yingjie" last="Sun">Yingjie Sun</name>
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<country xml:lang="fr">République populaire de Chine</country>
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<wicri:noRegion>200241</wicri:noRegion>
</affiliation>
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<author><name sortKey="Ding, Chan" sort="Ding, Chan" uniqKey="Ding C" first="Chan" last="Ding">Chan Ding</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, 200241, PR China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Disease and Zoonoses, Yang Zhou, 225009, PR China. Electronic address: shoveldeen@shvri.ac.cn.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, 200241, PR China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Disease and Zoonoses, Yang Zhou, 225009</wicri:regionArea>
<wicri:noRegion>225009</wicri:noRegion>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A549 Cells (MeSH)</term>
<term>Animals (MeSH)</term>
<term>Autophagosomes (metabolism)</term>
<term>Autophagosomes (virology)</term>
<term>Autophagy (MeSH)</term>
<term>Cell Line (MeSH)</term>
<term>Chickens (MeSH)</term>
<term>Fibroblasts (virology)</term>
<term>Giant Cells (metabolism)</term>
<term>Giant Cells (virology)</term>
<term>Hemagglutinins, Viral (genetics)</term>
<term>Humans (MeSH)</term>
<term>Intracellular Signaling Peptides and Proteins (MeSH)</term>
<term>Lysosomes (metabolism)</term>
<term>Lysosomes (virology)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (metabolism)</term>
<term>Mutation (MeSH)</term>
<term>Neuraminidase (genetics)</term>
<term>Newcastle Disease (pathology)</term>
<term>Newcastle disease virus (genetics)</term>
<term>Newcastle disease virus (pathogenicity)</term>
<term>Plasmids (genetics)</term>
<term>Protein Kinases (metabolism)</term>
<term>RNA, Small Interfering (MeSH)</term>
<term>Signal Transduction (MeSH)</term>
<term>Transfection (MeSH)</term>
<term>Viral Fusion Proteins (genetics)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Autophagie (MeSH)</term>
<term>Autophagosomes (métabolisme)</term>
<term>Autophagosomes (virologie)</term>
<term>Cellules A549 (MeSH)</term>
<term>Cellules géantes (métabolisme)</term>
<term>Cellules géantes (virologie)</term>
<term>Complexe-1 cible mécanistique de la rapamycine (métabolisme)</term>
<term>Fibroblastes (virologie)</term>
<term>Humains (MeSH)</term>
<term>Hémagglutinines virales (génétique)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Lysosomes (métabolisme)</term>
<term>Lysosomes (virologie)</term>
<term>Maladie de Newcastle (anatomopathologie)</term>
<term>Mutation (MeSH)</term>
<term>Petit ARN interférent (MeSH)</term>
<term>Plasmides (génétique)</term>
<term>Poulets (MeSH)</term>
<term>Protein kinases (métabolisme)</term>
<term>Protéines de fusion virale (génétique)</term>
<term>Protéines et peptides de signalisation intracellulaire (MeSH)</term>
<term>Sialidase (génétique)</term>
<term>Transduction du signal (MeSH)</term>
<term>Transfection (MeSH)</term>
<term>Virus de la maladie de Newcastle (génétique)</term>
<term>Virus de la maladie de Newcastle (pathogénicité)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Hemagglutinins, Viral</term>
<term>Neuraminidase</term>
<term>Viral Fusion Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Maladie de Newcastle</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Newcastle disease virus</term>
<term>Plasmids</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Hémagglutinines virales</term>
<term>Plasmides</term>
<term>Protéines de fusion virale</term>
<term>Sialidase</term>
<term>Virus de la maladie de Newcastle</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Autophagosomes</term>
<term>Giant Cells</term>
<term>Lysosomes</term>
<term>Mechanistic Target of Rapamycin Complex 1</term>
<term>Protein Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Autophagosomes</term>
<term>Cellules géantes</term>
<term>Complexe-1 cible mécanistique de la rapamycine</term>
<term>Lysosomes</term>
<term>Protein kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Newcastle disease virus</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus de la maladie de Newcastle</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Newcastle Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Autophagosomes</term>
<term>Cellules géantes</term>
<term>Fibroblastes</term>
<term>Lysosomes</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Autophagosomes</term>
<term>Fibroblasts</term>
<term>Giant Cells</term>
<term>Lysosomes</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>A549 Cells</term>
<term>Animals</term>
<term>Autophagy</term>
<term>Cell Line</term>
<term>Chickens</term>
<term>Humans</term>
<term>Intracellular Signaling Peptides and Proteins</term>
<term>Mutation</term>
<term>RNA, Small Interfering</term>
<term>Signal Transduction</term>
<term>Transfection</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Autophagie</term>
<term>Cellules A549</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Mutation</term>
<term>Petit ARN interférent</term>
<term>Poulets</term>
<term>Protéines et peptides de signalisation intracellulaire</term>
<term>Transduction du signal</term>
<term>Transfection</term>
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<front><div type="abstract" xml:lang="en">Autophagy triggered by glycoprotein-mediated membrane fusion has been reported for several paramyxoviruses. However, the function of HN and F glycoproteins of NDV and their role in autophagy induction have not been studied. Here, we found that co-transfection of HN and F of virulent NDV rapidly induced syncytium formation and triggered a steady state autophagy flux in adenocarcinomic human alveolar basal epithelial (A549) cells and chicken embryo fibroblast (DF-1) cells. Furthermore, we clearly identified that F and HN synergistically induced autophagosome fusion with lysosomes for subsequent degradation. The seven cleavage site mutations of F significantly decreased the autophagy induction, compared with those of wildtype virulent F. RNAi and pharmacological experiments suggested that autophagy benefitted membrane fusion and syncytium formation induced by F and HN of NDV. Activated F<sub>1</sub>
co-operated with HN to stimulate AMPK kinase and downstream ULK1 activation to suppress mTORC1 signaling. Our data described the synergistic role of HN and F in the induction of completed autophagic flux through the activation of AMPK- mTORC1- ULK1 pathway.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30658866</PMID>
<DateCompleted><Year>2019</Year>
<Month>04</Month>
<Day>19</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>04</Month>
<Day>19</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-2542</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>230</Volume>
<PubDate><Year>2019</Year>
<Month>Mar</Month>
</PubDate>
</JournalIssue>
<Title>Veterinary microbiology</Title>
<ISOAbbreviation>Vet Microbiol</ISOAbbreviation>
</Journal>
<ArticleTitle>Syncytia generated by hemagglutinin-neuraminidase and fusion proteins of virulent Newcastle disease virus induce complete autophagy by activating AMPK-mTORC1-ULK1 signaling>.</ArticleTitle>
<Pagination><MedlinePgn>283-290</MedlinePgn>
</Pagination>
<ELocationID EIdType="pii" ValidYN="Y">S0378-1135(18)31230-6</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.vetmic.2019.01.002</ELocationID>
<Abstract><AbstractText>Autophagy triggered by glycoprotein-mediated membrane fusion has been reported for several paramyxoviruses. However, the function of HN and F glycoproteins of NDV and their role in autophagy induction have not been studied. Here, we found that co-transfection of HN and F of virulent NDV rapidly induced syncytium formation and triggered a steady state autophagy flux in adenocarcinomic human alveolar basal epithelial (A549) cells and chicken embryo fibroblast (DF-1) cells. Furthermore, we clearly identified that F and HN synergistically induced autophagosome fusion with lysosomes for subsequent degradation. The seven cleavage site mutations of F significantly decreased the autophagy induction, compared with those of wildtype virulent F. RNAi and pharmacological experiments suggested that autophagy benefitted membrane fusion and syncytium formation induced by F and HN of NDV. Activated F<sub>1</sub>
co-operated with HN to stimulate AMPK kinase and downstream ULK1 activation to suppress mTORC1 signaling. Our data described the synergistic role of HN and F in the induction of completed autophagic flux through the activation of AMPK- mTORC1- ULK1 pathway.</AbstractText>
<CopyrightInformation>Copyright © 2019 Elsevier B.V. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ren</LastName>
<ForeName>Shanhui</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, 200241, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rehman</LastName>
<ForeName>Zaib Ur</ForeName>
<Initials>ZU</Initials>
<AffiliationInfo><Affiliation>Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, 200241, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shi</LastName>
<ForeName>Mengyu</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, 200241, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yang</LastName>
<ForeName>Bin</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>College of Veterinary Medicine, Xinjiang Agricultural University, Wulumuqi, 830052, Xinjiang, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Qu</LastName>
<ForeName>Yurong</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, 200241, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yang</LastName>
<ForeName>Xiao Feng</ForeName>
<Initials>XF</Initials>
<AffiliationInfo><Affiliation>Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, 200241, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shao</LastName>
<ForeName>Qi</ForeName>
<Initials>Q</Initials>
<AffiliationInfo><Affiliation>Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, 200241, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Meng</LastName>
<ForeName>Chunchun</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, 200241, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yang</LastName>
<ForeName>Zengqi</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>College of Veterinary Medicine, Northwest A&F University, Yangling, 712100, Shaanxi, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gao</LastName>
<ForeName>Xiaolong</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>College of Agriculture and Animal Husbandary, Qinghai University, Xining, Qinghai 810016, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sun</LastName>
<ForeName>Yingjie</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, 200241, PR China. Electronic address: sunyingjie@shvri.ac.cn.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ding</LastName>
<ForeName>Chan</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, 200241, PR China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Disease and Zoonoses, Yang Zhou, 225009, PR China. Electronic address: shoveldeen@shvri.ac.cn.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2019</Year>
<Month>01</Month>
<Day>04</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Netherlands</Country>
<MedlineTA>Vet Microbiol</MedlineTA>
<NlmUniqueID>7705469</NlmUniqueID>
<ISSNLinking>0378-1135</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D006389">Hemagglutinins, Viral</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D047908">Intracellular Signaling Peptides and Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D034741">RNA, Small Interfering</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014760">Viral Fusion Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.-</RegistryNumber>
<NameOfSubstance UI="D011494">Protein Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.1.-</RegistryNumber>
<NameOfSubstance UI="C086028">AMP-activated protein kinase kinase</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D000076222">Mechanistic Target of Rapamycin Complex 1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.2.1.18</RegistryNumber>
<NameOfSubstance UI="D009439">Neuraminidase</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000072283" MajorTopicYN="N">A549 Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071182" MajorTopicYN="N">Autophagosomes</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002645" MajorTopicYN="N">Chickens</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005347" MajorTopicYN="N">Fibroblasts</DescriptorName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015726" MajorTopicYN="N">Giant Cells</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006389" MajorTopicYN="N">Hemagglutinins, Viral</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D047908" MajorTopicYN="N">Intracellular Signaling Peptides and Proteins</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008247" MajorTopicYN="N">Lysosomes</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000076222" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 1</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009439" MajorTopicYN="N">Neuraminidase</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009521" MajorTopicYN="N">Newcastle Disease</DescriptorName>
<QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009522" MajorTopicYN="N">Newcastle disease virus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010957" MajorTopicYN="N">Plasmids</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011494" MajorTopicYN="N">Protein Kinases</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D034741" MajorTopicYN="N">RNA, Small Interfering</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014162" MajorTopicYN="N">Transfection</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014760" MajorTopicYN="N">Viral Fusion Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Autophagy</Keyword>
<Keyword MajorTopicYN="N">Fusion protein</Keyword>
<Keyword MajorTopicYN="N">Hemagglutinin-neuraminidase protein</Keyword>
<Keyword MajorTopicYN="N">Newcastle disease virus</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year>
<Month>10</Month>
<Day>20</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2019</Year>
<Month>01</Month>
<Day>02</Day>
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<PubMedPubDate PubStatus="accepted"><Year>2019</Year>
<Month>01</Month>
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<ArticleIdList><ArticleId IdType="pubmed">30658866</ArticleId>
<ArticleId IdType="pii">S0378-1135(18)31230-6</ArticleId>
<ArticleId IdType="doi">10.1016/j.vetmic.2019.01.002</ArticleId>
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<affiliations><list><country><li>République populaire de Chine</li>
</country>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Ren, Shanhui" sort="Ren, Shanhui" uniqKey="Ren S" first="Shanhui" last="Ren">Shanhui Ren</name>
</noRegion>
<name sortKey="Ding, Chan" sort="Ding, Chan" uniqKey="Ding C" first="Chan" last="Ding">Chan Ding</name>
<name sortKey="Gao, Xiaolong" sort="Gao, Xiaolong" uniqKey="Gao X" first="Xiaolong" last="Gao">Xiaolong Gao</name>
<name sortKey="Meng, Chunchun" sort="Meng, Chunchun" uniqKey="Meng C" first="Chunchun" last="Meng">Chunchun Meng</name>
<name sortKey="Qu, Yurong" sort="Qu, Yurong" uniqKey="Qu Y" first="Yurong" last="Qu">Yurong Qu</name>
<name sortKey="Rehman, Zaib Ur" sort="Rehman, Zaib Ur" uniqKey="Rehman Z" first="Zaib Ur" last="Rehman">Zaib Ur Rehman</name>
<name sortKey="Shao, Qi" sort="Shao, Qi" uniqKey="Shao Q" first="Qi" last="Shao">Qi Shao</name>
<name sortKey="Shi, Mengyu" sort="Shi, Mengyu" uniqKey="Shi M" first="Mengyu" last="Shi">Mengyu Shi</name>
<name sortKey="Sun, Yingjie" sort="Sun, Yingjie" uniqKey="Sun Y" first="Yingjie" last="Sun">Yingjie Sun</name>
<name sortKey="Yang, Bin" sort="Yang, Bin" uniqKey="Yang B" first="Bin" last="Yang">Bin Yang</name>
<name sortKey="Yang, Xiao Feng" sort="Yang, Xiao Feng" uniqKey="Yang X" first="Xiao Feng" last="Yang">Xiao Feng Yang</name>
<name sortKey="Yang, Zengqi" sort="Yang, Zengqi" uniqKey="Yang Z" first="Zengqi" last="Yang">Zengqi Yang</name>
</country>
</tree>
</affiliations>
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