RapamycinFungusV1, Main, Exploration, bibRecord, 000221

TIM-1 As a Signal Receptor Triggers Dengue Virus-Induced Autophagy.

Identifieur interne : 000221 ( Main/Exploration ); précédent : 000220; suivant : 000222

TIM-1 As a Signal Receptor Triggers Dengue Virus-Induced Autophagy.

Auteurs : Li-Wei Chu [Taïwan] ; Chia-Jui Yang [Taïwan] ; Kuan-Jen Peng [Taïwan] ; Pei-Ling Chen [Taïwan] ; Shuu-Jiun Wang [Taïwan] ; Yueh-Hsin Ping [Taïwan]

Source :

International journal of molecular sciences [ 1422-0067 ] ; 2019.

RBID : pubmed:31581681

Descripteurs français

KwdFr :
- Autophagie (MeSH), Autophagosomes (métabolisme), Dengue (métabolisme), Dengue (virologie), Humains (MeSH), Lignée cellulaire (MeSH), Marqueurs biologiques (MeSH), Modèles biologiques (MeSH), Récepteur cellulaire-1 du virus de l'hépatite A (métabolisme), Réplication virale (MeSH), Techniques de knock-down de gènes (MeSH), Transduction du signal (MeSH), Virus de la dengue (MeSH).
MESH :
- métabolisme : Autophagosomes, Dengue, Récepteur cellulaire-1 du virus de l'hépatite A.
- virologie : Dengue.
- Autophagie, Humains, Lignée cellulaire, Marqueurs biologiques, Modèles biologiques, Réplication virale, Techniques de knock-down de gènes, Transduction du signal, Virus de la dengue.

English descriptors

KwdEn :
- Autophagosomes (metabolism), Autophagy (MeSH), Biomarkers (MeSH), Cell Line (MeSH), Dengue (metabolism), Dengue (virology), Dengue Virus (MeSH), Gene Knockdown Techniques (MeSH), Hepatitis A Virus Cellular Receptor 1 (metabolism), Humans (MeSH), Models, Biological (MeSH), Signal Transduction (MeSH), Virus Replication (MeSH).
MESH :
- chemical , metabolism : Hepatitis A Virus Cellular Receptor 1.
- chemical : Biomarkers.
- metabolism : Autophagosomes, Dengue.
- virology : Dengue.
- Autophagy, Cell Line, Dengue Virus, Gene Knockdown Techniques, Humans, Models, Biological, Signal Transduction, Virus Replication.

Abstract

Dengue virus (DENV) infection triggers the activation of autophagy to facilitate the viral replication cycle from various aspects. Although a number of stimulators are proposed to activate autophagy, none of them appears prior to the uncoating process. Given that T-cell immunoglobulin and mucin domain 1 (TIM-1) receptor is a putative DENV receptor and promotes apoptotic body clearance by autophagy induction, it raises the possibility that TIM-1 may participate in the activation of DENV-induced autophagy. In this study, confocal images first revealed the co-localization of TIM-1 with autophagosomes in DENV-induced autophagy rather than rapamycin-induced autophagy, suggesting the co-transportation of TIM-1 with DENV during infection. The treatment of siRNA to knockdown TIM-1 expression in DENV-infected GFP-microtubule-associated protein light chain 3 (LC3)-Huh7.5 cells revealed that TIM-1 is required not only for DENV cellular internalization but also for autophagy activation. Furthermore, knockdown p85, a subunit of phosphoinositide 3-kinases (PI3Ks), which is co-localized with TIM-1 at rab5-positive endosomes caused the reduction of autophagy, indicating that TIM-1-mediated DENV-induced autophagy requires p85. Taken together, the current study uncovered TIM-1 as a novel factor for triggering autophagy in DENV infection through TIM-1-p85 axis, in addition to serving as a DENV receptor.

DOI: 10.3390/ijms20194893
PubMed: 31581681
PubMed Central: PMC6801812

Affiliations:

Taïwan

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000184
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Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Autophagosomes (metabolism)</term>
<term>Autophagy (MeSH)</term>
<term>Biomarkers (MeSH)</term>
<term>Cell Line (MeSH)</term>
<term>Dengue (metabolism)</term>
<term>Dengue (virology)</term>
<term>Dengue Virus (MeSH)</term>
<term>Gene Knockdown Techniques (MeSH)</term>
<term>Hepatitis A Virus Cellular Receptor 1 (metabolism)</term>
<term>Humans (MeSH)</term>
<term>Models, Biological (MeSH)</term>
<term>Signal Transduction (MeSH)</term>
<term>Virus Replication (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Autophagie (MeSH)</term>
<term>Autophagosomes (métabolisme)</term>
<term>Dengue (métabolisme)</term>
<term>Dengue (virologie)</term>
<term>Humains (MeSH)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Marqueurs biologiques (MeSH)</term>
<term>Modèles biologiques (MeSH)</term>
<term>Récepteur cellulaire-1 du virus de l'hépatite A (métabolisme)</term>
<term>Réplication virale (MeSH)</term>
<term>Techniques de knock-down de gènes (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
<term>Virus de la dengue (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Hepatitis A Virus Cellular Receptor 1</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Biomarkers</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Autophagosomes</term>
<term>Dengue</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Autophagosomes</term>
<term>Dengue</term>
<term>Récepteur cellulaire-1 du virus de l'hépatite A</term>
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<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Dengue</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Dengue</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Autophagy</term>
<term>Cell Line</term>
<term>Dengue Virus</term>
<term>Gene Knockdown Techniques</term>
<term>Humans</term>
<term>Models, Biological</term>
<term>Signal Transduction</term>
<term>Virus Replication</term>
</keywords>
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<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Marqueurs biologiques</term>
<term>Modèles biologiques</term>
<term>Réplication virale</term>
<term>Techniques de knock-down de gènes</term>
<term>Transduction du signal</term>
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<front><div type="abstract" xml:lang="en">Dengue virus (DENV) infection triggers the activation of autophagy to facilitate the viral replication cycle from various aspects. Although a number of stimulators are proposed to activate autophagy, none of them appears prior to the uncoating process. Given that T-cell immunoglobulin and mucin domain 1 (TIM-1) receptor is a putative DENV receptor and promotes apoptotic body clearance by autophagy induction, it raises the possibility that TIM-1 may participate in the activation of DENV-induced autophagy. In this study, confocal images first revealed the co-localization of TIM-1 with autophagosomes in DENV-induced autophagy rather than rapamycin-induced autophagy, suggesting the co-transportation of TIM-1 with DENV during infection. The treatment of siRNA to knockdown TIM-1 expression in DENV-infected GFP-microtubule-associated protein light chain 3 (LC3)-Huh7.5 cells revealed that TIM-1 is required not only for DENV cellular internalization but also for autophagy activation. Furthermore, knockdown p85, a subunit of phosphoinositide 3-kinases (PI3Ks), which is co-localized with TIM-1 at rab5-positive endosomes caused the reduction of autophagy, indicating that TIM-1-mediated DENV-induced autophagy requires p85. Taken together, the current study uncovered TIM-1 as a novel factor for triggering autophagy in DENV infection through TIM-1-p85 axis, in addition to serving as a DENV receptor.</div>
</front>
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<Title>International journal of molecular sciences</Title>
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<Abstract><AbstractText>Dengue virus (DENV) infection triggers the activation of autophagy to facilitate the viral replication cycle from various aspects. Although a number of stimulators are proposed to activate autophagy, none of them appears prior to the uncoating process. Given that T-cell immunoglobulin and mucin domain 1 (TIM-1) receptor is a putative DENV receptor and promotes apoptotic body clearance by autophagy induction, it raises the possibility that TIM-1 may participate in the activation of DENV-induced autophagy. In this study, confocal images first revealed the co-localization of TIM-1 with autophagosomes in DENV-induced autophagy rather than rapamycin-induced autophagy, suggesting the co-transportation of TIM-1 with DENV during infection. The treatment of siRNA to knockdown TIM-1 expression in DENV-infected GFP-microtubule-associated protein light chain 3 (LC3)-Huh7.5 cells revealed that TIM-1 is required not only for DENV cellular internalization but also for autophagy activation. Furthermore, knockdown p85, a subunit of phosphoinositide 3-kinases (PI3Ks), which is co-localized with TIM-1 at rab5-positive endosomes caused the reduction of autophagy, indicating that TIM-1-mediated DENV-induced autophagy requires p85. Taken together, the current study uncovered TIM-1 as a novel factor for triggering autophagy in DENV infection through TIM-1-p85 axis, in addition to serving as a DENV receptor.</AbstractText>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chu</LastName>
<ForeName>Li-Wei</ForeName>
<Initials>LW</Initials>
<AffiliationInfo><Affiliation>Institute of Biophotonics, National Yang-Ming University, Taipei 11221, Taiwan. nealchu125@gmail.com.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Brain Research Center, National Yang-Ming University, Taipei 11221, Taiwan. nealchu125@gmail.com.</Affiliation>
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<AffiliationInfo><Affiliation>Department of Internal Medicine, Far Eastern Memorial Hospital, New Taipei City 22060, Taiwan. yangcj1206@gmail.com.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Peng</LastName>
<ForeName>Kuan-Jen</ForeName>
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<ForeName>Pei-Ling</ForeName>
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<AffiliationInfo><Affiliation>Department and Institute of Pharmacology, National Yang-Ming University, Taipei 11221, Taiwan. s904158@gmail.com.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Shuu-Jiun</ForeName>
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<AffiliationInfo><Affiliation>Brain Research Center, National Yang-Ming University, Taipei 11221, Taiwan. sjwang@vghtpe.gov.tw.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Faculty of Medicine, National Yang-Ming University, Taipei 11221, Taiwan. sjwang@vghtpe.gov.tw.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Neurology, Neurological Institute, Taipei Veterans General Hospital, Taipei 11217, Taiwan. sjwang@vghtpe.gov.tw.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Ping</LastName>
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</AffiliationInfo>
<AffiliationInfo><Affiliation>Department and Institute of Pharmacology, National Yang-Ming University, Taipei 11221, Taiwan. yhping@ym.edu.tw.</Affiliation>
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<Agency>Ministry of Science and Technology, Taiwan</Agency>
<Country></Country>
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<Grant><GrantID>108DN01</GrantID>
<Agency>the National Yang-Ming University-Far Eastern Memorial Hospital Joint Research Program</Agency>
<Country></Country>
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<Grant><GrantID>107BRC- B201, B202, B203 & B204</GrantID>
<Agency>Brain Research Center, National Yang-Ming University from The Featured Areas Research Center Program within the framework of the Higher Education Sprout Project by the Ministry of Education (MOE) in Taiwan</Agency>
<Country></Country>
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	Serveur d'exploration sur la rapamycine et les champignons
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TIM-1 As a Signal Receptor Triggers Dengue Virus-Induced Autophagy.

TIM-1 As a Signal Receptor Triggers Dengue Virus-Induced Autophagy.

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