RapamycinFungusV1, Main, Exploration, bibRecord, 000359

Distinct role of 4E-BP1 and S6K1 in regulating autophagy and hepatitis B virus (HBV) replication.

Identifieur interne : 000359 ( Main/Exploration ); précédent : 000358; suivant : 000360

Distinct role of 4E-BP1 and S6K1 in regulating autophagy and hepatitis B virus (HBV) replication.

Auteurs : Quan Gao [République populaire de Chine] ; Bolin Hou [République populaire de Chine] ; Huaiyi Yang [République populaire de Chine] ; Xuejun Jiang [République populaire de Chine]

Source :

Life sciences [ 1879-0631 ] ; 2019.

RBID : pubmed:30690083

Descripteurs français

English descriptors

KwdEn :
- Adaptor Proteins, Signal Transducing (metabolism), Adaptor Proteins, Signal Transducing (physiology), Autophagy (drug effects), DNA Replication (drug effects), Hep G2 Cells (MeSH), Hepatitis B Surface Antigens (metabolism), Hepatitis B virus (metabolism), Hepatitis B virus (physiology), Humans (MeSH), Phosphoproteins (metabolism), Phosphoproteins (physiology), Phosphorylation (MeSH), Proto-Oncogene Proteins c-akt (metabolism), Ribosomal Protein S6 Kinases, 70-kDa (metabolism), Ribosomal Protein S6 Kinases, 70-kDa (physiology), Signal Transduction (drug effects), Sirolimus (pharmacology), TOR Serine-Threonine Kinases (physiology), Trans-Activators (drug effects), Virus Replication (drug effects).
MESH :
- chemical , drug effects : Trans-Activators.
- chemical , metabolism : Adaptor Proteins, Signal Transducing, Hepatitis B Surface Antigens, Phosphoproteins, Proto-Oncogene Proteins c-akt, Ribosomal Protein S6 Kinases, 70-kDa.
- chemical , pharmacology : Sirolimus.
- chemical , physiology : Adaptor Proteins, Signal Transducing, Phosphoproteins, Ribosomal Protein S6 Kinases, 70-kDa, TOR Serine-Threonine Kinases.
- drug effects : Autophagy, DNA Replication, Signal Transduction, Virus Replication.
- metabolism : Hepatitis B virus.
- physiology : Hepatitis B virus.
- Hep G2 Cells, Humans, Phosphorylation.

Abstract

AIMS

To investigate the role and underlying mechanism of 4E-BP1 and S6K1 in regulating autophagy and hepatitis B virus (HBV) replication.

MAIN METHODS

The mRNA relative expression of HBx and its DNA level were detected by real-time PCR. The relative levels of hepatitis B surface antigen (HBsAg) were measured by enzyme-linked immunosorbent assay (ELISA). HBx DNA level of HepG2 cells transfected with pcDNA3.1(+)-HBV1.3 plasmids were detected by Southern blot. Moreover, we determined autophagy through electron microscopy, confocal microscopy and Western blot.

KEY FINDINGS

Rapamycin promoted autophagy and the X protein synthesis concomitantly with elevation in Akt phosphorylation and Beclin1 expression. Either Beclin1 or Akt depletion suppresses the Rapa-enhanced HBV replication, whereas mTOR silencing inhibited HBV replication concurring with a decreased in both S6K1 and 4E-BP1 phosphorylation. Unexpectedly, Akt inhibitor suppressed Rapa-dependent autophagic flux and increased the level of p62/SQSTM1. While S6K1 ablation impaired autophagy and decreased X protein expression, 4E-BP1 silencing slightly influenced autophagy and increased X protein level.

SIGNIFICANCE

The underlying mechanism of 4E-BP1 and S6K1, two main downstream effectors of mTOR, in mediating HBV replication and HBV-induced autophagy remains largely unknown. Here, we propose that Akt is required for both HBV replication and Rapa-induced autophagy, and 4E-BP1 and S6K1 play a distinct role in the virus replication and autophagic process.

DOI: 10.1016/j.lfs.2019.01.039
PubMed: 30690083

Affiliations:

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

to stream Main, to step Corpus: 000359
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Le document en format XML

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<term>Adaptor Proteins, Signal Transducing (physiology)</term>
<term>Autophagy (drug effects)</term>
<term>DNA Replication (drug effects)</term>
<term>Hep G2 Cells (MeSH)</term>
<term>Hepatitis B Surface Antigens (metabolism)</term>
<term>Hepatitis B virus (metabolism)</term>
<term>Hepatitis B virus (physiology)</term>
<term>Humans (MeSH)</term>
<term>Phosphoproteins (metabolism)</term>
<term>Phosphoproteins (physiology)</term>
<term>Phosphorylation (MeSH)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>Ribosomal Protein S6 Kinases, 70-kDa (metabolism)</term>
<term>Ribosomal Protein S6 Kinases, 70-kDa (physiology)</term>
<term>Signal Transduction (drug effects)</term>
<term>Sirolimus (pharmacology)</term>
<term>TOR Serine-Threonine Kinases (physiology)</term>
<term>Trans-Activators (drug effects)</term>
<term>Virus Replication (drug effects)</term>
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<term>Autophagie (effets des médicaments et des substances chimiques)</term>
<term>Cellules HepG2 (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Phosphoprotéines (métabolisme)</term>
<term>Phosphoprotéines (physiologie)</term>
<term>Phosphorylation (MeSH)</term>
<term>Protéines adaptatrices de la transduction du signal (métabolisme)</term>
<term>Protéines adaptatrices de la transduction du signal (physiologie)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
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<term>Ribosomal Protein S6 Kinases, 70-kDa (physiologie)</term>
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<term>Virus de l'hépatite B (physiologie)</term>
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<term>Hepatitis B Surface Antigens</term>
<term>Phosphoproteins</term>
<term>Proto-Oncogene Proteins c-akt</term>
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<term>Phosphoproteins</term>
<term>Ribosomal Protein S6 Kinases, 70-kDa</term>
<term>TOR Serine-Threonine Kinases</term>
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<term>DNA Replication</term>
<term>Signal Transduction</term>
<term>Virus Replication</term>
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<term>Protéines proto-oncogènes c-akt</term>
<term>Ribosomal Protein S6 Kinases, 70-kDa</term>
<term>Virus de l'hépatite B</term>
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<term>Protéines adaptatrices de la transduction du signal</term>
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<front><div type="abstract" xml:lang="en"><p><b>AIMS</b>
</p>
<p>To investigate the role and underlying mechanism of 4E-BP1 and S6K1 in regulating autophagy and hepatitis B virus (HBV) replication.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>MAIN METHODS</b>
</p>
<p>The mRNA relative expression of HBx and its DNA level were detected by real-time PCR. The relative levels of hepatitis B surface antigen (HBsAg) were measured by enzyme-linked immunosorbent assay (ELISA). HBx DNA level of HepG2 cells transfected with pcDNA3.1(+)-HBV1.3 plasmids were detected by Southern blot. Moreover, we determined autophagy through electron microscopy, confocal microscopy and Western blot.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>KEY FINDINGS</b>
</p>
<p>Rapamycin promoted autophagy and the X protein synthesis concomitantly with elevation in Akt phosphorylation and Beclin1 expression. Either Beclin1 or Akt depletion suppresses the Rapa-enhanced HBV replication, whereas mTOR silencing inhibited HBV replication concurring with a decreased in both S6K1 and 4E-BP1 phosphorylation. Unexpectedly, Akt inhibitor suppressed Rapa-dependent autophagic flux and increased the level of p62/SQSTM1. While S6K1 ablation impaired autophagy and decreased X protein expression, 4E-BP1 silencing slightly influenced autophagy and increased X protein level.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>SIGNIFICANCE</b>
</p>
<p>The underlying mechanism of 4E-BP1 and S6K1, two main downstream effectors of mTOR, in mediating HBV replication and HBV-induced autophagy remains largely unknown. Here, we propose that Akt is required for both HBV replication and Rapa-induced autophagy, and 4E-BP1 and S6K1 play a distinct role in the virus replication and autophagic process.</p>
</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30690083</PMID>
<DateCompleted><Year>2019</Year>
<Month>02</Month>
<Day>15</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>02</Month>
<Day>15</Day>
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<JournalIssue CitedMedium="Internet"><Volume>220</Volume>
<PubDate><Year>2019</Year>
<Month>Mar</Month>
<Day>01</Day>
</PubDate>
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<Title>Life sciences</Title>
<ISOAbbreviation>Life Sci</ISOAbbreviation>
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<ArticleTitle>Distinct role of 4E-BP1 and S6K1 in regulating autophagy and hepatitis B virus (HBV) replication.</ArticleTitle>
<Pagination><MedlinePgn>1-7</MedlinePgn>
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<Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">To investigate the role and underlying mechanism of 4E-BP1 and S6K1 in regulating autophagy and hepatitis B virus (HBV) replication.</AbstractText>
<AbstractText Label="MAIN METHODS" NlmCategory="METHODS">The mRNA relative expression of HBx and its DNA level were detected by real-time PCR. The relative levels of hepatitis B surface antigen (HBsAg) were measured by enzyme-linked immunosorbent assay (ELISA). HBx DNA level of HepG2 cells transfected with pcDNA3.1(+)-HBV1.3 plasmids were detected by Southern blot. Moreover, we determined autophagy through electron microscopy, confocal microscopy and Western blot.</AbstractText>
<AbstractText Label="KEY FINDINGS" NlmCategory="RESULTS">Rapamycin promoted autophagy and the X protein synthesis concomitantly with elevation in Akt phosphorylation and Beclin1 expression. Either Beclin1 or Akt depletion suppresses the Rapa-enhanced HBV replication, whereas mTOR silencing inhibited HBV replication concurring with a decreased in both S6K1 and 4E-BP1 phosphorylation. Unexpectedly, Akt inhibitor suppressed Rapa-dependent autophagic flux and increased the level of p62/SQSTM1. While S6K1 ablation impaired autophagy and decreased X protein expression, 4E-BP1 silencing slightly influenced autophagy and increased X protein level.</AbstractText>
<AbstractText Label="SIGNIFICANCE" NlmCategory="CONCLUSIONS">The underlying mechanism of 4E-BP1 and S6K1, two main downstream effectors of mTOR, in mediating HBV replication and HBV-induced autophagy remains largely unknown. Here, we propose that Akt is required for both HBV replication and Rapa-induced autophagy, and 4E-BP1 and S6K1 play a distinct role in the virus replication and autophagic process.</AbstractText>
<CopyrightInformation>Copyright © 2019 Elsevier Inc. All rights reserved.</CopyrightInformation>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gao</LastName>
<ForeName>Quan</ForeName>
<Initials>Q</Initials>
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</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Jiang</LastName>
<ForeName>Xuejun</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China. Electronic address: jiangxj@im.ac.cn.</Affiliation>
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<PubMedPubDate PubStatus="revised"><Year>2019</Year>
<Month>01</Month>
<Day>13</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2019</Year>
<Month>01</Month>
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<ArticleIdList><ArticleId IdType="pubmed">30690083</ArticleId>
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<affiliations><list><country><li>République populaire de Chine</li>
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	Serveur d'exploration sur la rapamycine et les champignons
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Serveur d'exploration sur la rapamycine et les champignons

Distinct role of 4E-BP1 and S6K1 in regulating autophagy and hepatitis B virus (HBV) replication.

Distinct role of 4E-BP1 and S6K1 in regulating autophagy and hepatitis B virus (HBV) replication.

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