RapamycinFungusV1, Main, Exploration, bibRecord, 000589

Hepatitis B Virus Surface Antigen Enhances the Sensitivity of Hepatocytes to Fas-Mediated Apoptosis via Suppression of AKT Phosphorylation.

Identifieur interne : 000589 ( Main/Exploration ); précédent : 000588; suivant : 000590

Hepatitis B Virus Surface Antigen Enhances the Sensitivity of Hepatocytes to Fas-Mediated Apoptosis via Suppression of AKT Phosphorylation.

Auteurs : Zhen-Tang Jing ; Wei Liu [République populaire de Chine] ; Shu-Xiang Wu ; Yun He ; Yan-Ting Lin ; Wan-Nan Chen [République populaire de Chine] ; Xin-Jian Lin ; Xu Lin [République populaire de Chine]

Source :

Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2018.

RBID : pubmed:30171166

Descripteurs français

KwdFr :
- Acétates (administration et posologie), Acétates (pharmacologie), Adenoviridae (génétique), Animaux (MeSH), Anticorps monoclonaux (métabolisme), Antigènes CD95 (immunologie), Antigènes CD95 (métabolisme), Antigènes de surface du virus de l'hépatite B (métabolisme), Apoptose (MeSH), Benzopyranes (administration et posologie), Benzopyranes (pharmacologie), Caspase 8 (métabolisme), Cellules HepG2 (MeSH), Cellules cultivées (MeSH), Défaillance hépatique aigüe (anatomopathologie), Défaillance hépatique aigüe (métabolisme), Humains (MeSH), Hépatite B (anatomopathologie), Hépatite B (métabolisme), Hépatocytes (physiologie), Hépatocytes (virologie), Modèles animaux de maladie humaine (MeSH), Mâle (MeSH), Phosphorylation (MeSH), Protéine de régulation de l'apoptose CASP8 et FADD-like (métabolisme), Protéines proto-oncogènes c-akt (agonistes), Protéines proto-oncogènes c-akt (métabolisme), Souris (MeSH), Souris de lignée C57BL (MeSH), Virus de l'hépatite B (physiologie).
MESH :
- administration et posologie : Acétates, Benzopyranes.
- agonistes : Protéines proto-oncogènes c-akt.
- anatomopathologie : Défaillance hépatique aigüe, Hépatite B.
- génétique : Adenoviridae.
- immunologie : Antigènes CD95.
- métabolisme : Anticorps monoclonaux, Antigènes CD95, Antigènes de surface du virus de l'hépatite B, Caspase 8, Défaillance hépatique aigüe, Hépatite B, Protéine de régulation de l'apoptose CASP8 et FADD-like, Protéines proto-oncogènes c-akt.
- pharmacologie : Acétates, Benzopyranes.
- physiologie : Hépatocytes, Virus de l'hépatite B.
- virologie : Hépatocytes.
- Animaux, Apoptose, Cellules HepG2, Cellules cultivées, Humains, Modèles animaux de maladie humaine, Mâle, Phosphorylation, Souris, Souris de lignée C57BL.

English descriptors

KwdEn :
- Acetates (administration & dosage), Acetates (pharmacology), Adenoviridae (genetics), Animals (MeSH), Antibodies, Monoclonal (metabolism), Apoptosis (MeSH), Benzopyrans (administration & dosage), Benzopyrans (pharmacology), CASP8 and FADD-Like Apoptosis Regulating Protein (metabolism), Caspase 8 (metabolism), Cells, Cultured (MeSH), Disease Models, Animal (MeSH), Hep G2 Cells (MeSH), Hepatitis B (metabolism), Hepatitis B (pathology), Hepatitis B Surface Antigens (metabolism), Hepatitis B virus (physiology), Hepatocytes (physiology), Hepatocytes (virology), Humans (MeSH), Liver Failure, Acute (metabolism), Liver Failure, Acute (pathology), Male (MeSH), Mice (MeSH), Mice, Inbred C57BL (MeSH), Phosphorylation (MeSH), Proto-Oncogene Proteins c-akt (agonists), Proto-Oncogene Proteins c-akt (metabolism), fas Receptor (immunology), fas Receptor (metabolism).
MESH :
- chemical , administration & dosage : Acetates, Benzopyrans.
- chemical , agonists : Proto-Oncogene Proteins c-akt.
- chemical , immunology : fas Receptor.
- chemical , metabolism : Antibodies, Monoclonal, CASP8 and FADD-Like Apoptosis Regulating Protein, Caspase 8, Hepatitis B Surface Antigens, Proto-Oncogene Proteins c-akt, fas Receptor.
- chemical , pharmacology : Acetates, Benzopyrans.
- genetics : Adenoviridae.
- metabolism : Hepatitis B, Liver Failure, Acute.
- pathology : Hepatitis B, Liver Failure, Acute.
- physiology : Hepatitis B virus, Hepatocytes.
- virology : Hepatocytes.
- Animals, Apoptosis, Cells, Cultured, Disease Models, Animal, Hep G2 Cells, Humans, Male, Mice, Mice, Inbred C57BL, Phosphorylation.

Abstract

The Fas receptor/ligand system plays a prominent role in hepatic apoptosis and hepatocyte death. Although hepatitis B virus (HBV) surface Ag (HBsAg) is the most abundant HBV protein in the liver and peripheral blood of patients with chronic HBV infection, its role in Fas-mediated hepatocyte apoptosis has not been disclosed. In this study, we report that HBsAg sensitizes HepG2 cells to agonistic anti-Fas Ab CH11-induced apoptosis through increasing the formation of SDS-stable Fas aggregation and procaspase-8 cleavage but decreasing both the expression of cellular FLIP_L/S and the recruitment of FLIP_L/S at the death-inducing signaling complex (DISC). Notably, HBsAg increased endoplasmic reticulum stress and consequently reduced AKT phosphorylation by deactivation of phosphoinositide-dependent kinase-1 (PDPK1) and mechanistic target of rapamycin complex 2 (mTORC2), leading to enhancement of Fas-mediated apoptosis. In a mouse model, expression of HBsAg in mice injected with recombinant adenovirus-associated virus 8 aggravated Jo2-induced acute liver failure, which could be effectively attenuated by the AKT activator SC79. Based on these results, it is concluded that HBsAg predisposes hepatocytes to Fas-mediated apoptosis and mice to acute liver failure via suppression of AKT prosurviving activity, suggesting that interventions directed at enhancing the activation or functional activity of AKT may be of therapeutic value in Fas-mediated progressive liver cell injury and liver diseases.

DOI: 10.4049/jimmunol.1800732
PubMed: 30171166
PubMed Central: PMC6176106

Affiliations:

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Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acetates (administration & dosage)</term>
<term>Acetates (pharmacology)</term>
<term>Adenoviridae (genetics)</term>
<term>Animals (MeSH)</term>
<term>Antibodies, Monoclonal (metabolism)</term>
<term>Apoptosis (MeSH)</term>
<term>Benzopyrans (administration & dosage)</term>
<term>Benzopyrans (pharmacology)</term>
<term>CASP8 and FADD-Like Apoptosis Regulating Protein (metabolism)</term>
<term>Caspase 8 (metabolism)</term>
<term>Cells, Cultured (MeSH)</term>
<term>Disease Models, Animal (MeSH)</term>
<term>Hep G2 Cells (MeSH)</term>
<term>Hepatitis B (metabolism)</term>
<term>Hepatitis B (pathology)</term>
<term>Hepatitis B Surface Antigens (metabolism)</term>
<term>Hepatitis B virus (physiology)</term>
<term>Hepatocytes (physiology)</term>
<term>Hepatocytes (virology)</term>
<term>Humans (MeSH)</term>
<term>Liver Failure, Acute (metabolism)</term>
<term>Liver Failure, Acute (pathology)</term>
<term>Male (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Phosphorylation (MeSH)</term>
<term>Proto-Oncogene Proteins c-akt (agonists)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>fas Receptor (immunology)</term>
<term>fas Receptor (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Acétates (administration et posologie)</term>
<term>Acétates (pharmacologie)</term>
<term>Adenoviridae (génétique)</term>
<term>Animaux (MeSH)</term>
<term>Anticorps monoclonaux (métabolisme)</term>
<term>Antigènes CD95 (immunologie)</term>
<term>Antigènes CD95 (métabolisme)</term>
<term>Antigènes de surface du virus de l'hépatite B (métabolisme)</term>
<term>Apoptose (MeSH)</term>
<term>Benzopyranes (administration et posologie)</term>
<term>Benzopyranes (pharmacologie)</term>
<term>Caspase 8 (métabolisme)</term>
<term>Cellules HepG2 (MeSH)</term>
<term>Cellules cultivées (MeSH)</term>
<term>Défaillance hépatique aigüe (anatomopathologie)</term>
<term>Défaillance hépatique aigüe (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Hépatite B (anatomopathologie)</term>
<term>Hépatite B (métabolisme)</term>
<term>Hépatocytes (physiologie)</term>
<term>Hépatocytes (virologie)</term>
<term>Modèles animaux de maladie humaine (MeSH)</term>
<term>Mâle (MeSH)</term>
<term>Phosphorylation (MeSH)</term>
<term>Protéine de régulation de l'apoptose CASP8 et FADD-like (métabolisme)</term>
<term>Protéines proto-oncogènes c-akt (agonistes)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Virus de l'hépatite B (physiologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Acetates</term>
<term>Benzopyrans</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="agonists" xml:lang="en"><term>Proto-Oncogene Proteins c-akt</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>fas Receptor</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antibodies, Monoclonal</term>
<term>CASP8 and FADD-Like Apoptosis Regulating Protein</term>
<term>Caspase 8</term>
<term>Hepatitis B Surface Antigens</term>
<term>Proto-Oncogene Proteins c-akt</term>
<term>fas Receptor</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Acetates</term>
<term>Benzopyrans</term>
</keywords>
<keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Acétates</term>
<term>Benzopyranes</term>
</keywords>
<keywords scheme="MESH" qualifier="agonistes" xml:lang="fr"><term>Protéines proto-oncogènes c-akt</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Défaillance hépatique aigüe</term>
<term>Hépatite B</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adenoviridae</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Adenoviridae</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Antigènes CD95</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Hepatitis B</term>
<term>Liver Failure, Acute</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Anticorps monoclonaux</term>
<term>Antigènes CD95</term>
<term>Antigènes de surface du virus de l'hépatite B</term>
<term>Caspase 8</term>
<term>Défaillance hépatique aigüe</term>
<term>Hépatite B</term>
<term>Protéine de régulation de l'apoptose CASP8 et FADD-like</term>
<term>Protéines proto-oncogènes c-akt</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Hepatitis B</term>
<term>Liver Failure, Acute</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Acétates</term>
<term>Benzopyranes</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Hépatocytes</term>
<term>Virus de l'hépatite B</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Hepatitis B virus</term>
<term>Hepatocytes</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Hépatocytes</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Hepatocytes</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Apoptosis</term>
<term>Cells, Cultured</term>
<term>Disease Models, Animal</term>
<term>Hep G2 Cells</term>
<term>Humans</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Phosphorylation</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Apoptose</term>
<term>Cellules HepG2</term>
<term>Cellules cultivées</term>
<term>Humains</term>
<term>Modèles animaux de maladie humaine</term>
<term>Mâle</term>
<term>Phosphorylation</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
</keywords>
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<front><div type="abstract" xml:lang="en">The Fas receptor/ligand system plays a prominent role in hepatic apoptosis and hepatocyte death. Although hepatitis B virus (HBV) surface Ag (HBsAg) is the most abundant HBV protein in the liver and peripheral blood of patients with chronic HBV infection, its role in Fas-mediated hepatocyte apoptosis has not been disclosed. In this study, we report that HBsAg sensitizes HepG2 cells to agonistic anti-Fas Ab CH11-induced apoptosis through increasing the formation of SDS-stable Fas aggregation and procaspase-8 cleavage but decreasing both the expression of cellular FLIP<sub>L/S</sub>
 and the recruitment of FLIP<sub>L/S</sub>
 at the death-inducing signaling complex (DISC). Notably, HBsAg increased endoplasmic reticulum stress and consequently reduced AKT phosphorylation by deactivation of phosphoinositide-dependent kinase-1 (PDPK1) and mechanistic target of rapamycin complex 2 (mTORC2), leading to enhancement of Fas-mediated apoptosis. In a mouse model, expression of HBsAg in mice injected with recombinant adenovirus-associated virus 8 aggravated Jo2-induced acute liver failure, which could be effectively attenuated by the AKT activator SC79. Based on these results, it is concluded that HBsAg predisposes hepatocytes to Fas-mediated apoptosis and mice to acute liver failure via suppression of AKT prosurviving activity, suggesting that interventions directed at enhancing the activation or functional activity of AKT may be of therapeutic value in Fas-mediated progressive liver cell injury and liver diseases.</div>
</front>
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<DateCompleted><Year>2019</Year>
<Month>07</Month>
<Day>22</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>07</Month>
<Day>22</Day>
</DateRevised>
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<JournalIssue CitedMedium="Internet"><Volume>201</Volume>
<Issue>8</Issue>
<PubDate><Year>2018</Year>
<Month>10</Month>
<Day>15</Day>
</PubDate>
</JournalIssue>
<Title>Journal of immunology (Baltimore, Md. : 1950)</Title>
<ISOAbbreviation>J Immunol</ISOAbbreviation>
</Journal>
<ArticleTitle>Hepatitis B Virus Surface Antigen Enhances the Sensitivity of Hepatocytes to Fas-Mediated Apoptosis via Suppression of AKT Phosphorylation.</ArticleTitle>
<Pagination><MedlinePgn>2303-2314</MedlinePgn>
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<Abstract><AbstractText>The Fas receptor/ligand system plays a prominent role in hepatic apoptosis and hepatocyte death. Although hepatitis B virus (HBV) surface Ag (HBsAg) is the most abundant HBV protein in the liver and peripheral blood of patients with chronic HBV infection, its role in Fas-mediated hepatocyte apoptosis has not been disclosed. In this study, we report that HBsAg sensitizes HepG2 cells to agonistic anti-Fas Ab CH11-induced apoptosis through increasing the formation of SDS-stable Fas aggregation and procaspase-8 cleavage but decreasing both the expression of cellular FLIP<sub>L/S</sub>
 and the recruitment of FLIP<sub>L/S</sub>
 at the death-inducing signaling complex (DISC). Notably, HBsAg increased endoplasmic reticulum stress and consequently reduced AKT phosphorylation by deactivation of phosphoinositide-dependent kinase-1 (PDPK1) and mechanistic target of rapamycin complex 2 (mTORC2), leading to enhancement of Fas-mediated apoptosis. In a mouse model, expression of HBsAg in mice injected with recombinant adenovirus-associated virus 8 aggravated Jo2-induced acute liver failure, which could be effectively attenuated by the AKT activator SC79. Based on these results, it is concluded that HBsAg predisposes hepatocytes to Fas-mediated apoptosis and mice to acute liver failure via suppression of AKT prosurviving activity, suggesting that interventions directed at enhancing the activation or functional activity of AKT may be of therapeutic value in Fas-mediated progressive liver cell injury and liver diseases.</AbstractText>
<CopyrightInformation>Copyright © 2018 by The American Association of Immunologists, Inc.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jing</LastName>
<ForeName>Zhen-Tang</ForeName>
<Initials>ZT</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Ministry of Education for Gastrointestinal Cancer, School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China; and.</Affiliation>
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<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Wei</ForeName>
<Initials>W</Initials>
<Identifier Source="ORCID">0000-0001-7118-815X</Identifier>
<AffiliationInfo><Affiliation>Key Laboratory of Ministry of Education for Gastrointestinal Cancer, School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China; and.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Key Laboratory of Tumor Microbiology, Department of Medical Microbiology, Fujian Medical University, Fuzhou 350004, China.</Affiliation>
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<ForeName>Shu-Xiang</ForeName>
<Initials>SX</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Ministry of Education for Gastrointestinal Cancer, School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China; and.</Affiliation>
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<ForeName>Yun</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Ministry of Education for Gastrointestinal Cancer, School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China; and.</Affiliation>
</AffiliationInfo>
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<ForeName>Yan-Ting</ForeName>
<Initials>YT</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Ministry of Education for Gastrointestinal Cancer, School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China; and.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Wan-Nan</ForeName>
<Initials>WN</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Ministry of Education for Gastrointestinal Cancer, School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China; and.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Key Laboratory of Tumor Microbiology, Department of Medical Microbiology, Fujian Medical University, Fuzhou 350004, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lin</LastName>
<ForeName>Xin-Jian</ForeName>
<Initials>XJ</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Ministry of Education for Gastrointestinal Cancer, School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China; and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lin</LastName>
<ForeName>Xu</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Ministry of Education for Gastrointestinal Cancer, School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China; and linxu@mail.fjmu.edu.cn.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Key Laboratory of Tumor Microbiology, Department of Medical Microbiology, Fujian Medical University, Fuzhou 350004, China.</Affiliation>
</AffiliationInfo>
</Author>
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<Language>eng</Language>
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<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>08</Month>
<Day>31</Day>
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<CommentsCorrectionsList><CommentsCorrections RefType="ErratumIn"><RefSource>J Immunol. 2020 Jul 1;205(1):300-301</RefSource>
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<name sortKey="Jing, Zhen Tang" sort="Jing, Zhen Tang" uniqKey="Jing Z" first="Zhen-Tang" last="Jing">Zhen-Tang Jing</name>
<name sortKey="Lin, Xin Jian" sort="Lin, Xin Jian" uniqKey="Lin X" first="Xin-Jian" last="Lin">Xin-Jian Lin</name>
<name sortKey="Lin, Yan Ting" sort="Lin, Yan Ting" uniqKey="Lin Y" first="Yan-Ting" last="Lin">Yan-Ting Lin</name>
<name sortKey="Wu, Shu Xiang" sort="Wu, Shu Xiang" uniqKey="Wu S" first="Shu-Xiang" last="Wu">Shu-Xiang Wu</name>
</noCountry>
<country name="République populaire de Chine"><region name="Fujian"><name sortKey="Liu, Wei" sort="Liu, Wei" uniqKey="Liu W" first="Wei" last="Liu">Wei Liu</name>
</region>
<name sortKey="Chen, Wan Nan" sort="Chen, Wan Nan" uniqKey="Chen W" first="Wan-Nan" last="Chen">Wan-Nan Chen</name>
<name sortKey="Lin, Xu" sort="Lin, Xu" uniqKey="Lin X" first="Xu" last="Lin">Xu Lin</name>
<name sortKey="Lin, Xu" sort="Lin, Xu" uniqKey="Lin X" first="Xu" last="Lin">Xu Lin</name>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000589 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000589 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Bois
   |area=    RapamycinFungusV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:30171166
   |texte=   Hepatitis B Virus Surface Antigen Enhances the Sensitivity of Hepatocytes to Fas-Mediated Apoptosis via Suppression of AKT Phosphorylation.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i   -Sk "pubmed:30171166" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd   \
       | NlmPubMed2Wicri -a RapamycinFungusV1

This area was generated with Dilib version V0.6.38.
Data generation: Thu Nov 19 21:55:41 2020. Site generation: Thu Nov 19 22:00:39 2020

	Serveur d'exploration sur la rapamycine et les champignons
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur la rapamycine et les champignons

Hepatitis B Virus Surface Antigen Enhances the Sensitivity of Hepatocytes to Fas-Mediated Apoptosis via Suppression of AKT Phosphorylation.

Hepatitis B Virus Surface Antigen Enhances the Sensitivity of Hepatocytes to Fas-Mediated Apoptosis via Suppression of AKT Phosphorylation.

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