Serveur d'exploration SRAS

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.

The SARS-Coronavirus Membrane protein induces apoptosis through modulating the Akt survival pathway.

Identifieur interne : 003578 ( Main/Exploration ); précédent : 003577; suivant : 003579

The SARS-Coronavirus Membrane protein induces apoptosis through modulating the Akt survival pathway.

Auteurs : Chak-Ming Chan [République populaire de Chine] ; Cheuk-Wing Ma ; Wood-Yee Chan ; Ho Yin Edwin Chan

Source :

RBID : pubmed:17306213

Descripteurs français

English descriptors

Abstract

A number of viral gene products are capable of triggering apoptotic cell death through interfering with cellular signaling cascades, including the Akt kinase pathway. In this study, the pro-apoptotic role of the SARS-CoV Membrane (M) structural protein is described. We found that the SARS-CoV M protein induced apoptosis in both HEK293T cells and transgenic Drosophila. We further showed that M protein-induced apoptosis involved mitochondrial release of cytochrome c protein, and could be suppressed by caspase inhibitors. Over-expression of M caused a dominant rough-eye phenotype in adult Drosophila. By performing a forward genetic modifier screen, we identified phosphoinositide-dependent kinase-1 (PDK-1) as a dominant suppressor of M-induced apoptotic cell death. Both PDK-1 and Akt kinases play essential roles in the cell survival signaling pathway. Altogether, our data show that SARS-CoV M protein induces apoptosis through the modulation of the cellular Akt pro-survival pathway and mitochondrial cytochrome c release.

DOI: 10.1016/j.abb.2007.01.012
PubMed: 17306213


Affiliations:


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


Le document en format XML

<record>
<TEI>
<teiHeader>
<fileDesc>
<titleStmt>
<title xml:lang="en">The SARS-Coronavirus Membrane protein induces apoptosis through modulating the Akt survival pathway.</title>
<author>
<name sortKey="Chan, Chak Ming" sort="Chan, Chak Ming" uniqKey="Chan C" first="Chak-Ming" last="Chan">Chak-Ming Chan</name>
<affiliation wicri:level="4">
<nlm:affiliation>Laboratory of Drosophila Research, Department of Biochemistry, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Laboratory of Drosophila Research, Department of Biochemistry, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR</wicri:regionArea>
<orgName type="university">Université chinoise de Hong Kong</orgName>
<placeName>
<settlement type="city">Sha Tin</settlement>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Ma, Cheuk Wing" sort="Ma, Cheuk Wing" uniqKey="Ma C" first="Cheuk-Wing" last="Ma">Cheuk-Wing Ma</name>
</author>
<author>
<name sortKey="Chan, Wood Yee" sort="Chan, Wood Yee" uniqKey="Chan W" first="Wood-Yee" last="Chan">Wood-Yee Chan</name>
</author>
<author>
<name sortKey="Chan, Ho Yin Edwin" sort="Chan, Ho Yin Edwin" uniqKey="Chan H" first="Ho Yin Edwin" last="Chan">Ho Yin Edwin Chan</name>
</author>
</titleStmt>
<publicationStmt>
<idno type="wicri:source">PubMed</idno>
<date when="2007">2007</date>
<idno type="RBID">pubmed:17306213</idno>
<idno type="pmid">17306213</idno>
<idno type="doi">10.1016/j.abb.2007.01.012</idno>
<idno type="wicri:Area/PubMed/Corpus">001E94</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001E94</idno>
<idno type="wicri:Area/PubMed/Curation">001E94</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001E94</idno>
<idno type="wicri:Area/PubMed/Checkpoint">001C66</idno>
<idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001C66</idno>
<idno type="wicri:Area/Ncbi/Merge">001874</idno>
<idno type="wicri:Area/Ncbi/Curation">001874</idno>
<idno type="wicri:Area/Ncbi/Checkpoint">001874</idno>
<idno type="wicri:doubleKey">0003-9861:2007:Chan C:the:sars:coronavirus</idno>
<idno type="wicri:Area/Main/Merge">003690</idno>
<idno type="wicri:Area/Main/Curation">003578</idno>
<idno type="wicri:Area/Main/Exploration">003578</idno>
</publicationStmt>
<sourceDesc>
<biblStruct>
<analytic>
<title xml:lang="en">The SARS-Coronavirus Membrane protein induces apoptosis through modulating the Akt survival pathway.</title>
<author>
<name sortKey="Chan, Chak Ming" sort="Chan, Chak Ming" uniqKey="Chan C" first="Chak-Ming" last="Chan">Chak-Ming Chan</name>
<affiliation wicri:level="4">
<nlm:affiliation>Laboratory of Drosophila Research, Department of Biochemistry, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Laboratory of Drosophila Research, Department of Biochemistry, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR</wicri:regionArea>
<orgName type="university">Université chinoise de Hong Kong</orgName>
<placeName>
<settlement type="city">Sha Tin</settlement>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Ma, Cheuk Wing" sort="Ma, Cheuk Wing" uniqKey="Ma C" first="Cheuk-Wing" last="Ma">Cheuk-Wing Ma</name>
</author>
<author>
<name sortKey="Chan, Wood Yee" sort="Chan, Wood Yee" uniqKey="Chan W" first="Wood-Yee" last="Chan">Wood-Yee Chan</name>
</author>
<author>
<name sortKey="Chan, Ho Yin Edwin" sort="Chan, Ho Yin Edwin" uniqKey="Chan H" first="Ho Yin Edwin" last="Chan">Ho Yin Edwin Chan</name>
</author>
</analytic>
<series>
<title level="j">Archives of biochemistry and biophysics</title>
<idno type="ISSN">0003-9861</idno>
<imprint>
<date when="2007" type="published">2007</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="KwdEn" xml:lang="en">
<term>Animals</term>
<term>Animals, Genetically Modified</term>
<term>Apoptosis (physiology)</term>
<term>Cell Line</term>
<term>Cell Survival</term>
<term>Drosophila</term>
<term>Humans</term>
<term>Kidney (pathology)</term>
<term>Oncogene Protein v-akt (metabolism)</term>
<term>Phosphorylation</term>
<term>SARS Virus (metabolism)</term>
<term>Signal Transduction (physiology)</term>
<term>Viral Matrix Proteins (genetics)</term>
<term>Viral Matrix Proteins (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr">
<term>Animal génétiquement modifié</term>
<term>Animaux</term>
<term>Apoptose (physiologie)</term>
<term>Drosophila</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Phosphorylation</term>
<term>Protéine oncogène v-akt (métabolisme)</term>
<term>Protéines de la matrice virale (génétique)</term>
<term>Protéines de la matrice virale (métabolisme)</term>
<term>Rein (anatomopathologie)</term>
<term>Survie cellulaire</term>
<term>Transduction du signal (physiologie)</term>
<term>Virus du SRAS (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en">
<term>Viral Matrix Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en">
<term>Oncogene Protein v-akt</term>
<term>Viral Matrix Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr">
<term>Rein</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr">
<term>Protéines de la matrice virale</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en">
<term>SARS Virus</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr">
<term>Protéine oncogène v-akt</term>
<term>Protéines de la matrice virale</term>
<term>Virus du SRAS</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en">
<term>Kidney</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr">
<term>Apoptose</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en">
<term>Apoptosis</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Animals</term>
<term>Animals, Genetically Modified</term>
<term>Cell Line</term>
<term>Cell Survival</term>
<term>Drosophila</term>
<term>Humans</term>
<term>Phosphorylation</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr">
<term>Animal génétiquement modifié</term>
<term>Animaux</term>
<term>Drosophila</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Phosphorylation</term>
<term>Survie cellulaire</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">A number of viral gene products are capable of triggering apoptotic cell death through interfering with cellular signaling cascades, including the Akt kinase pathway. In this study, the pro-apoptotic role of the SARS-CoV Membrane (M) structural protein is described. We found that the SARS-CoV M protein induced apoptosis in both HEK293T cells and transgenic Drosophila. We further showed that M protein-induced apoptosis involved mitochondrial release of cytochrome c protein, and could be suppressed by caspase inhibitors. Over-expression of M caused a dominant rough-eye phenotype in adult Drosophila. By performing a forward genetic modifier screen, we identified phosphoinositide-dependent kinase-1 (PDK-1) as a dominant suppressor of M-induced apoptotic cell death. Both PDK-1 and Akt kinases play essential roles in the cell survival signaling pathway. Altogether, our data show that SARS-CoV M protein induces apoptosis through the modulation of the cellular Akt pro-survival pathway and mitochondrial cytochrome c release.</div>
</front>
</TEI>
<affiliations>
<list>
<country>
<li>République populaire de Chine</li>
</country>
<settlement>
<li>Sha Tin</li>
</settlement>
<orgName>
<li>Université chinoise de Hong Kong</li>
</orgName>
</list>
<tree>
<noCountry>
<name sortKey="Chan, Ho Yin Edwin" sort="Chan, Ho Yin Edwin" uniqKey="Chan H" first="Ho Yin Edwin" last="Chan">Ho Yin Edwin Chan</name>
<name sortKey="Chan, Wood Yee" sort="Chan, Wood Yee" uniqKey="Chan W" first="Wood-Yee" last="Chan">Wood-Yee Chan</name>
<name sortKey="Ma, Cheuk Wing" sort="Ma, Cheuk Wing" uniqKey="Ma C" first="Cheuk-Wing" last="Ma">Cheuk-Wing Ma</name>
</noCountry>
<country name="République populaire de Chine">
<noRegion>
<name sortKey="Chan, Chak Ming" sort="Chan, Chak Ming" uniqKey="Chan C" first="Chak-Ming" last="Chan">Chak-Ming Chan</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Sante/explor/SrasV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 003578 | SxmlIndent | more

Ou

HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 003578 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Sante
   |area=    SrasV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:17306213
   |texte=   The SARS-Coronavirus Membrane protein induces apoptosis through modulating the Akt survival pathway.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i   -Sk "pubmed:17306213" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd   \
       | NlmPubMed2Wicri -a SrasV1 

Wicri

This area was generated with Dilib version V0.6.33.
Data generation: Tue Apr 28 14:49:16 2020. Site generation: Sat Mar 27 22:06:49 2021