The SARS-Coronavirus Membrane protein induces apoptosis through modulating the Akt survival pathway.
Identifieur interne : 001C66 ( PubMed/Checkpoint ); précédent : 001C65; suivant : 001C67The 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 ChanSource :
- Archives of biochemistry and biophysics [ 0003-9861 ] ; 2007.
Descripteurs français
- KwdFr :
- Animal génétiquement modifié, Animaux, Apoptose (physiologie), Drosophila, Humains, Lignée cellulaire, Phosphorylation, Protéine oncogène v-akt (métabolisme), Protéines de la matrice virale (génétique), Protéines de la matrice virale (métabolisme), Rein (anatomopathologie), Survie cellulaire, Transduction du signal (physiologie), Virus du SRAS (métabolisme).
- MESH :
- anatomopathologie : Rein.
- génétique : Protéines de la matrice virale.
- métabolisme : Protéine oncogène v-akt, Protéines de la matrice virale, Virus du SRAS.
- physiologie : Apoptose, Transduction du signal.
- Animal génétiquement modifié, Animaux, Drosophila, Humains, Lignée cellulaire, Phosphorylation, Survie cellulaire.
English descriptors
- KwdEn :
- Animals, Animals, Genetically Modified, Apoptosis (physiology), Cell Line, Cell Survival, Drosophila, Humans, Kidney (pathology), Oncogene Protein v-akt (metabolism), Phosphorylation, SARS Virus (metabolism), Signal Transduction (physiology), Viral Matrix Proteins (genetics), Viral Matrix Proteins (metabolism).
- MESH :
- chemical , genetics : Viral Matrix Proteins.
- chemical , metabolism : Oncogene Protein v-akt, Viral Matrix Proteins.
- metabolism : SARS Virus.
- pathology : Kidney.
- physiology : Apoptosis, Signal Transduction.
- Animals, Animals, Genetically Modified, Cell Line, Cell Survival, Drosophila, Humans, Phosphorylation.
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:
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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></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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17306213</PMID><DateCompleted><Year>2007</Year><Month>05</Month><Day>18</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0003-9861</ISSN><JournalIssue CitedMedium="Print"><Volume>459</Volume><Issue>2</Issue><PubDate><Year>2007</Year><Month>Mar</Month><Day>15</Day></PubDate></JournalIssue><Title>Archives of biochemistry and biophysics</Title><ISOAbbreviation>Arch. Biochem. Biophys.</ISOAbbreviation></Journal><ArticleTitle>The SARS-Coronavirus Membrane protein induces apoptosis through modulating the Akt survival pathway.</ArticleTitle><Pagination><MedlinePgn>197-207</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chan</LastName><ForeName>Chak-Ming</ForeName><Initials>CM</Initials><AffiliationInfo><Affiliation>Laboratory of Drosophila Research, Department of Biochemistry, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Cheuk-Wing</ForeName><Initials>CW</Initials></Author><Author ValidYN="Y"><LastName>Chan</LastName><ForeName>Wood-Yee</ForeName><Initials>WY</Initials></Author><Author ValidYN="Y"><LastName>Chan</LastName><ForeName>Ho Yin Edwin</ForeName><Initials>HY</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType 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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)
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