Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-XL protein.
Identifieur interne : 001E46 ( PubMed/Corpus ); précédent : 001E45; suivant : 001E47Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-XL protein.
Auteurs : Ying-Xim Tan ; Timothy H P. Tan ; Marvin J-R Lee ; Puay-Yoke Tham ; Vithiagaran Gunalan ; Julian Druce ; Chris Birch ; Mike Catton ; Nai Yang Fu ; Victor C. Yu ; Yee-Joo TanSource :
- Journal of virology [ 0022-538X ] ; 2007.
English descriptors
- KwdEn :
- Amino Acid Sequence, Animals, Apoptosis, Chlorocebus aethiops, Gene Deletion, Humans, Immunoprecipitation, Mitochondria (metabolism), Molecular Sequence Data, Mutation, Protein Structure, Tertiary, Sequence Homology, Amino Acid, Vero Cells, Viral Matrix Proteins (metabolism), Viral Matrix Proteins (physiology), Viral Proteins (metabolism), Viral Proteins (physiology), bcl-X Protein (metabolism).
- MESH :
- chemical , metabolism : Viral Matrix Proteins, Viral Proteins, bcl-X Protein.
- metabolism : Mitochondria.
- chemical , physiology : Viral Matrix Proteins, Viral Proteins.
- Amino Acid Sequence, Animals, Apoptosis, Chlorocebus aethiops, Gene Deletion, Humans, Immunoprecipitation, Molecular Sequence Data, Mutation, Protein Structure, Tertiary, Sequence Homology, Amino Acid, Vero Cells.
Abstract
The severe acute respiratory syndrome coronavirus (SARS-CoV) 7a protein, which is not expressed by other known coronaviruses, can induce apoptosis in various cell lines. In this study, we show that the overexpression of Bcl-XL, a prosurvival member of the Bcl-2 family, blocks 7a-induced apoptosis, suggesting that the mechanism for apoptosis induction by 7a is at the level of or upstream from the Bcl-2 family. Coimmunoprecipitation experiments showed that 7a interacts with Bcl-XL and other prosurvival proteins (Bcl-2, Bcl-w, Mcl-1, and A1) but not with the proapoptotic proteins (Bax, Bak, Bad, and Bid). A good correlation between the abilities of 7a deletion mutants to induce apoptosis and to interact with Bcl-XL was observed, suggesting that 7a triggers apoptosis by interfering directly with the prosurvival function of Bcl-XL. Interestingly, amino acids 224 and 225 within the C-terminal transmembrane domain of Bcl-XL are essential for the interaction with the 7a protein, although the BH3 domain of Bcl-XL also contributes to this interaction. In addition, fractionation experiments showed that 7a colocalized with Bcl-XL at the endoplasmic reticulum as well as the mitochondria, suggesting that they may form complexes in different membranous compartments.
DOI: 10.1128/JVI.00090-07
PubMed: 17428862
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pubmed:17428862Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-XL protein.</title><author><name sortKey="Tan, Ying Xim" sort="Tan, Ying Xim" uniqKey="Tan Y" first="Ying-Xim" last="Tan">Ying-Xim Tan</name><affiliation><nlm:affiliation>Collaborative Anti-Viral Research Group, Institute of Molecular and Cell Biology, 61 Biopolis Drive, Proteos, Singapore 138673, Republic of Singapore.</nlm:affiliation></affiliation></author><author><name sortKey="Tan, Timothy H P" sort="Tan, Timothy H P" uniqKey="Tan T" first="Timothy H P" last="Tan">Timothy H P. Tan</name></author><author><name sortKey="Lee, Marvin J R" sort="Lee, Marvin J R" uniqKey="Lee M" first="Marvin J-R" last="Lee">Marvin J-R Lee</name></author><author><name sortKey="Tham, Puay Yoke" sort="Tham, Puay Yoke" uniqKey="Tham P" first="Puay-Yoke" last="Tham">Puay-Yoke Tham</name></author><author><name sortKey="Gunalan, Vithiagaran" sort="Gunalan, Vithiagaran" uniqKey="Gunalan V" first="Vithiagaran" last="Gunalan">Vithiagaran Gunalan</name></author><author><name sortKey="Druce, Julian" sort="Druce, Julian" uniqKey="Druce J" first="Julian" last="Druce">Julian Druce</name></author><author><name sortKey="Birch, Chris" sort="Birch, Chris" uniqKey="Birch C" first="Chris" last="Birch">Chris Birch</name></author><author><name sortKey="Catton, Mike" sort="Catton, Mike" uniqKey="Catton M" first="Mike" last="Catton">Mike Catton</name></author><author><name sortKey="Fu, Nai Yang" sort="Fu, Nai Yang" uniqKey="Fu N" first="Nai Yang" last="Fu">Nai Yang Fu</name></author><author><name sortKey="Yu, Victor C" sort="Yu, Victor C" uniqKey="Yu V" first="Victor C" last="Yu">Victor C. Yu</name></author><author><name sortKey="Tan, Yee Joo" sort="Tan, Yee Joo" uniqKey="Tan Y" first="Yee-Joo" last="Tan">Yee-Joo Tan</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="RBID">pubmed:17428862</idno><idno type="pmid">17428862</idno><idno type="doi">10.1128/JVI.00090-07</idno><idno type="wicri:Area/PubMed/Corpus">001E46</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001E46</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-XL protein.</title><author><name sortKey="Tan, Ying Xim" sort="Tan, Ying Xim" uniqKey="Tan Y" first="Ying-Xim" last="Tan">Ying-Xim Tan</name><affiliation><nlm:affiliation>Collaborative Anti-Viral Research Group, Institute of Molecular and Cell Biology, 61 Biopolis Drive, Proteos, Singapore 138673, Republic of Singapore.</nlm:affiliation></affiliation></author><author><name sortKey="Tan, Timothy H P" sort="Tan, Timothy H P" uniqKey="Tan T" first="Timothy H P" last="Tan">Timothy H P. Tan</name></author><author><name sortKey="Lee, Marvin J R" sort="Lee, Marvin J R" uniqKey="Lee M" first="Marvin J-R" last="Lee">Marvin J-R Lee</name></author><author><name sortKey="Tham, Puay Yoke" sort="Tham, Puay Yoke" uniqKey="Tham P" first="Puay-Yoke" last="Tham">Puay-Yoke Tham</name></author><author><name sortKey="Gunalan, Vithiagaran" sort="Gunalan, Vithiagaran" uniqKey="Gunalan V" first="Vithiagaran" last="Gunalan">Vithiagaran Gunalan</name></author><author><name sortKey="Druce, Julian" sort="Druce, Julian" uniqKey="Druce J" first="Julian" last="Druce">Julian Druce</name></author><author><name sortKey="Birch, Chris" sort="Birch, Chris" uniqKey="Birch C" first="Chris" last="Birch">Chris Birch</name></author><author><name sortKey="Catton, Mike" sort="Catton, Mike" uniqKey="Catton M" first="Mike" last="Catton">Mike Catton</name></author><author><name sortKey="Fu, Nai Yang" sort="Fu, Nai Yang" uniqKey="Fu N" first="Nai Yang" last="Fu">Nai Yang Fu</name></author><author><name sortKey="Yu, Victor C" sort="Yu, Victor C" uniqKey="Yu V" first="Victor C" last="Yu">Victor C. Yu</name></author><author><name sortKey="Tan, Yee Joo" sort="Tan, Yee Joo" uniqKey="Tan Y" first="Yee-Joo" last="Tan">Yee-Joo Tan</name></author></analytic><series><title level="j">Journal of virology</title><idno type="ISSN">0022-538X</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amino Acid Sequence</term><term>Animals</term><term>Apoptosis</term><term>Chlorocebus aethiops</term><term>Gene Deletion</term><term>Humans</term><term>Immunoprecipitation</term><term>Mitochondria (metabolism)</term><term>Molecular Sequence Data</term><term>Mutation</term><term>Protein Structure, Tertiary</term><term>Sequence Homology, Amino Acid</term><term>Vero Cells</term><term>Viral Matrix Proteins (metabolism)</term><term>Viral Matrix Proteins (physiology)</term><term>Viral Proteins (metabolism)</term><term>Viral Proteins (physiology)</term><term>bcl-X Protein (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Viral Matrix Proteins</term><term>Viral Proteins</term><term>bcl-X Protein</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mitochondria</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Viral Matrix Proteins</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Amino Acid Sequence</term><term>Animals</term><term>Apoptosis</term><term>Chlorocebus aethiops</term><term>Gene Deletion</term><term>Humans</term><term>Immunoprecipitation</term><term>Molecular Sequence Data</term><term>Mutation</term><term>Protein Structure, Tertiary</term><term>Sequence Homology, Amino Acid</term><term>Vero Cells</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The severe acute respiratory syndrome coronavirus (SARS-CoV) 7a protein, which is not expressed by other known coronaviruses, can induce apoptosis in various cell lines. In this study, we show that the overexpression of Bcl-XL, a prosurvival member of the Bcl-2 family, blocks 7a-induced apoptosis, suggesting that the mechanism for apoptosis induction by 7a is at the level of or upstream from the Bcl-2 family. Coimmunoprecipitation experiments showed that 7a interacts with Bcl-XL and other prosurvival proteins (Bcl-2, Bcl-w, Mcl-1, and A1) but not with the proapoptotic proteins (Bax, Bak, Bad, and Bid). A good correlation between the abilities of 7a deletion mutants to induce apoptosis and to interact with Bcl-XL was observed, suggesting that 7a triggers apoptosis by interfering directly with the prosurvival function of Bcl-XL. Interestingly, amino acids 224 and 225 within the C-terminal transmembrane domain of Bcl-XL are essential for the interaction with the 7a protein, although the BH3 domain of Bcl-XL also contributes to this interaction. In addition, fractionation experiments showed that 7a colocalized with Bcl-XL at the endoplasmic reticulum as well as the mitochondria, suggesting that they may form complexes in different membranous compartments.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17428862</PMID><DateCompleted><Year>2007</Year><Month>07</Month><Day>11</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0022-538X</ISSN><JournalIssue CitedMedium="Print"><Volume>81</Volume><Issue>12</Issue><PubDate><Year>2007</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-XL protein.</ArticleTitle><Pagination><MedlinePgn>6346-55</MedlinePgn></Pagination><Abstract><AbstractText>The severe acute respiratory syndrome coronavirus (SARS-CoV) 7a protein, which is not expressed by other known coronaviruses, can induce apoptosis in various cell lines. In this study, we show that the overexpression of Bcl-XL, a prosurvival member of the Bcl-2 family, blocks 7a-induced apoptosis, suggesting that the mechanism for apoptosis induction by 7a is at the level of or upstream from the Bcl-2 family. Coimmunoprecipitation experiments showed that 7a interacts with Bcl-XL and other prosurvival proteins (Bcl-2, Bcl-w, Mcl-1, and A1) but not with the proapoptotic proteins (Bax, Bak, Bad, and Bid). A good correlation between the abilities of 7a deletion mutants to induce apoptosis and to interact with Bcl-XL was observed, suggesting that 7a triggers apoptosis by interfering directly with the prosurvival function of Bcl-XL. Interestingly, amino acids 224 and 225 within the C-terminal transmembrane domain of Bcl-XL are essential for the interaction with the 7a protein, although the BH3 domain of Bcl-XL also contributes to this interaction. In addition, fractionation experiments showed that 7a colocalized with Bcl-XL at the endoplasmic reticulum as well as the mitochondria, suggesting that they may form complexes in different membranous compartments.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tan</LastName><ForeName>Ying-Xim</ForeName><Initials>YX</Initials><AffiliationInfo><Affiliation>Collaborative Anti-Viral Research Group, Institute of Molecular and Cell Biology, 61 Biopolis Drive, Proteos, Singapore 138673, Republic of Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tan</LastName><ForeName>Timothy H P</ForeName><Initials>TH</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Marvin J-R</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>Tham</LastName><ForeName>Puay-Yoke</ForeName><Initials>PY</Initials></Author><Author ValidYN="Y"><LastName>Gunalan</LastName><ForeName>Vithiagaran</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Druce</LastName><ForeName>Julian</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Birch</LastName><ForeName>Chris</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Catton</LastName><ForeName>Mike</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Fu</LastName><ForeName>Nai Yang</ForeName><Initials>NY</Initials></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Victor C</ForeName><Initials>VC</Initials></Author><Author ValidYN="Y"><LastName>Tan</LastName><ForeName>Yee-Joo</ForeName><Initials>YJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2007</Year><Month>04</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Virol</MedlineTA><NlmUniqueID>0113724</NlmUniqueID><ISSNLinking>0022-538X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014763">Viral Matrix Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014764">Viral Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051020">bcl-X Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C488151">sars7a protein, SARS virus</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000595" MajorTopicYN="N">Amino Acid Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" 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