Bcl-xL inhibits T-cell apoptosis induced by expression of SARS coronavirus E protein in the absence of growth factors.
Identifieur interne : 002618 ( PubMed/Corpus ); précédent : 002617; suivant : 002619Bcl-xL inhibits T-cell apoptosis induced by expression of SARS coronavirus E protein in the absence of growth factors.
Auteurs : Yu Yang ; Zeyu Xiong ; Sheng Zhang ; Yan Yan ; Justin Nguyen ; Bernard Ng ; Huifang Lu ; John Brendese ; Fan Yang ; Hong Wang ; Xiao-Feng YangSource :
- The Biochemical journal [ 1470-8728 ] ; 2005.
English descriptors
- KwdEn :
- Amino Acid Sequence, Apoptosis, Gene Expression Regulation, Viral, Growth Substances (metabolism), Humans, Jurkat Cells, Molecular Sequence Data, Protein Structure, Tertiary, SARS Virus (physiology), T-Lymphocytes (cytology), T-Lymphocytes (metabolism), T-Lymphocytes (virology), Viral Envelope Proteins (genetics), Viral Envelope Proteins (metabolism), bcl-X Protein (metabolism).
- MESH :
- chemical , genetics : Viral Envelope Proteins.
- chemical , metabolism : Growth Substances, Viral Envelope Proteins, bcl-X Protein.
- cytology : T-Lymphocytes.
- metabolism : T-Lymphocytes.
- physiology : SARS Virus.
- virology : T-Lymphocytes.
- Amino Acid Sequence, Apoptosis, Gene Expression Regulation, Viral, Humans, Jurkat Cells, Molecular Sequence Data, Protein Structure, Tertiary.
Abstract
One of the hallmark findings in patients suffering from SARS (severe acute respiratory syndrome) is lymphopenia, which is the result of massive lymphocyte death. SARS-CoV (SARS coronavirus), a novel coronavirus that has been etiologically associated with SARS cases, is homologous with MHV (murine hepatitis coronavirus), and MHV small envelope E protein is capable of inducing apoptosis. We hypothesized that SARS-CoV encodes a small envelope E protein that is homologous with MHV E protein, thus inducing T-cell apoptosis. To test this hypothesis, a cDNA encoding SARS-CoV E protein was created using whole gene synthesis. Our results showed that SARS-CoV E protein induced apoptosis in the transfected Jurkat T-cells, which was amplified to higher apoptosis rates in the absence of growth factors. However, apoptosis was inhibited by overexpressed antiapoptotic protein Bcl-xL. Moreover, we found that SARS-CoV E protein interacted with Bcl-xL in vitro and endogenous Bcl-xL in vivo and that Bcl-xL interaction with SARS-CoV E protein was mediated by BH3 (Bcl-2 homology domain 3) of Bcl-xL. Finally, we identified a novel BH3-like region located in the C-terminal cytosolic domain of SARS-CoV E protein, which mediates its binding to Bcl-xL. These results demonstrate, for the first time, a novel molecular mechanism of T-cell apoptosis that contributes to the SARS-CoV-induced lymphopenia observed in most SARS patients.
DOI: 10.1042/BJ20050698
PubMed: 16048439
Links to Exploration step
pubmed:16048439Le document en format XML
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Nguyen</name></author><author><name sortKey="Ng, Bernard" sort="Ng, Bernard" uniqKey="Ng B" first="Bernard" last="Ng">Bernard Ng</name></author><author><name sortKey="Lu, Huifang" sort="Lu, Huifang" uniqKey="Lu H" first="Huifang" last="Lu">Huifang Lu</name></author><author><name sortKey="Brendese, John" sort="Brendese, John" uniqKey="Brendese J" first="John" last="Brendese">John Brendese</name></author><author><name sortKey="Yang, Fan" sort="Yang, Fan" uniqKey="Yang F" first="Fan" last="Yang">Fan Yang</name></author><author><name sortKey="Wang, Hong" sort="Wang, Hong" uniqKey="Wang H" first="Hong" last="Wang">Hong Wang</name></author><author><name sortKey="Yang, Xiao Feng" sort="Yang, Xiao Feng" uniqKey="Yang X" first="Xiao-Feng" last="Yang">Xiao-Feng Yang</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:16048439</idno><idno type="pmid">16048439</idno><idno type="doi">10.1042/BJ20050698</idno><idno 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last="Yan">Yan Yan</name></author><author><name sortKey="Nguyen, Justin" sort="Nguyen, Justin" uniqKey="Nguyen J" first="Justin" last="Nguyen">Justin Nguyen</name></author><author><name sortKey="Ng, Bernard" sort="Ng, Bernard" uniqKey="Ng B" first="Bernard" last="Ng">Bernard Ng</name></author><author><name sortKey="Lu, Huifang" sort="Lu, Huifang" uniqKey="Lu H" first="Huifang" last="Lu">Huifang Lu</name></author><author><name sortKey="Brendese, John" sort="Brendese, John" uniqKey="Brendese J" first="John" last="Brendese">John Brendese</name></author><author><name sortKey="Yang, Fan" sort="Yang, Fan" uniqKey="Yang F" first="Fan" last="Yang">Fan Yang</name></author><author><name sortKey="Wang, Hong" sort="Wang, Hong" uniqKey="Wang H" first="Hong" last="Wang">Hong Wang</name></author><author><name sortKey="Yang, Xiao Feng" sort="Yang, Xiao Feng" uniqKey="Yang X" first="Xiao-Feng" last="Yang">Xiao-Feng Yang</name></author></analytic><series><title level="j">The Biochemical journal</title><idno type="eISSN">1470-8728</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amino Acid Sequence</term><term>Apoptosis</term><term>Gene Expression Regulation, Viral</term><term>Growth Substances (metabolism)</term><term>Humans</term><term>Jurkat Cells</term><term>Molecular Sequence Data</term><term>Protein Structure, Tertiary</term><term>SARS Virus (physiology)</term><term>T-Lymphocytes (cytology)</term><term>T-Lymphocytes (metabolism)</term><term>T-Lymphocytes (virology)</term><term>Viral Envelope Proteins (genetics)</term><term>Viral Envelope Proteins (metabolism)</term><term>bcl-X Protein (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Viral Envelope Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Growth Substances</term><term>Viral Envelope Proteins</term><term>bcl-X Protein</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Amino Acid Sequence</term><term>Apoptosis</term><term>Gene Expression Regulation, Viral</term><term>Humans</term><term>Jurkat Cells</term><term>Molecular Sequence Data</term><term>Protein Structure, Tertiary</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">One of the hallmark findings in patients suffering from SARS (severe acute respiratory syndrome) is lymphopenia, which is the result of massive lymphocyte death. SARS-CoV (SARS coronavirus), a novel coronavirus that has been etiologically associated with SARS cases, is homologous with MHV (murine hepatitis coronavirus), and MHV small envelope E protein is capable of inducing apoptosis. We hypothesized that SARS-CoV encodes a small envelope E protein that is homologous with MHV E protein, thus inducing T-cell apoptosis. To test this hypothesis, a cDNA encoding SARS-CoV E protein was created using whole gene synthesis. Our results showed that SARS-CoV E protein induced apoptosis in the transfected Jurkat T-cells, which was amplified to higher apoptosis rates in the absence of growth factors. However, apoptosis was inhibited by overexpressed antiapoptotic protein Bcl-xL. Moreover, we found that SARS-CoV E protein interacted with Bcl-xL in vitro and endogenous Bcl-xL in vivo and that Bcl-xL interaction with SARS-CoV E protein was mediated by BH3 (Bcl-2 homology domain 3) of Bcl-xL. Finally, we identified a novel BH3-like region located in the C-terminal cytosolic domain of SARS-CoV E protein, which mediates its binding to Bcl-xL. These results demonstrate, for the first time, a novel molecular mechanism of T-cell apoptosis that contributes to the SARS-CoV-induced lymphopenia observed in most SARS patients.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16048439</PMID><DateCompleted><Year>2006</Year><Month>02</Month><Day>21</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1470-8728</ISSN><JournalIssue CitedMedium="Internet"><Volume>392</Volume><Issue>Pt 1</Issue><PubDate><Year>2005</Year><Month>Nov</Month><Day>15</Day></PubDate></JournalIssue><Title>The Biochemical journal</Title><ISOAbbreviation>Biochem. J.</ISOAbbreviation></Journal><ArticleTitle>Bcl-xL inhibits T-cell apoptosis induced by expression of SARS coronavirus E protein in the absence of growth factors.</ArticleTitle><Pagination><MedlinePgn>135-43</MedlinePgn></Pagination><Abstract><AbstractText>One of the hallmark findings in patients suffering from SARS (severe acute respiratory syndrome) is lymphopenia, which is the result of massive lymphocyte death. SARS-CoV (SARS coronavirus), a novel coronavirus that has been etiologically associated with SARS cases, is homologous with MHV (murine hepatitis coronavirus), and MHV small envelope E protein is capable of inducing apoptosis. We hypothesized that SARS-CoV encodes a small envelope E protein that is homologous with MHV E protein, thus inducing T-cell apoptosis. To test this hypothesis, a cDNA encoding SARS-CoV E protein was created using whole gene synthesis. Our results showed that SARS-CoV E protein induced apoptosis in the transfected Jurkat T-cells, which was amplified to higher apoptosis rates in the absence of growth factors. However, apoptosis was inhibited by overexpressed antiapoptotic protein Bcl-xL. Moreover, we found that SARS-CoV E protein interacted with Bcl-xL in vitro and endogenous Bcl-xL in vivo and that Bcl-xL interaction with SARS-CoV E protein was mediated by BH3 (Bcl-2 homology domain 3) of Bcl-xL. Finally, we identified a novel BH3-like region located in the C-terminal cytosolic domain of SARS-CoV E protein, which mediates its binding to Bcl-xL. These results demonstrate, for the first time, a novel molecular mechanism of T-cell apoptosis that contributes to the SARS-CoV-induced lymphopenia observed in most SARS patients.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Yu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Medicine, Laboratory of Immunopathology, Biology of Inflammation Center, Baylor College of Medicine, Houston, TX 77030, U.S.A.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xiong</LastName><ForeName>Zeyu</ForeName><Initials>Z</Initials></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Sheng</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Yan</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Nguyen</LastName><ForeName>Justin</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Ng</LastName><ForeName>Bernard</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Huifang</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Brendese</LastName><ForeName>John</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Fan</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Hong</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Xiao-Feng</ForeName><Initials>XF</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>K08 AI054514</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P20 CA103698</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI054514</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 DK56238</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DK056238</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Biochem J</MedlineTA><NlmUniqueID>2984726R</NlmUniqueID><ISSNLinking>0264-6021</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C494811">BCL2L1 protein, 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