SrasV1, PascalFrancis, Corpus, bibRecord, 000363

Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-XL protein

Identifieur interne : 000363 ( PascalFrancis/Corpus ); précédent : 000362; suivant : 000364

Induction 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 Tan

Source :

Journal of virology [ 0022-538X ] ; 2007.

RBID : Pascal:07-0315403

Descripteurs français

Pascal (Inist)
- Coronavirus, Apoptose, Mort cellulaire, Protéine, Virologie, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Apoptosis, Cell death, Coronavirus, Protein, Severe acute respiratory syndrome, Virology.

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-X_L, 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-X_L and other prosurvival proteins (Bcl-2, Bcl-w, Mcl-1, and Al) 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-X_L was observed, suggesting that 7a triggers apoptosis by interfering directly with the prosurvival function of Bcl-X_L. Interestingly, amino acids 224 and 225 within the C-terminal transmembrane domain of Bcl-X_L are essential for the interaction with the 7a protein, although the BH3 domain of Bcl-X_L also contributes to this interaction. In addition, fractionation experiments showed that 7a colocalized with Bcl-X_L at the endoplasmic reticulum as well as the mitochondria, suggesting that they may form complexes in different membranous compartments.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A08	`01`	`1`	`ENG`	`@1 Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-X_L protein`
A11	`01`	`1`		`@1 TAN (Ying-Xim)`
A11	`02`	`1`		`@1 TAN (Timothy H. P.)`
A11	`03`	`1`		`@1 LEE (Marvin J.-R.)`
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A11	`05`	`1`		`@1 GUNALAN (Vithiagaran)`
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A14	`01`			`@1 Collaborative Anti-Viral Research Group, Institute of Molecular and Cell Biology @2 Singapore @3 SGP @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 11 aut.`
A14	`02`			`@1 Victorian Infectious Diseases Reference Laboratory @2 North Melbourne, Victoria @3 AUS @Z 6 aut. @Z 7 aut. @Z 8 aut.`
A14	`03`			`@1 Mechanisms of Apoptosis in Mammalian Cells Group, Institute of Molecular and Cell Biology @2 Singapore @3 SGP @Z 9 aut. @Z 10 aut.`
A20				`@1 6346-6355`
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A44				`@0 0000 @1 © 2007 INIST-CNRS. All rights reserved.`
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C01	`01`		`ENG`	@0 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-X_L, 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-X_L and other prosurvival proteins (Bcl-2, Bcl-w, Mcl-1, and Al) 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-X_L was observed, suggesting that 7a triggers apoptosis by interfering directly with the prosurvival function of Bcl-X_L. Interestingly, amino acids 224 and 225 within the C-terminal transmembrane domain of Bcl-X_L are essential for the interaction with the 7a protein, although the BH3 domain of Bcl-X_L also contributes to this interaction. In addition, fractionation experiments showed that 7a colocalized with Bcl-X_L at the endoplasmic reticulum as well as the mitochondria, suggesting that they may form complexes in different membranous compartments.
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C03	`02`	`X`	`SPA`	`@0 Apoptosis @5 05`
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C03	`05`	`X`	`FRE`	`@0 Virologie @5 08`
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C03	`06`	`X`	`FRE`	`@0 Syndrome respiratoire aigu sévère @2 NM @5 14`
C03	`06`	`X`	`ENG`	`@0 Severe acute respiratory syndrome @2 NM @5 14`
C03	`06`	`X`	`SPA`	`@0 Síndrome respiratorio agudo severo @2 NM @5 14`
C07	`01`	`X`	`FRE`	`@0 Coronaviridae @2 NW`
C07	`01`	`X`	`ENG`	`@0 Coronaviridae @2 NW`
C07	`01`	`X`	`SPA`	`@0 Coronaviridae @2 NW`
C07	`02`	`X`	`FRE`	`@0 Nidovirales @2 NW`
C07	`02`	`X`	`ENG`	`@0 Nidovirales @2 NW`
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C07	`04`	`X`	`FRE`	`@0 Appareil respiratoire pathologie @5 13`
C07	`04`	`X`	`ENG`	`@0 Respiratory disease @5 13`
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C07	`05`	`X`	`FRE`	`@0 Virose`
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C07	`05`	`X`	`SPA`	`@0 Virosis`
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C07	`07`	`X`	`SPA`	`@0 Pulmón patología @5 16`
N21				`@1 204`
N44	`01`			`@1 OTO`
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Format Inist (serveur)

NO :	PASCAL 07-0315403 INIST
ET :	Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-X_L protein
AU :	TAN (Ying-Xim); TAN (Timothy H. P.); LEE (Marvin J.-R.); THAM (Puay-Yoke); GUNALAN (Vithiagaran); DRUCE (Julian); BIRCH (Chris); CATTON (Mike); NAI YANG FU; YU (Victor C.); TAN (Yee-Joo)
AF :	Collaborative Anti-Viral Research Group, Institute of Molecular and Cell Biology/Singapore /Singapour (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 11 aut.); Victorian Infectious Diseases Reference Laboratory/North Melbourne, Victoria/Australie (6 aut., 7 aut., 8 aut.); Mechanisms of Apoptosis in Mammalian Cells Group, Institute of Molecular and Cell Biology/Singapore/Singapour (9 aut., 10 aut.)
DT :	Publication en série; Niveau analytique
SO :	Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2007; Vol. 81; No. 12; Pp. 6346-6355; Bibl. 40 ref.
LA :	Anglais
EA :	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-X_L, 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-X_L and other prosurvival proteins (Bcl-2, Bcl-w, Mcl-1, and Al) 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-X_L was observed, suggesting that 7a triggers apoptosis by interfering directly with the prosurvival function of Bcl-X_L. Interestingly, amino acids 224 and 225 within the C-terminal transmembrane domain of Bcl-X_L are essential for the interaction with the 7a protein, although the BH3 domain of Bcl-X_L also contributes to this interaction. In addition, fractionation experiments showed that 7a colocalized with Bcl-X_L at the endoplasmic reticulum as well as the mitochondria, suggesting that they may form complexes in different membranous compartments.
CC :	002A05C10
FD :	Coronavirus; Apoptose; Mort cellulaire; Protéine; Virologie; Syndrome respiratoire aigu sévère
FG :	Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie
ED :	Coronavirus; Apoptosis; Cell death; Protein; Virology; Severe acute respiratory syndrome
EG :	Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease
SD :	Coronavirus; Apoptosis; Muerte celular; Proteína; Virología; Síndrome respiratorio agudo severo
LO :	INIST-13592.354000149881670190
ID :	07-0315403

Links to Exploration step

Pascal:07-0315403

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-X<sub>L</sub>
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<author><name sortKey="Tham, Puay Yoke" sort="Tham, Puay Yoke" uniqKey="Tham P" first="Puay-Yoke" last="Tham">Puay-Yoke Tham</name>
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<author><name sortKey="Gunalan, Vithiagaran" sort="Gunalan, Vithiagaran" uniqKey="Gunalan V" first="Vithiagaran" last="Gunalan">Vithiagaran Gunalan</name>
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<author><name sortKey="Druce, Julian" sort="Druce, Julian" uniqKey="Druce J" first="Julian" last="Druce">Julian Druce</name>
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<author><name sortKey="Birch, Chris" sort="Birch, Chris" uniqKey="Birch C" first="Chris" last="Birch">Chris Birch</name>
<affiliation><inist:fA14 i1="02"><s1>Victorian Infectious Diseases Reference Laboratory</s1>
<s2>North Melbourne, Victoria</s2>
<s3>AUS</s3>
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<author><name sortKey="Catton, Mike" sort="Catton, Mike" uniqKey="Catton M" first="Mike" last="Catton">Mike Catton</name>
<affiliation><inist:fA14 i1="02"><s1>Victorian Infectious Diseases Reference Laboratory</s1>
<s2>North Melbourne, Victoria</s2>
<s3>AUS</s3>
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<author><name sortKey="Nai Yang Fu" sort="Nai Yang Fu" uniqKey="Nai Yang Fu" last="Nai Yang Fu">NAI YANG FU</name>
<affiliation><inist:fA14 i1="03"><s1>Mechanisms of Apoptosis in Mammalian Cells Group, Institute of Molecular and Cell Biology</s1>
<s2>Singapore</s2>
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</author>
<author><name sortKey="Yu, Victor C" sort="Yu, Victor C" uniqKey="Yu V" first="Victor C." last="Yu">Victor C. Yu</name>
<affiliation><inist:fA14 i1="03"><s1>Mechanisms of Apoptosis in Mammalian Cells Group, Institute of Molecular and Cell Biology</s1>
<s2>Singapore</s2>
<s3>SGP</s3>
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</affiliation>
</author>
<author><name sortKey="Tan, Yee Joo" sort="Tan, Yee Joo" uniqKey="Tan Y" first="Yee-Joo" last="Tan">Yee-Joo Tan</name>
<affiliation><inist:fA14 i1="01"><s1>Collaborative Anti-Viral Research Group, Institute of Molecular and Cell Biology</s1>
<s2>Singapore </s2>
<s3>SGP</s3>
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<series><title level="j" type="main">Journal of virology</title>
<title level="j" type="abbreviated">J. virol.</title>
<idno type="ISSN">0022-538X</idno>
<imprint><date when="2007">2007</date>
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<seriesStmt><title level="j" type="main">Journal of virology</title>
<title level="j" type="abbreviated">J. virol.</title>
<idno type="ISSN">0022-538X</idno>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis</term>
<term>Cell death</term>
<term>Coronavirus</term>
<term>Protein</term>
<term>Severe acute respiratory syndrome</term>
<term>Virology</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Coronavirus</term>
<term>Apoptose</term>
<term>Mort cellulaire</term>
<term>Protéine</term>
<term>Virologie</term>
<term>Syndrome respiratoire aigu sévère</term>
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<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-X<sub>L</sub>
, 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-X<sub>L</sub>
 and other prosurvival proteins (Bcl-2, Bcl-w, Mcl-1, and Al) 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-X<sub>L</sub>
 was observed, suggesting that 7a triggers apoptosis by interfering directly with the prosurvival function of Bcl-X<sub>L</sub>
. Interestingly, amino acids 224 and 225 within the C-terminal transmembrane domain of Bcl-X<sub>L</sub>
 are essential for the interaction with the 7a protein, although the BH3 domain of Bcl-X<sub>L</sub>
 also contributes to this interaction. In addition, fractionation experiments showed that 7a colocalized with Bcl-X<sub>L</sub>
 at the endoplasmic reticulum as well as the mitochondria, suggesting that they may form complexes in different membranous compartments.</div>
</front>
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<fA11 i1="01" i2="1"><s1>TAN (Ying-Xim)</s1>
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<fC01 i1="01" l="ENG"><s0>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-X<sub>L</sub>
, 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-X<sub>L</sub>
 and other prosurvival proteins (Bcl-2, Bcl-w, Mcl-1, and Al) 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-X<sub>L</sub>
 was observed, suggesting that 7a triggers apoptosis by interfering directly with the prosurvival function of Bcl-X<sub>L</sub>
. Interestingly, amino acids 224 and 225 within the C-terminal transmembrane domain of Bcl-X<sub>L</sub>
 are essential for the interaction with the 7a protein, although the BH3 domain of Bcl-X<sub>L</sub>
 also contributes to this interaction. In addition, fractionation experiments showed that 7a colocalized with Bcl-X<sub>L</sub>
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<server><NO>PASCAL 07-0315403 INIST</NO>
<ET>Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-X<sub>L</sub>
 protein</ET>
<AU>TAN (Ying-Xim); TAN (Timothy H. P.); LEE (Marvin J.-R.); THAM (Puay-Yoke); GUNALAN (Vithiagaran); DRUCE (Julian); BIRCH (Chris); CATTON (Mike); NAI YANG FU; YU (Victor C.); TAN (Yee-Joo)</AU>
<AF>Collaborative Anti-Viral Research Group, Institute of Molecular and Cell Biology/Singapore /Singapour (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 11 aut.); Victorian Infectious Diseases Reference Laboratory/North Melbourne, Victoria/Australie (6 aut., 7 aut., 8 aut.); Mechanisms of Apoptosis in Mammalian Cells Group, Institute of Molecular and Cell Biology/Singapore/Singapour (9 aut., 10 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2007; Vol. 81; No. 12; Pp. 6346-6355; Bibl. 40 ref.</SO>
<LA>Anglais</LA>
<EA>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-X<sub>L</sub>
, 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-X<sub>L</sub>
 and other prosurvival proteins (Bcl-2, Bcl-w, Mcl-1, and Al) 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-X<sub>L</sub>
 was observed, suggesting that 7a triggers apoptosis by interfering directly with the prosurvival function of Bcl-X<sub>L</sub>
. Interestingly, amino acids 224 and 225 within the C-terminal transmembrane domain of Bcl-X<sub>L</sub>
 are essential for the interaction with the 7a protein, although the BH3 domain of Bcl-X<sub>L</sub>
 also contributes to this interaction. In addition, fractionation experiments showed that 7a colocalized with Bcl-X<sub>L</sub>
 at the endoplasmic reticulum as well as the mitochondria, suggesting that they may form complexes in different membranous compartments.</EA>
<CC>002A05C10</CC>
<FD>Coronavirus; Apoptose; Mort cellulaire; Protéine; Virologie; Syndrome respiratoire aigu sévère</FD>
<FG>Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie</FG>
<ED>Coronavirus; Apoptosis; Cell death; Protein; Virology; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease</EG>
<SD>Coronavirus; Apoptosis; Muerte celular; Proteína; Virología; Síndrome respiratorio agudo severo</SD>
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Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-XL protein

Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-XL protein

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