The SARS-coronavirus membrane protein induces apoptosis via interfering with PDK1-PKB/Akt signalling.
Identifieur interne : 000F01 ( PubMed/Checkpoint ); précédent : 000F00; suivant : 000F02The SARS-coronavirus membrane protein induces apoptosis via interfering with PDK1-PKB/Akt signalling.
Auteurs : Ho Tsoi [République populaire de Chine] ; Li Li [République populaire de Chine] ; Zhefan S. Chen [République populaire de Chine] ; Kwok-Fai Lau [République populaire de Chine] ; Stephen K W. Tsui [République populaire de Chine] ; Ho Yin Edwin Chan [République populaire de Chine]Source :
- The Biochemical journal [ 1470-8728 ] ; 2014.
Descripteurs français
- KwdFr :
- Apoptose, Caspases (métabolisme), Cellules HEK293, Humains, Liaison aux protéines, Motifs et domaines d'intéraction protéique, Protein-Serine-Threonine Kinases (métabolisme), Protéines de la matrice virale (), Protéines de la matrice virale (métabolisme), Protéines proto-oncogènes c-akt (métabolisme), Transduction du signal (), Virus du SRAS (métabolisme).
- MESH :
English descriptors
- KwdEn :
- Apoptosis, Caspases (metabolism), HEK293 Cells, Humans, Protein Binding, Protein Interaction Domains and Motifs, Protein-Serine-Threonine Kinases (metabolism), Proto-Oncogene Proteins c-akt (metabolism), Pyruvate Dehydrogenase (Acetyl-Transferring) Kinase, SARS Virus (metabolism), Signal Transduction (drug effects), Viral Matrix Proteins (chemistry), Viral Matrix Proteins (metabolism).
- MESH :
- chemical , chemistry : Viral Matrix Proteins.
- chemical , metabolism : Caspases, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins c-akt, Viral Matrix Proteins.
- drug effects : Signal Transduction.
- metabolism : SARS Virus.
- Apoptosis, HEK293 Cells, Humans, Protein Binding, Protein Interaction Domains and Motifs, Pyruvate Dehydrogenase (Acetyl-Transferring) Kinase.
Abstract
A number of viral gene products are capable of inducing apoptosis by interfering with various cellular signalling cascades. We previously reported the pro-apoptotic property of the SARS-CoV (severe acute respiratory syndrome coronavirus) M (membrane)-protein and a down-regulation of the phosphorylation level of the cell-survival protein PKB (protein kinase B)/Akt in cells expressing M-protein. We also showed that overexpression of PDK1 (3-phosphoinositide-dependent protein kinase 1), the immediate upstream kinase of PKB/Akt, suppressed M-induced apoptosis. This illustrates that M-protein perturbs the PDK1 and PKB/Akt cell survival signalling pathway. In the present study, we demonstrated that the C-terminus of M-protein interacts with the PH (pleckstrin homology) domain of PDK1. This interaction disrupted the association between PDK1 and PKB/Akt, and led to down-regulation of PKB/Akt activity. This subsequently reduced the level of the phosphorylated forkhead transcription factor FKHRL1 and ASK (apoptosis signal-regulating kinase), and led to the activation of caspases 8 and 9. Altogether, our data demonstrate that the SARS-CoV M-protein induces apoptosis through disrupting the interaction of PDK1 with PKB/Akt, and this causes the activation of apoptosis. Our work highlights that the SARS-CoV M protein is highly pro-apoptotic and is capable of simultaneously inducing apoptosis via initiating caspases 8 and 9. Preventing the interaction between M-protein and PDK1 is a plausible therapeutic approach to target the pro-apoptotic property of SARS-CoV.
DOI: 10.1042/BJ20131461
PubMed: 25271362
Affiliations:
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pubmed:25271362Le document en format XML
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<front><div type="abstract" xml:lang="en">A number of viral gene products are capable of inducing apoptosis by interfering with various cellular signalling cascades. We previously reported the pro-apoptotic property of the SARS-CoV (severe acute respiratory syndrome coronavirus) M (membrane)-protein and a down-regulation of the phosphorylation level of the cell-survival protein PKB (protein kinase B)/Akt in cells expressing M-protein. We also showed that overexpression of PDK1 (3-phosphoinositide-dependent protein kinase 1), the immediate upstream kinase of PKB/Akt, suppressed M-induced apoptosis. This illustrates that M-protein perturbs the PDK1 and PKB/Akt cell survival signalling pathway. In the present study, we demonstrated that the C-terminus of M-protein interacts with the PH (pleckstrin homology) domain of PDK1. This interaction disrupted the association between PDK1 and PKB/Akt, and led to down-regulation of PKB/Akt activity. This subsequently reduced the level of the phosphorylated forkhead transcription factor FKHRL1 and ASK (apoptosis signal-regulating kinase), and led to the activation of caspases 8 and 9. Altogether, our data demonstrate that the SARS-CoV M-protein induces apoptosis through disrupting the interaction of PDK1 with PKB/Akt, and this causes the activation of apoptosis. Our work highlights that the SARS-CoV M protein is highly pro-apoptotic and is capable of simultaneously inducing apoptosis via initiating caspases 8 and 9. Preventing the interaction between M-protein and PDK1 is a plausible therapeutic approach to target the pro-apoptotic property of SARS-CoV. </div>
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<Abstract><AbstractText>A number of viral gene products are capable of inducing apoptosis by interfering with various cellular signalling cascades. We previously reported the pro-apoptotic property of the SARS-CoV (severe acute respiratory syndrome coronavirus) M (membrane)-protein and a down-regulation of the phosphorylation level of the cell-survival protein PKB (protein kinase B)/Akt in cells expressing M-protein. We also showed that overexpression of PDK1 (3-phosphoinositide-dependent protein kinase 1), the immediate upstream kinase of PKB/Akt, suppressed M-induced apoptosis. This illustrates that M-protein perturbs the PDK1 and PKB/Akt cell survival signalling pathway. In the present study, we demonstrated that the C-terminus of M-protein interacts with the PH (pleckstrin homology) domain of PDK1. This interaction disrupted the association between PDK1 and PKB/Akt, and led to down-regulation of PKB/Akt activity. This subsequently reduced the level of the phosphorylated forkhead transcription factor FKHRL1 and ASK (apoptosis signal-regulating kinase), and led to the activation of caspases 8 and 9. Altogether, our data demonstrate that the SARS-CoV M-protein induces apoptosis through disrupting the interaction of PDK1 with PKB/Akt, and this causes the activation of apoptosis. Our work highlights that the SARS-CoV M protein is highly pro-apoptotic and is capable of simultaneously inducing apoptosis via initiating caspases 8 and 9. Preventing the interaction between M-protein and PDK1 is a plausible therapeutic approach to target the pro-apoptotic property of SARS-CoV. </AbstractText>
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<affiliations><list><country><li>République populaire de Chine</li>
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<settlement><li>Sha Tin</li>
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<orgName><li>Université chinoise de Hong Kong</li>
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<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="Chen, Zhefan S" sort="Chen, Zhefan S" uniqKey="Chen Z" first="Zhefan S" last="Chen">Zhefan S. Chen</name>
<name sortKey="Lau, Kwok Fai" sort="Lau, Kwok Fai" uniqKey="Lau K" first="Kwok-Fai" last="Lau">Kwok-Fai Lau</name>
<name sortKey="Li, Li" sort="Li, Li" uniqKey="Li L" first="Li" last="Li">Li Li</name>
<name sortKey="Tsui, Stephen K W" sort="Tsui, Stephen K W" uniqKey="Tsui S" first="Stephen K W" last="Tsui">Stephen K W. Tsui</name>
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