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Activation of NF-kappaB by the full-length nucleocapsid protein of the SARS coronavirus.

Identifieur interne : 004941 ( Main/Exploration ); précédent : 004940; suivant : 004942

Activation of NF-kappaB by the full-length nucleocapsid protein of the SARS coronavirus.

Auteurs : Qing-Jiao Liao [République populaire de Chine] ; Lin-Bai Ye ; Khalid Amine Timani ; Ying-Chun Zeng ; Ying-Long She ; Li Ye ; Zheng-Hui Wu

Source :

RBID : pubmed:16143815

Descripteurs français

English descriptors

Abstract

The severe acute respiratory syndrome coronavirus (SARS-CoV) is the major causative agent for the worldwide outbreak of SARS in 2003. The mechanism by which SARS-CoV causes atypical pneumonia remains unclear. The nuclear factor kappa B (NF-kappaB) is a key transcription factor that activates numerous genes involved in cellular immune response and inflammation. Many studies have shown that NF-kappaB plays an important role in the pathogenesis of lung diseases. In this study, we investigated the possible regulatory interaction between the SARS-CoV nucleocapsid (N) protein and NF-kappaB by luciferase activity assay. Our results showed that the SARS-CoV N protein can significantly activate NF-kappaB only in Vero E6 cells, which are susceptible to SARS-CoV infection, but not in Vero or HeLa cells. This suggests that NF-kappaB activation is cell-specific. Furthermore, NF-kappaB activation in Vero E6 cells expressing the N protein is dose-dependent. Further experiments showed that there is more than one function domain in the N protein responsible for NF-kappaB activation. Our data indicated the possible role of the N protein in the pathogenesis of SARS.

DOI: 10.1111/j.1745-7270.2005.00082.x
PubMed: 16143815


Affiliations:


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Le document en format XML

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<term>Mutation</term>
<term>NF-kappa B (physiology)</term>
<term>Nuclear Localization Signals</term>
<term>Nucleocapsid Proteins (chemistry)</term>
<term>Nucleocapsid Proteins (genetics)</term>
<term>Nucleocapsid Proteins (pharmacology)</term>
<term>Nucleocapsid Proteins (physiology)</term>
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<term>Humains</term>
<term>Mutation</term>
<term>Protéines nucléocapside ()</term>
<term>Protéines nucléocapside (génétique)</term>
<term>Protéines nucléocapside (pharmacologie)</term>
<term>Protéines nucléocapside (physiologie)</term>
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<div type="abstract" xml:lang="en">The severe acute respiratory syndrome coronavirus (SARS-CoV) is the major causative agent for the worldwide outbreak of SARS in 2003. The mechanism by which SARS-CoV causes atypical pneumonia remains unclear. The nuclear factor kappa B (NF-kappaB) is a key transcription factor that activates numerous genes involved in cellular immune response and inflammation. Many studies have shown that NF-kappaB plays an important role in the pathogenesis of lung diseases. In this study, we investigated the possible regulatory interaction between the SARS-CoV nucleocapsid (N) protein and NF-kappaB by luciferase activity assay. Our results showed that the SARS-CoV N protein can significantly activate NF-kappaB only in Vero E6 cells, which are susceptible to SARS-CoV infection, but not in Vero or HeLa cells. This suggests that NF-kappaB activation is cell-specific. Furthermore, NF-kappaB activation in Vero E6 cells expressing the N protein is dose-dependent. Further experiments showed that there is more than one function domain in the N protein responsible for NF-kappaB activation. Our data indicated the possible role of the N protein in the pathogenesis of SARS.</div>
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