SrasV1, Ncbi, Merge, bibRecord, 001422

Nucleocapsid protein of SARS-CoV activates the expression of cyclooxygenase-2 by binding directly to regulatory elements for nuclear factor-kappa B and CCAAT/enhancer binding protein.

Identifieur interne : 001422 ( Ncbi/Merge ); précédent : 001421; suivant : 001423

Nucleocapsid protein of SARS-CoV activates the expression of cyclooxygenase-2 by binding directly to regulatory elements for nuclear factor-kappa B and CCAAT/enhancer binding protein.

Auteurs : Xiaohong Yan [République populaire de Chine] ; Qian Hao ; Yongxin Mu ; Khalid Amine Timani ; Linbai Ye ; Ying Zhu ; Jianguo Wu

Source :

The international journal of biochemistry & cell biology [ 1357-2725 ] ; 2006.

RBID : pubmed:16546436

Descripteurs français

English descriptors

KwdEn :
- Amino Acid Sequence, Binding Sites (genetics), CCAAT-Enhancer-Binding Protein-beta (metabolism), Cell Line, Chromatin Immunoprecipitation, Cyclooxygenase 2 (genetics), Cyclooxygenase 2 (metabolism), Electrophoretic Mobility Shift Assay, Gene Expression Regulation, Enzymologic, Humans, Mutagenesis, Site-Directed (methods), Mutation, NF-kappa B (metabolism), Nucleocapsid Proteins (genetics), Nucleocapsid Proteins (metabolism), Nucleocapsid Proteins (physiology), Plasmids (genetics), Promoter Regions, Genetic (genetics), Protein Binding, SARS Virus (genetics), SARS Virus (metabolism), Transcriptional Activation.
MESH :
- chemical , genetics : Cyclooxygenase 2, Nucleocapsid Proteins.
- chemical , metabolism : CCAAT-Enhancer-Binding Protein-beta, Cyclooxygenase 2, NF-kappa B, Nucleocapsid Proteins.
- genetics : Binding Sites, Plasmids, Promoter Regions, Genetic, SARS Virus.
- metabolism : SARS Virus.
- methods : Mutagenesis, Site-Directed.
- chemical , physiology : Nucleocapsid Proteins.
- Amino Acid Sequence, Cell Line, Chromatin Immunoprecipitation, Electrophoretic Mobility Shift Assay, Gene Expression Regulation, Enzymologic, Humans, Mutation, Protein Binding, Transcriptional Activation.

Abstract

SARS-associated coronavirus (SARS-CoV) causes inflammation and damage to the lungs resulting in severe acute respiratory syndrome. To evaluate the molecular mechanisms behind this event, we investigated the roles of SARS-CoV proteins in regulation of the proinflammatory factor, cyclooxygenase-2 (COX-2). Individual viral proteins were tested for their abilities to regulate COX-2 gene expression. Results showed that the COX-2 promoter was activated by the nucleocapsid (N) protein in a concentration-dependent manner. Western blot analysis indicated that N protein was sufficient to stimulate the production of COX-2 protein in mammalian cells. COX-2 promoter mutations suggested that activation of COX-2 transcription depended on two regulatory elements, a nuclear factor-kappa B (NF-kappaB) binding site, and a CCAAT/enhancer binding protein (C/EBP) binding site. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) demonstrated that SARS-CoV N protein bound directly to these regulatory sequences. Protein mutation analysis revealed that a Lys-rich motif of N protein acted as a nuclear localization signal and was essential for the activation of COX-2. In addition, a Leu-rich motif was found to be required for the N protein function. A sequence of 68 residuals was identified as a potential DNA-binding domain essential for activating COX-2 expression. We propose that SARS-CoV N protein causes inflammation of the lungs by activating COX-2 gene expression by binding directly to the promoter resulting in inflammation through multiple COX-2 signaling cascades.

DOI: 10.1016/j.biocel.2006.02.003
PubMed: 16546436

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Le document en format XML

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<front><div type="abstract" xml:lang="en">SARS-associated coronavirus (SARS-CoV) causes inflammation and damage to the lungs resulting in severe acute respiratory syndrome. To evaluate the molecular mechanisms behind this event, we investigated the roles of SARS-CoV proteins in regulation of the proinflammatory factor, cyclooxygenase-2 (COX-2). Individual viral proteins were tested for their abilities to regulate COX-2 gene expression. Results showed that the COX-2 promoter was activated by the nucleocapsid (N) protein in a concentration-dependent manner. Western blot analysis indicated that N protein was sufficient to stimulate the production of COX-2 protein in mammalian cells. COX-2 promoter mutations suggested that activation of COX-2 transcription depended on two regulatory elements, a nuclear factor-kappa B (NF-kappaB) binding site, and a CCAAT/enhancer binding protein (C/EBP) binding site. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) demonstrated that SARS-CoV N protein bound directly to these regulatory sequences. Protein mutation analysis revealed that a Lys-rich motif of N protein acted as a nuclear localization signal and was essential for the activation of COX-2. In addition, a Leu-rich motif was found to be required for the N protein function. A sequence of 68 residuals was identified as a potential DNA-binding domain essential for activating COX-2 expression. We propose that SARS-CoV N protein causes inflammation of the lungs by activating COX-2 gene expression by binding directly to the promoter resulting in inflammation through multiple COX-2 signaling cascades.</div>
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<Abstract><AbstractText>SARS-associated coronavirus (SARS-CoV) causes inflammation and damage to the lungs resulting in severe acute respiratory syndrome. To evaluate the molecular mechanisms behind this event, we investigated the roles of SARS-CoV proteins in regulation of the proinflammatory factor, cyclooxygenase-2 (COX-2). Individual viral proteins were tested for their abilities to regulate COX-2 gene expression. Results showed that the COX-2 promoter was activated by the nucleocapsid (N) protein in a concentration-dependent manner. Western blot analysis indicated that N protein was sufficient to stimulate the production of COX-2 protein in mammalian cells. COX-2 promoter mutations suggested that activation of COX-2 transcription depended on two regulatory elements, a nuclear factor-kappa B (NF-kappaB) binding site, and a CCAAT/enhancer binding protein (C/EBP) binding site. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) demonstrated that SARS-CoV N protein bound directly to these regulatory sequences. Protein mutation analysis revealed that a Lys-rich motif of N protein acted as a nuclear localization signal and was essential for the activation of COX-2. In addition, a Leu-rich motif was found to be required for the N protein function. A sequence of 68 residuals was identified as a potential DNA-binding domain essential for activating COX-2 expression. We propose that SARS-CoV N protein causes inflammation of the lungs by activating COX-2 gene expression by binding directly to the promoter resulting in inflammation through multiple COX-2 signaling cascades.</AbstractText>
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<ReferenceList><Reference><Citation>Proteomics. 2005 Mar;5(4):925-37</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15759315</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Proc Natl Acad Sci U S A. 2001 Jun 5;98(12):6905-10</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11381123</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Biochem Biophys Res Commun. 2004 Apr 2;316(2):476-83</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15020242</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>J Virol. 2004 Dec;78(23):12964-74</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15542648</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Viral Immunol. 2003;16(4):447-60</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14733733</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Mol Pharmacol. 2002 Aug;62(2):326-33</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12130685</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Acta Biochim Biophys Sin (Shanghai). 2004 Nov;36(11):754-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15514849</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>J Biol Chem. 2002 Mar 1;277(9):6923-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11741938</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Genomics Proteomics Bioinformatics. 2003 May;1(2):145-54</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15626344</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Science. 2003 May 30;300(5624):1394-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12730500</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>J Virol. 2001 Oct;75(19):9345-56</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11533198</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>J Virol. 2003 Mar;77(5):2922-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12584316</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Eur J Biochem. 2000 Dec;267(23):6798-809</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11082190</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Science. 2003 May 30;300(5624):1399-404</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12730501</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1953-66</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12690092</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Genes Dev. 1991 Sep;5(9):1553-67</Citation>
<ArticleIdList><ArticleId IdType="pubmed">1884998</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Biochem Biophys Res Commun. 1998 Mar 27;244(3):819-24</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9535750</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>J Biol Chem. 2001 Jun 1;276(22):18897-904</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11278846</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>J Clin Invest. 2002 Dec;110(12):1831-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12488433</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1995-2005</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12671061</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>J Biol Chem. 2003 Feb 14;278(7):4770-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12471036</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Biochem Biophys Res Commun. 2003 Nov 28;311(4):870-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14623261</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Gut. 2004 Nov;53(11):1665-72</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15479690</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Biochem J. 2004 Oct 1;383(Pt 1):13-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15294014</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>J Biol Chem. 1998 Oct 16;273(42):27686-94</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9765305</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Virus Genes. 2005 Jan;30(1):93-102</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15744567</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>J Virol. 2004 Sep;78(18):9721-30</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15331705</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
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Nucleocapsid protein of SARS-CoV activates the expression of cyclooxygenase-2 by binding directly to regulatory elements for nuclear factor-kappa B and CCAAT/enhancer binding protein.

Nucleocapsid protein of SARS-CoV activates the expression of cyclooxygenase-2 by binding directly to regulatory elements for nuclear factor-kappa B and CCAAT/enhancer binding protein.

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