SrasV1, PubMed, Corpus, bibRecord, 001E29

Signal transduction in SARS-CoV-infected cells.

Identifieur interne : 001E29 ( PubMed/Corpus ); précédent : 001E28; suivant : 001E30

Signal transduction in SARS-CoV-infected cells.

Auteurs : T. Mizutani

Source :

Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2007.

RBID : pubmed:17470913

English descriptors

KwdEn :
- Animals, Apoptosis, Cell Survival, Chlorocebus aethiops, Cytokines (biosynthesis), Genes, Viral, Humans, MAP Kinase Signaling System, Proto-Oncogene Proteins c-akt (metabolism), SARS Virus (genetics), SARS Virus (immunology), SARS Virus (physiology), Severe Acute Respiratory Syndrome (virology), Signal Transduction, Transcription Factors (metabolism), Vero Cells.
MESH :
- chemical , biosynthesis : Cytokines.
- chemical , metabolism : Proto-Oncogene Proteins c-akt, Transcription Factors.
- genetics : SARS Virus.
- immunology : SARS Virus.
- physiology : SARS Virus.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Apoptosis, Cell Survival, Chlorocebus aethiops, Genes, Viral, Humans, MAP Kinase Signaling System, Signal Transduction, Vero Cells.

Abstract

Severe acute respiratory syndrome (SARS) is a newly found infectious disease that is caused by a novel human coronavirus, SARS coronavirus (SARS-CoV). Because the mortality rate of SARS patients is very high, understanding the pathological mechanisms of SARS not only in vivo but in vitro is important for the prevention of SARS. Activation of signaling pathways caused by SARS-CoV infection leads to the phosphorylation and activation of downstream molecules. Two conflicting cellular programs, apoptosis to eliminate virus-infected cells and survival to delay apoptosis by producing antiviral cytokines, occur in SARS patients. Recent studies regarding SARS and SARS-CoV have clarified that activation of mitogen-activated protein kinases (MAPKs) plays important roles in upregulation of cytokine expression and apoptosis both in vitro and in vivo. Both Akt and p38 MAPK are keys for determination of cell survival or death in SARS-CoV-infected cells in vitro. Agents being developed to target these signaling cascades may be important for the design of anti-SARS-CoV drugs. This review highlights recent progress regarding SARS-CoV biology, especially signal transduction in SARS-CoV-infected cells.

DOI: 10.1196/annals.1408.006
PubMed: 17470913

Links to Exploration step

pubmed:17470913

Le document en format XML

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<author><name sortKey="Mizutani, T" sort="Mizutani, T" uniqKey="Mizutani T" first="T" last="Mizutani">T. Mizutani</name>
<affiliation><nlm:affiliation>Department of Virology 1, National Institute of Infectious Diseases, Gakuen 4-7-1, Musashimurayama, Tokyo, Japan. tmizutan@nih.go.jp</nlm:affiliation>
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<author><name sortKey="Mizutani, T" sort="Mizutani, T" uniqKey="Mizutani T" first="T" last="Mizutani">T. Mizutani</name>
<affiliation><nlm:affiliation>Department of Virology 1, National Institute of Infectious Diseases, Gakuen 4-7-1, Musashimurayama, Tokyo, Japan. tmizutan@nih.go.jp</nlm:affiliation>
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<series><title level="j">Annals of the New York Academy of Sciences</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Apoptosis</term>
<term>Cell Survival</term>
<term>Chlorocebus aethiops</term>
<term>Cytokines (biosynthesis)</term>
<term>Genes, Viral</term>
<term>Humans</term>
<term>MAP Kinase Signaling System</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>SARS Virus (genetics)</term>
<term>SARS Virus (immunology)</term>
<term>SARS Virus (physiology)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
<term>Signal Transduction</term>
<term>Transcription Factors (metabolism)</term>
<term>Vero Cells</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Cytokines</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Proto-Oncogene Proteins c-akt</term>
<term>Transcription Factors</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>SARS Virus</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>SARS Virus</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Apoptosis</term>
<term>Cell Survival</term>
<term>Chlorocebus aethiops</term>
<term>Genes, Viral</term>
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<front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) is a newly found infectious disease that is caused by a novel human coronavirus, SARS coronavirus (SARS-CoV). Because the mortality rate of SARS patients is very high, understanding the pathological mechanisms of SARS not only in vivo but in vitro is important for the prevention of SARS. Activation of signaling pathways caused by SARS-CoV infection leads to the phosphorylation and activation of downstream molecules. Two conflicting cellular programs, apoptosis to eliminate virus-infected cells and survival to delay apoptosis by producing antiviral cytokines, occur in SARS patients. Recent studies regarding SARS and SARS-CoV have clarified that activation of mitogen-activated protein kinases (MAPKs) plays important roles in upregulation of cytokine expression and apoptosis both in vitro and in vivo. Both Akt and p38 MAPK are keys for determination of cell survival or death in SARS-CoV-infected cells in vitro. Agents being developed to target these signaling cascades may be important for the design of anti-SARS-CoV drugs. This review highlights recent progress regarding SARS-CoV biology, especially signal transduction in SARS-CoV-infected cells.</div>
</front>
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<DateCompleted><Year>2007</Year>
<Month>06</Month>
<Day>14</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>12</Month>
<Day>10</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Print">0077-8923</ISSN>
<JournalIssue CitedMedium="Print"><Volume>1102</Volume>
<PubDate><Year>2007</Year>
<Month>Apr</Month>
</PubDate>
</JournalIssue>
<Title>Annals of the New York Academy of Sciences</Title>
<ISOAbbreviation>Ann. N. Y. Acad. Sci.</ISOAbbreviation>
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<ArticleTitle>Signal transduction in SARS-CoV-infected cells.</ArticleTitle>
<Pagination><MedlinePgn>86-95</MedlinePgn>
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<Abstract><AbstractText>Severe acute respiratory syndrome (SARS) is a newly found infectious disease that is caused by a novel human coronavirus, SARS coronavirus (SARS-CoV). Because the mortality rate of SARS patients is very high, understanding the pathological mechanisms of SARS not only in vivo but in vitro is important for the prevention of SARS. Activation of signaling pathways caused by SARS-CoV infection leads to the phosphorylation and activation of downstream molecules. Two conflicting cellular programs, apoptosis to eliminate virus-infected cells and survival to delay apoptosis by producing antiviral cytokines, occur in SARS patients. Recent studies regarding SARS and SARS-CoV have clarified that activation of mitogen-activated protein kinases (MAPKs) plays important roles in upregulation of cytokine expression and apoptosis both in vitro and in vivo. Both Akt and p38 MAPK are keys for determination of cell survival or death in SARS-CoV-infected cells in vitro. Agents being developed to target these signaling cascades may be important for the design of anti-SARS-CoV drugs. This review highlights recent progress regarding SARS-CoV biology, especially signal transduction in SARS-CoV-infected cells.</AbstractText>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mizutani</LastName>
<ForeName>T</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Department of Virology 1, National Institute of Infectious Diseases, Gakuen 4-7-1, Musashimurayama, Tokyo, Japan. tmizutan@nih.go.jp</Affiliation>
</AffiliationInfo>
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<Language>eng</Language>
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<Chemical><RegistryNumber>0</RegistryNumber>
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<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
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<MeshHeading><DescriptorName UI="D002470" MajorTopicYN="Y">Cell Survival</DescriptorName>
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<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
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<MeshHeading><DescriptorName UI="D020935" MajorTopicYN="N">MAP Kinase Signaling System</DescriptorName>
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<MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014709" MajorTopicYN="N">Vero Cells</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<NumberOfReferences>43</NumberOfReferences>
</MedlineCitation>
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<Day>2</Day>
<Hour>9</Hour>
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Signal transduction in SARS-CoV-infected cells.

Signal transduction in SARS-CoV-infected cells.

Source :

English descriptors

Abstract

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki