Severe acute respiratory syndrome coronavirus 7a accessory protein is a viral structural protein.
Identifieur interne : 001573 ( Ncbi/Merge ); précédent : 001572; suivant : 001574Severe acute respiratory syndrome coronavirus 7a accessory protein is a viral structural protein.
Auteurs : Cheng Huang [États-Unis] ; Naoto Ito ; Chien-Te K. Tseng ; Shinji MakinoSource :
- Journal of virology [ 0022-538X ] ; 2006.
Descripteurs français
- KwdFr :
- Assemblage viral, Cellules cultivées, Humains, Immunoprécipitation, Plasmides, Protéines de la matrice virale (physiologie), Protéines virales (physiologie), Protéines virales structurales (physiologie), Rein (embryologie), Rein (virologie), Syndrome respiratoire aigu sévère (virologie), Technique de Western, Virus du SRAS (physiologie).
- MESH :
- embryologie : Rein.
- physiologie : Protéines de la matrice virale, Protéines virales, Protéines virales structurales, Virus du SRAS.
- virologie : Rein, Syndrome respiratoire aigu sévère.
- Assemblage viral, Cellules cultivées, Humains, Immunoprécipitation, Plasmides, Technique de Western.
English descriptors
- KwdEn :
- Blotting, Western, Cells, Cultured, Humans, Immunoprecipitation, Kidney (embryology), Kidney (virology), Plasmids, SARS Virus (physiology), Severe Acute Respiratory Syndrome (virology), Viral Matrix Proteins (physiology), Viral Proteins (physiology), Viral Structural Proteins (physiology), Virus Assembly.
- MESH :
- chemical , physiology : Viral Matrix Proteins, Viral Proteins, Viral Structural Proteins.
- embryology : Kidney.
- physiology : SARS Virus.
- virology : Kidney, Severe Acute Respiratory Syndrome.
- Blotting, Western, Cells, Cultured, Humans, Immunoprecipitation, Plasmids, Virus Assembly.
Abstract
Severe acute respiratory syndrome coronavirus (SCoV) 7a protein is one of the viral accessory proteins. In expressing cells, 7a protein exhibits a variety of biological activities, including induction of apoptosis, activation of the mitogen-activated protein kinase signaling pathway, inhibition of host protein translation, and suppression of cell growth progression. Analysis of SCoV particles that were purified by either sucrose gradient equilibrium centrifugation or a virus capture assay, in which intact SCoV particles were specifically immunoprecipitated by anti-S protein monoclonal antibody, demonstrated that 7a protein was associated with purified SCoV particles. Coexpression of 7a protein with SCoV S, M, N, and E proteins resulted in production of virus-like particles (VLPs) carrying 7a protein, while 7a protein was not released from cells expressing 7a protein alone. Although interaction between 7a protein and another SCoV accessory protein, 3a, has been reported, 3a protein was dispensable for assembly of 7a protein into VLPs. S protein was not required for the 7a protein incorporation into VLPs, and yet 7a protein interacted with S protein in coexpressing cells. These data established that, in addition to 3a protein, 7a protein was a SCoV accessory protein identified as a SCoV structural protein.
DOI: 10.1128/JVI.00414-06
PubMed: 16840309
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Tseng</name></author><author><name sortKey="Makino, Shinji" sort="Makino, Shinji" uniqKey="Makino S" first="Shinji" last="Makino">Shinji Makino</name></author></analytic><series><title level="j">Journal of virology</title><idno type="ISSN">0022-538X</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Blotting, Western</term><term>Cells, Cultured</term><term>Humans</term><term>Immunoprecipitation</term><term>Kidney (embryology)</term><term>Kidney (virology)</term><term>Plasmids</term><term>SARS Virus (physiology)</term><term>Severe Acute Respiratory Syndrome (virology)</term><term>Viral Matrix Proteins (physiology)</term><term>Viral Proteins (physiology)</term><term>Viral Structural Proteins (physiology)</term><term>Virus Assembly</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Assemblage viral</term><term>Cellules cultivées</term><term>Humains</term><term>Immunoprécipitation</term><term>Plasmides</term><term>Protéines de la matrice virale (physiologie)</term><term>Protéines virales (physiologie)</term><term>Protéines virales structurales (physiologie)</term><term>Rein (embryologie)</term><term>Rein (virologie)</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Technique de Western</term><term>Virus du SRAS (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Viral Matrix Proteins</term><term>Viral Proteins</term><term>Viral Structural Proteins</term></keywords><keywords scheme="MESH" qualifier="embryologie" xml:lang="fr"><term>Rein</term></keywords><keywords scheme="MESH" qualifier="embryology" xml:lang="en"><term>Kidney</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Protéines de la matrice virale</term><term>Protéines virales</term><term>Protéines virales structurales</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Rein</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Kidney</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Blotting, Western</term><term>Cells, Cultured</term><term>Humans</term><term>Immunoprecipitation</term><term>Plasmids</term><term>Virus Assembly</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Assemblage viral</term><term>Cellules cultivées</term><term>Humains</term><term>Immunoprécipitation</term><term>Plasmides</term><term>Technique de Western</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome coronavirus (SCoV) 7a protein is one of the viral accessory proteins. In expressing cells, 7a protein exhibits a variety of biological activities, including induction of apoptosis, activation of the mitogen-activated protein kinase signaling pathway, inhibition of host protein translation, and suppression of cell growth progression. Analysis of SCoV particles that were purified by either sucrose gradient equilibrium centrifugation or a virus capture assay, in which intact SCoV particles were specifically immunoprecipitated by anti-S protein monoclonal antibody, demonstrated that 7a protein was associated with purified SCoV particles. Coexpression of 7a protein with SCoV S, M, N, and E proteins resulted in production of virus-like particles (VLPs) carrying 7a protein, while 7a protein was not released from cells expressing 7a protein alone. Although interaction between 7a protein and another SCoV accessory protein, 3a, has been reported, 3a protein was dispensable for assembly of 7a protein into VLPs. S protein was not required for the 7a protein incorporation into VLPs, and yet 7a protein interacted with S protein in coexpressing cells. These data established that, in addition to 3a protein, 7a protein was a SCoV accessory protein identified as a SCoV structural protein.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16840309</PMID><DateCompleted><Year>2006</Year><Month>08</Month><Day>18</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-538X</ISSN><JournalIssue CitedMedium="Print"><Volume>80</Volume><Issue>15</Issue><PubDate><Year>2006</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Severe acute respiratory syndrome coronavirus 7a accessory protein is a viral structural protein.</ArticleTitle><Pagination><MedlinePgn>7287-94</MedlinePgn></Pagination><Abstract><AbstractText>Severe acute respiratory syndrome coronavirus (SCoV) 7a protein is one of the viral accessory proteins. In expressing cells, 7a protein exhibits a variety of biological activities, including induction of apoptosis, activation of the mitogen-activated protein kinase signaling pathway, inhibition of host protein translation, and suppression of cell growth progression. Analysis of SCoV particles that were purified by either sucrose gradient equilibrium centrifugation or a virus capture assay, in which intact SCoV particles were specifically immunoprecipitated by anti-S protein monoclonal antibody, demonstrated that 7a protein was associated with purified SCoV particles. Coexpression of 7a protein with SCoV S, M, N, and E proteins resulted in production of virus-like particles (VLPs) carrying 7a protein, while 7a protein was not released from cells expressing 7a protein alone. Although interaction between 7a protein and another SCoV accessory protein, 3a, has been reported, 3a protein was dispensable for assembly of 7a protein into VLPs. S protein was not required for the 7a protein incorporation into VLPs, and yet 7a protein interacted with S protein in coexpressing cells. These data established that, in addition to 3a protein, 7a protein was a SCoV accessory protein identified as a SCoV structural protein.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Cheng</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, The University of Texas Medical Branch at Galveston, Galveston, TX 77555-1019, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ito</LastName><ForeName>Naoto</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Tseng</LastName><ForeName>Chien-Te K</ForeName><Initials>CT</Initials></Author><Author ValidYN="Y"><LastName>Makino</LastName><ForeName>Shinji</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>N01AI30039</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>N01 AI 30039</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 AI029984</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI 29984</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI029984</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J 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Tseng</name></noCountry><country name="États-Unis"><region name="Texas"><name sortKey="Huang, Cheng" sort="Huang, Cheng" uniqKey="Huang C" first="Cheng" last="Huang">Cheng Huang</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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