MAVS-mediated apoptosis and its inhibition by viral proteins.
Identifieur interne : 002A78 ( Main/Exploration ); précédent : 002A77; suivant : 002A79MAVS-mediated apoptosis and its inhibition by viral proteins.
Auteurs : Yu Lei [États-Unis] ; Chris B. Moore ; Rachael M. Liesman ; Brian P. O'Connor ; Daniel T. Bergstralh ; Zhijian J. Chen ; Raymond J. Pickles ; Jenny P-Y TingSource :
- PloS one [ 1932-6203 ] ; 2009.
Descripteurs français
- KwdFr :
- Animaux, Apoptose (immunologie), Apoptose (physiologie), Caspases (métabolisme), Cellules cultivées, Facteur de transcription NF-kappa B (métabolisme), Facteur-3 de régulation d'interféron (antagonistes et inhibiteurs), Facteur-3 de régulation d'interféron (génétique), Humains, Interactions hôte-pathogène (immunologie), Interactions hôte-pathogène (physiologie), Interféron de type I (biosynthèse), Lignée cellulaire, Mitochondries (métabolisme), Modèles biologiques, Petit ARN interférent (génétique), Protéines adaptatrices de la transduction du signal (), Protéines adaptatrices de la transduction du signal (déficit), Protéines adaptatrices de la transduction du signal (génétique), Protéines adaptatrices de la transduction du signal (physiologie), Protéines virales (physiologie), Protéines virales non structurales (physiologie), RNA replicase (physiologie), Souris, Souris knockout, Structure tertiaire des protéines, Séquence nucléotidique, Virus Sendai (pathogénicité).
- MESH :
- antagonistes et inhibiteurs : Facteur-3 de régulation d'interféron.
- biosynthèse : Interféron de type I.
- déficit : Protéines adaptatrices de la transduction du signal.
- génétique : Facteur-3 de régulation d'interféron, Petit ARN interférent, Protéines adaptatrices de la transduction du signal.
- immunologie : Apoptose, Interactions hôte-pathogène.
- métabolisme : Caspases, Facteur de transcription NF-kappa B, Mitochondries.
- pathogénicité : Virus Sendai.
- physiologie : Apoptose, Interactions hôte-pathogène, Protéines adaptatrices de la transduction du signal, Protéines virales, Protéines virales non structurales, RNA replicase.
- Animaux, Cellules cultivées, Humains, Lignée cellulaire, Modèles biologiques, Protéines adaptatrices de la transduction du signal, Souris, Souris knockout, Structure tertiaire des protéines, Séquence nucléotidique.
English descriptors
- KwdEn :
- Adaptor Proteins, Signal Transducing (chemistry), Adaptor Proteins, Signal Transducing (deficiency), Adaptor Proteins, Signal Transducing (genetics), Adaptor Proteins, Signal Transducing (physiology), Animals, Apoptosis (immunology), Apoptosis (physiology), Base Sequence, Caspases (metabolism), Cell Line, Cells, Cultured, Host-Pathogen Interactions (immunology), Host-Pathogen Interactions (physiology), Humans, Interferon Regulatory Factor-3 (antagonists & inhibitors), Interferon Regulatory Factor-3 (genetics), Interferon Type I (biosynthesis), Mice, Mice, Knockout, Mitochondria (metabolism), Models, Biological, NF-kappa B (metabolism), Protein Structure, Tertiary, RNA Replicase (physiology), RNA, Small Interfering (genetics), Sendai virus (pathogenicity), Viral Nonstructural Proteins (physiology), Viral Proteins (physiology).
- MESH :
- chemical , antagonists & inhibitors : Interferon Regulatory Factor-3.
- chemical , biosynthesis : Interferon Type I.
- chemical , chemistry : Adaptor Proteins, Signal Transducing.
- chemical , deficiency : Adaptor Proteins, Signal Transducing.
- chemical , genetics : Adaptor Proteins, Signal Transducing, Interferon Regulatory Factor-3, RNA, Small Interfering.
- chemical , metabolism : Caspases, NF-kappa B.
- chemical , physiology : Adaptor Proteins, Signal Transducing, RNA Replicase, Viral Nonstructural Proteins, Viral Proteins.
- immunology : Apoptosis, Host-Pathogen Interactions.
- metabolism : Mitochondria.
- pathogenicity : Sendai virus.
- physiology : Apoptosis, Host-Pathogen Interactions.
- Animals, Base Sequence, Cell Line, Cells, Cultured, Humans, Mice, Mice, Knockout, Models, Biological, Protein Structure, Tertiary.
Abstract
Host responses to viral infection include both immune activation and programmed cell death. The mitochondrial antiviral signaling adaptor, MAVS (IPS-1, VISA or Cardif) is critical for host defenses to viral infection by inducing type-1 interferons (IFN-I), however its role in virus-induced apoptotic responses has not been elucidated.
DOI: 10.1371/journal.pone.0005466
PubMed: 19404494
Affiliations:
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Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptor Proteins, Signal Transducing (chemistry)</term>
<term>Adaptor Proteins, Signal Transducing (deficiency)</term>
<term>Adaptor Proteins, Signal Transducing (genetics)</term>
<term>Adaptor Proteins, Signal Transducing (physiology)</term>
<term>Animals</term>
<term>Apoptosis (immunology)</term>
<term>Apoptosis (physiology)</term>
<term>Base Sequence</term>
<term>Caspases (metabolism)</term>
<term>Cell Line</term>
<term>Cells, Cultured</term>
<term>Host-Pathogen Interactions (immunology)</term>
<term>Host-Pathogen Interactions (physiology)</term>
<term>Humans</term>
<term>Interferon Regulatory Factor-3 (antagonists & inhibitors)</term>
<term>Interferon Regulatory Factor-3 (genetics)</term>
<term>Interferon Type I (biosynthesis)</term>
<term>Mice</term>
<term>Mice, Knockout</term>
<term>Mitochondria (metabolism)</term>
<term>Models, Biological</term>
<term>NF-kappa B (metabolism)</term>
<term>Protein Structure, Tertiary</term>
<term>RNA Replicase (physiology)</term>
<term>RNA, Small Interfering (genetics)</term>
<term>Sendai virus (pathogenicity)</term>
<term>Viral Nonstructural Proteins (physiology)</term>
<term>Viral Proteins (physiology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Apoptose (immunologie)</term>
<term>Apoptose (physiologie)</term>
<term>Caspases (métabolisme)</term>
<term>Cellules cultivées</term>
<term>Facteur de transcription NF-kappa B (métabolisme)</term>
<term>Facteur-3 de régulation d'interféron (antagonistes et inhibiteurs)</term>
<term>Facteur-3 de régulation d'interféron (génétique)</term>
<term>Humains</term>
<term>Interactions hôte-pathogène (immunologie)</term>
<term>Interactions hôte-pathogène (physiologie)</term>
<term>Interféron de type I (biosynthèse)</term>
<term>Lignée cellulaire</term>
<term>Mitochondries (métabolisme)</term>
<term>Modèles biologiques</term>
<term>Petit ARN interférent (génétique)</term>
<term>Protéines adaptatrices de la transduction du signal ()</term>
<term>Protéines adaptatrices de la transduction du signal (déficit)</term>
<term>Protéines adaptatrices de la transduction du signal (génétique)</term>
<term>Protéines adaptatrices de la transduction du signal (physiologie)</term>
<term>Protéines virales (physiologie)</term>
<term>Protéines virales non structurales (physiologie)</term>
<term>RNA replicase (physiologie)</term>
<term>Souris</term>
<term>Souris knockout</term>
<term>Structure tertiaire des protéines</term>
<term>Séquence nucléotidique</term>
<term>Virus Sendai (pathogénicité)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Interferon Regulatory Factor-3</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Interferon Type I</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term>
<term>Interferon Regulatory Factor-3</term>
<term>RNA, Small Interfering</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspases</term>
<term>NF-kappa B</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term>
<term>RNA Replicase</term>
<term>Viral Nonstructural Proteins</term>
<term>Viral Proteins</term>
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<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Facteur-3 de régulation d'interféron</term>
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<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Interféron de type I</term>
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</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur-3 de régulation d'interféron</term>
<term>Petit ARN interférent</term>
<term>Protéines adaptatrices de la transduction du signal</term>
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<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Apoptose</term>
<term>Interactions hôte-pathogène</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Apoptosis</term>
<term>Host-Pathogen Interactions</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspases</term>
<term>Facteur de transcription NF-kappa B</term>
<term>Mitochondries</term>
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<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Sendai virus</term>
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<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus Sendai</term>
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<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Apoptose</term>
<term>Interactions hôte-pathogène</term>
<term>Protéines adaptatrices de la transduction du signal</term>
<term>Protéines virales</term>
<term>Protéines virales non structurales</term>
<term>RNA replicase</term>
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<term>Host-Pathogen Interactions</term>
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<term>Base Sequence</term>
<term>Cell Line</term>
<term>Cells, Cultured</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Knockout</term>
<term>Models, Biological</term>
<term>Protein Structure, Tertiary</term>
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<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules cultivées</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Modèles biologiques</term>
<term>Protéines adaptatrices de la transduction du signal</term>
<term>Souris</term>
<term>Souris knockout</term>
<term>Structure tertiaire des protéines</term>
<term>Séquence nucléotidique</term>
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<front><div type="abstract" xml:lang="en">Host responses to viral infection include both immune activation and programmed cell death. The mitochondrial antiviral signaling adaptor, MAVS (IPS-1, VISA or Cardif) is critical for host defenses to viral infection by inducing type-1 interferons (IFN-I), however its role in virus-induced apoptotic responses has not been elucidated.</div>
</front>
</TEI>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Caroline du Nord</li>
</region>
</list>
<tree><noCountry><name sortKey="Bergstralh, Daniel T" sort="Bergstralh, Daniel T" uniqKey="Bergstralh D" first="Daniel T" last="Bergstralh">Daniel T. Bergstralh</name>
<name sortKey="Chen, Zhijian J" sort="Chen, Zhijian J" uniqKey="Chen Z" first="Zhijian J" last="Chen">Zhijian J. Chen</name>
<name sortKey="Liesman, Rachael M" sort="Liesman, Rachael M" uniqKey="Liesman R" first="Rachael M" last="Liesman">Rachael M. Liesman</name>
<name sortKey="Moore, Chris B" sort="Moore, Chris B" uniqKey="Moore C" first="Chris B" last="Moore">Chris B. Moore</name>
<name sortKey="O Connor, Brian P" sort="O Connor, Brian P" uniqKey="O Connor B" first="Brian P" last="O'Connor">Brian P. O'Connor</name>
<name sortKey="Pickles, Raymond J" sort="Pickles, Raymond J" uniqKey="Pickles R" first="Raymond J" last="Pickles">Raymond J. Pickles</name>
<name sortKey="Ting, Jenny P Y" sort="Ting, Jenny P Y" uniqKey="Ting J" first="Jenny P-Y" last="Ting">Jenny P-Y Ting</name>
</noCountry>
<country name="États-Unis"><region name="Caroline du Nord"><name sortKey="Lei, Yu" sort="Lei, Yu" uniqKey="Lei Y" first="Yu" last="Lei">Yu Lei</name>
</region>
</country>
</tree>
</affiliations>
</record>
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