StressCovidV1, Main, Exploration, bibRecord, 000E92

mTOR/p70S6K signaling distinguishes routine, maintenance-level autophagy from autophagic cell death during influenza A infection.

Identifieur interne : 000E92 ( Main/Exploration ); précédent : 000E91; suivant : 000E93

mTOR/p70S6K signaling distinguishes routine, maintenance-level autophagy from autophagic cell death during influenza A infection.

Auteurs : Emmanuel Datan [États-Unis] ; Alireza Shirazian [États-Unis] ; Shawna Benjamin [États-Unis] ; Demetrius Matassov [États-Unis] ; Antonella Tinari [Italie] ; Walter Malorni [Italie] ; Richard A. Lockshin [États-Unis] ; Adolfo Garcia-Sastre [États-Unis] ; Zahra Zakeri [États-Unis]

Source :

Virology [ 1096-0341 ] ; 2014.

RBID : pubmed:24606695

Descripteurs français

KwdFr :
- Apoptose, Autophagie, Complexes multiprotéiques (génétique), Complexes multiprotéiques (métabolisme), Grippe humaine (enzymologie), Grippe humaine (génétique), Grippe humaine (physiopathologie), Humains, Phosphatidylinositol 3-kinases (génétique), Phosphatidylinositol 3-kinases (métabolisme), Ribosomal Protein S6 Kinases, 70-kDa (génétique), Ribosomal Protein S6 Kinases, 70-kDa (métabolisme), Sérine-thréonine kinases TOR (génétique), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal, Virus de la grippe A (génétique), Virus de la grippe A (physiologie).
MESH :
- enzymologie : Grippe humaine.
- génétique : Complexes multiprotéiques, Grippe humaine, Phosphatidylinositol 3-kinases, Ribosomal Protein S6 Kinases, 70-kDa, Sérine-thréonine kinases TOR, Virus de la grippe A.
- métabolisme : Complexes multiprotéiques, Phosphatidylinositol 3-kinases, Ribosomal Protein S6 Kinases, 70-kDa, Sérine-thréonine kinases TOR.
- physiologie : Virus de la grippe A.
- physiopathologie : Grippe humaine.
- Apoptose, Autophagie, Humains, Transduction du signal.

English descriptors

KwdEn :
- Apoptosis, Autophagy, Humans, Influenza A virus (genetics), Influenza A virus (physiology), Influenza, Human (enzymology), Influenza, Human (genetics), Influenza, Human (physiopathology), Mechanistic Target of Rapamycin Complex 1, Mechanistic Target of Rapamycin Complex 2, Multiprotein Complexes (genetics), Multiprotein Complexes (metabolism), Phosphatidylinositol 3-Kinases (genetics), Phosphatidylinositol 3-Kinases (metabolism), Ribosomal Protein S6 Kinases, 70-kDa (genetics), Ribosomal Protein S6 Kinases, 70-kDa (metabolism), Signal Transduction, TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (metabolism).
MESH :
- chemical , genetics : Multiprotein Complexes, Phosphatidylinositol 3-Kinases, Ribosomal Protein S6 Kinases, 70-kDa, TOR Serine-Threonine Kinases.
- chemical , metabolism : Multiprotein Complexes, Phosphatidylinositol 3-Kinases, Ribosomal Protein S6 Kinases, 70-kDa, TOR Serine-Threonine Kinases.
- chemical : Mechanistic Target of Rapamycin Complex 1, Mechanistic Target of Rapamycin Complex 2.
- enzymology : Influenza, Human.
- genetics : Influenza A virus, Influenza, Human.
- physiology : Influenza A virus.
- physiopathology : Influenza, Human.
- Apoptosis, Autophagy, Humans, Signal Transduction.

Abstract

Autophagy, a stress response activated in influenza A virus infection helps the cell avoid apoptosis. However, in the absence of apoptosis infected cells undergo vastly expanded autophagy and nevertheless die in the presence of necrostatin but not of autophagy inhibitors. Combinations of inhibitors indicate that the controls of protective and lethal autophagy are different. Infection that triggers apoptosis also triggers canonical autophagy signaling exhibiting transient PI3K and mTORC1 activity. In terminal autophagy phospho-mTOR(Ser2448) is suppressed while mTORC1, PI3K and mTORC2 activities increase. mTORC1 substrate p70S6K becomes highly phosphorylated while its activity, now regulated by mTORC2, is required for LC3-II formation. Inhibition of mTORC2/p70S6K, unlike that of PI3K/mTORC1, blocks expanded autophagy in the absence of apoptosis but not moderate autophagy. Inhibitors of expanded autophagy limit virus reproduction. Thus expanded, lethal autophagy is activated by a signaling mechanism different from autophagy that helps cells survive toxic or stressful episodes.

DOI: 10.1016/j.virol.2014.01.008
PubMed: 24606695

Affiliations:

Le document en format XML

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<term>Autophagy</term>
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<term>Influenza A virus (physiology)</term>
<term>Influenza, Human (enzymology)</term>
<term>Influenza, Human (genetics)</term>
<term>Influenza, Human (physiopathology)</term>
<term>Mechanistic Target of Rapamycin Complex 1</term>
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<term>Phosphatidylinositol 3-Kinases (metabolism)</term>
<term>Ribosomal Protein S6 Kinases, 70-kDa (genetics)</term>
<term>Ribosomal Protein S6 Kinases, 70-kDa (metabolism)</term>
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<term>TOR Serine-Threonine Kinases (genetics)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
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<term>Autophagie</term>
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<term>Transduction du signal</term>
<term>Virus de la grippe A (génétique)</term>
<term>Virus de la grippe A (physiologie)</term>
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<term>Phosphatidylinositol 3-Kinases</term>
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<term>Phosphatidylinositol 3-kinases</term>
<term>Ribosomal Protein S6 Kinases, 70-kDa</term>
<term>Sérine-thréonine kinases TOR</term>
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<front><div type="abstract" xml:lang="en">Autophagy, a stress response activated in influenza A virus infection helps the cell avoid apoptosis. However, in the absence of apoptosis infected cells undergo vastly expanded autophagy and nevertheless die in the presence of necrostatin but not of autophagy inhibitors. Combinations of inhibitors indicate that the controls of protective and lethal autophagy are different. Infection that triggers apoptosis also triggers canonical autophagy signaling exhibiting transient PI3K and mTORC1 activity. In terminal autophagy phospho-mTOR(Ser2448) is suppressed while mTORC1, PI3K and mTORC2 activities increase. mTORC1 substrate p70S6K becomes highly phosphorylated while its activity, now regulated by mTORC2, is required for LC3-II formation. Inhibition of mTORC2/p70S6K, unlike that of PI3K/mTORC1, blocks expanded autophagy in the absence of apoptosis but not moderate autophagy. Inhibitors of expanded autophagy limit virus reproduction. Thus expanded, lethal autophagy is activated by a signaling mechanism different from autophagy that helps cells survive toxic or stressful episodes. </div>
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EXPLOR_STEP=$WICRI_ROOT/Sante/explor/StressCovidV1/Data/Main/Exploration

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000E92 | SxmlIndent | more

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{{Explor lien
   |wiki=    Sante
   |area=    StressCovidV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:24606695
   |texte=   mTOR/p70S6K signaling distinguishes routine, maintenance-level autophagy from autophagic cell death during influenza A infection.
}}

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       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd   \
       | NlmPubMed2Wicri -a StressCovidV1

This area was generated with Dilib version V0.6.33.
Data generation: Wed May 6 16:44:09 2020. Site generation: Sun Mar 28 08:26:57 2021

Serveur d'exploration Stress et Covid

mTOR/p70S6K signaling distinguishes routine, maintenance-level autophagy from autophagic cell death during influenza A infection.

mTOR/p70S6K signaling distinguishes routine, maintenance-level autophagy from autophagic cell death during influenza A infection.

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Pour générer des pages wiki

	Serveur d'exploration Stress et Covid
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.