RapamycinFungusV1, Main, Exploration, bibRecord, 000022

Transcriptional block of AMPK-induced autophagy promotes glutamate excitotoxicity in nutrient-deprived SH-SY5Y neuroblastoma cells.

Identifieur interne : 000022 ( Main/Exploration ); précédent : 000021; suivant : 000023

Transcriptional block of AMPK-induced autophagy promotes glutamate excitotoxicity in nutrient-deprived SH-SY5Y neuroblastoma cells.

Auteurs : Ljubica Vucicevic [Serbie] ; Maja Misirkic [Serbie] ; Darko Ciric [Serbie] ; Tamara Martinovic [Serbie] ; Maja Jovanovic [Serbie] ; Aleksandra Isakovic [Serbie] ; Ivanka Markovic [Serbie] ; Jasna Saponjic [Serbie] ; Marc Foretz [France] ; Yoana Rabanal-Ruiz [Royaume-Uni, Espagne] ; Viktor I. Korolchuk [Royaume-Uni] ; Vladimir Trajkovic [Serbie]

Source :

Cellular and molecular life sciences : CMLS [ 1420-9071 ] ; 2020.

RBID : pubmed:31720741

Descripteurs français

English descriptors

KwdEn :
- AMP-Activated Protein Kinases (genetics), AMP-Activated Protein Kinases (metabolism), Autophagosomes (metabolism), Autophagy (drug effects), Autophagy-Related Protein-1 Homolog (metabolism), Beclin-1 (metabolism), Cell Line, Tumor (MeSH), Energy Metabolism (drug effects), Forkhead Box Protein O3 (metabolism), Glutamic Acid (toxicity), Humans (MeSH), Ibotenic Acid (pharmacology), Intracellular Signaling Peptides and Proteins (metabolism), Mechanistic Target of Rapamycin Complex 1 (metabolism), Memantine (pharmacology), Microtubule-Associated Proteins (genetics), Microtubule-Associated Proteins (metabolism), Necrosis (MeSH), Neuroblastoma (metabolism), Neuroblastoma (pathology), Nutrients (deficiency), Receptors, N-Methyl-D-Aspartate (agonists), Receptors, N-Methyl-D-Aspartate (metabolism), Sequestosome-1 Protein (genetics), Sequestosome-1 Protein (metabolism), Transcription, Genetic (drug effects).
MESH :
- chemical , agonists : Receptors, N-Methyl-D-Aspartate.
- chemical , genetics : AMP-Activated Protein Kinases, Microtubule-Associated Proteins, Sequestosome-1 Protein.
- chemical , metabolism : AMP-Activated Protein Kinases, Autophagy-Related Protein-1 Homolog, Beclin-1, Forkhead Box Protein O3, Intracellular Signaling Peptides and Proteins, Mechanistic Target of Rapamycin Complex 1, Microtubule-Associated Proteins, Receptors, N-Methyl-D-Aspartate, Sequestosome-1 Protein.
- deficiency : Nutrients.
- drug effects : Autophagy, Energy Metabolism, Transcription, Genetic.
- metabolism : Autophagosomes, Neuroblastoma.
- pathology : Neuroblastoma.
- chemical , pharmacology : Ibotenic Acid, Memantine.
- chemical , toxicity : Glutamic Acid.
- Cell Line, Tumor, Humans, Necrosis.

Abstract

We investigated the role of autophagy, a controlled lysosomal degradation of cellular macromolecules and organelles, in glutamate excitotoxicity during nutrient deprivation in vitro. The incubation in low-glucose serum/amino acid-free cell culture medium synergized with glutamate in increasing AMP/ATP ratio and causing excitotoxic necrosis in SH-SY5Y human neuroblastoma cells. Glutamate suppressed starvation-triggered autophagy, as confirmed by diminished intracellular acidification, lower LC3 punctuation and LC3-I conversion to autophagosome-associated LC3-II, reduced expression of proautophagic beclin-1 and ATG5, increase of the selective autophagic target NBR1, and decreased number of autophagic vesicles. Similar results were observed in PC12 rat pheochromocytoma cells. Both glutamate-mediated excitotoxicity and autophagy inhibition in starved SH-SY5Y cells were reverted by NMDA antagonist memantine and mimicked by NMDA agonists D-aspartate and ibotenate. Glutamate reduced starvation-triggered phosphorylation of the energy sensor AMP-activated protein kinase (AMPK) without affecting the activity of mammalian target of rapamycin complex 1, a major negative regulator of autophagy. This was associated with reduced mRNA levels of autophagy transcriptional activators (FOXO3, ATF4) and molecules involved in autophagy initiation (ULK1, ATG13, FIP200), autophagosome nucleation/elongation (ATG14, beclin-1, ATG5), and autophagic cargo delivery to autophagosomes (SQSTM1). Glutamate-mediated transcriptional repression of autophagy was alleviated by overexpression of constitutively active AMPK. Genetic or pharmacological AMPK activation by AMPK overexpression or metformin, as well as genetic or pharmacological autophagy induction by TFEB overexpression or lithium chloride, reduced the sensitivity of nutrient-deprived SH-SY5Y cells to glutamate excitotoxicity. These data indicate that transcriptional inhibition of AMPK-dependent cytoprotective autophagy is involved in glutamate-mediated excitotoxicity during nutrient deprivation in vitro.

DOI: 10.1007/s00018-019-03356-2
PubMed: 31720741

Affiliations:

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Le document en format XML

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<country xml:lang="fr">Espagne</country>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Transcriptional block of AMPK-induced autophagy promotes glutamate excitotoxicity in nutrient-deprived SH-SY5Y neuroblastoma cells.</title>
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<author><name sortKey="Ciric, Darko" sort="Ciric, Darko" uniqKey="Ciric D" first="Darko" last="Ciric">Darko Ciric</name>
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<author><name sortKey="Markovic, Ivanka" sort="Markovic, Ivanka" uniqKey="Markovic I" first="Ivanka" last="Markovic">Ivanka Markovic</name>
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<country xml:lang="fr">Serbie</country>
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<author><name sortKey="Saponjic, Jasna" sort="Saponjic, Jasna" uniqKey="Saponjic J" first="Jasna" last="Saponjic">Jasna Saponjic</name>
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<country xml:lang="fr">Serbie</country>
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<author><name sortKey="Foretz, Marc" sort="Foretz, Marc" uniqKey="Foretz M" first="Marc" last="Foretz">Marc Foretz</name>
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<country xml:lang="fr">France</country>
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<settlement type="city">Paris</settlement>
</placeName>
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<affiliation wicri:level="3"><nlm:affiliation>CNRS UMR8104, Paris, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
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<placeName><region type="region">Île-de-France</region>
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<affiliation wicri:level="4"><nlm:affiliation>Université Paris Descartes, Sorbonne Paris cité, Paris, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
<wicri:regionArea>Université Paris Descartes, Sorbonne Paris cité, Paris</wicri:regionArea>
<placeName><region type="region">Île-de-France</region>
<region type="old region">Île-de-France</region>
<settlement type="city">Paris</settlement>
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<author><name sortKey="Rabanal Ruiz, Yoana" sort="Rabanal Ruiz, Yoana" uniqKey="Rabanal Ruiz Y" first="Yoana" last="Rabanal-Ruiz">Yoana Rabanal-Ruiz</name>
<affiliation wicri:level="1"><nlm:affiliation>Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne, UK.</nlm:affiliation>
<country xml:lang="fr">Royaume-Uni</country>
<wicri:regionArea>Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne</wicri:regionArea>
<wicri:noRegion>Newcastle upon Tyne</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Regional Center for Biomedical Research, University of Castilla-La Mancha, Ciudad Real, Spain.</nlm:affiliation>
<country xml:lang="fr">Espagne</country>
<wicri:regionArea>Regional Center for Biomedical Research, University of Castilla-La Mancha, Ciudad Real</wicri:regionArea>
<wicri:noRegion>Ciudad Real</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Korolchuk, Viktor I" sort="Korolchuk, Viktor I" uniqKey="Korolchuk V" first="Viktor I" last="Korolchuk">Viktor I. Korolchuk</name>
<affiliation wicri:level="1"><nlm:affiliation>Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne, UK.</nlm:affiliation>
<country xml:lang="fr">Royaume-Uni</country>
<wicri:regionArea>Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne</wicri:regionArea>
<wicri:noRegion>Newcastle upon Tyne</wicri:noRegion>
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<author><name sortKey="Trajkovic, Vladimir" sort="Trajkovic, Vladimir" uniqKey="Trajkovic V" first="Vladimir" last="Trajkovic">Vladimir Trajkovic</name>
<affiliation wicri:level="1"><nlm:affiliation>Faculty of Medicine, Institute of Microbiology and Immunology, University of Belgrade, Dr. Subotica 1, 11000, Belgrade, Serbia. vladimir.trajkovic@med.bg.ac.rs.</nlm:affiliation>
<country xml:lang="fr">Serbie</country>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>AMP-Activated Protein Kinases (genetics)</term>
<term>AMP-Activated Protein Kinases (metabolism)</term>
<term>Autophagosomes (metabolism)</term>
<term>Autophagy (drug effects)</term>
<term>Autophagy-Related Protein-1 Homolog (metabolism)</term>
<term>Beclin-1 (metabolism)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Energy Metabolism (drug effects)</term>
<term>Forkhead Box Protein O3 (metabolism)</term>
<term>Glutamic Acid (toxicity)</term>
<term>Humans (MeSH)</term>
<term>Ibotenic Acid (pharmacology)</term>
<term>Intracellular Signaling Peptides and Proteins (metabolism)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (metabolism)</term>
<term>Memantine (pharmacology)</term>
<term>Microtubule-Associated Proteins (genetics)</term>
<term>Microtubule-Associated Proteins (metabolism)</term>
<term>Necrosis (MeSH)</term>
<term>Neuroblastoma (metabolism)</term>
<term>Neuroblastoma (pathology)</term>
<term>Nutrients (deficiency)</term>
<term>Receptors, N-Methyl-D-Aspartate (agonists)</term>
<term>Receptors, N-Methyl-D-Aspartate (metabolism)</term>
<term>Sequestosome-1 Protein (genetics)</term>
<term>Sequestosome-1 Protein (metabolism)</term>
<term>Transcription, Genetic (drug effects)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>AMP-Activated Protein Kinases (génétique)</term>
<term>AMP-Activated Protein Kinases (métabolisme)</term>
<term>Acide glutamique (toxicité)</term>
<term>Acide iboténique (pharmacologie)</term>
<term>Autophagie (effets des médicaments et des substances chimiques)</term>
<term>Autophagosomes (métabolisme)</term>
<term>Bécline-1 (métabolisme)</term>
<term>Complexe-1 cible mécanistique de la rapamycine (métabolisme)</term>
<term>Homologue de la protéine-1 associée à l'autophagie (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Mémantine (pharmacologie)</term>
<term>Métabolisme énergétique (effets des médicaments et des substances chimiques)</term>
<term>Neuroblastome (anatomopathologie)</term>
<term>Neuroblastome (métabolisme)</term>
<term>Nutriments (déficit)</term>
<term>Nécrose (MeSH)</term>
<term>Protéine O3 à motif en tête de fourche (métabolisme)</term>
<term>Protéines associées aux microtubules (génétique)</term>
<term>Protéines associées aux microtubules (métabolisme)</term>
<term>Protéines et peptides de signalisation intracellulaire (métabolisme)</term>
<term>Récepteurs du N-méthyl-D-aspartate (agonistes)</term>
<term>Récepteurs du N-méthyl-D-aspartate (métabolisme)</term>
<term>Séquestosome-1 (génétique)</term>
<term>Séquestosome-1 (métabolisme)</term>
<term>Transcription génétique (effets des médicaments et des substances chimiques)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="agonists" xml:lang="en"><term>Receptors, N-Methyl-D-Aspartate</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>AMP-Activated Protein Kinases</term>
<term>Microtubule-Associated Proteins</term>
<term>Sequestosome-1 Protein</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>AMP-Activated Protein Kinases</term>
<term>Autophagy-Related Protein-1 Homolog</term>
<term>Beclin-1</term>
<term>Forkhead Box Protein O3</term>
<term>Intracellular Signaling Peptides and Proteins</term>
<term>Mechanistic Target of Rapamycin Complex 1</term>
<term>Microtubule-Associated Proteins</term>
<term>Receptors, N-Methyl-D-Aspartate</term>
<term>Sequestosome-1 Protein</term>
</keywords>
<keywords scheme="MESH" qualifier="agonistes" xml:lang="fr"><term>Récepteurs du N-méthyl-D-aspartate</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Neuroblastome</term>
</keywords>
<keywords scheme="MESH" qualifier="deficiency" xml:lang="en"><term>Nutrients</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term>
<term>Energy Metabolism</term>
<term>Transcription, Genetic</term>
</keywords>
<keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Nutriments</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Autophagie</term>
<term>Métabolisme énergétique</term>
<term>Transcription génétique</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>AMP-Activated Protein Kinases</term>
<term>Protéines associées aux microtubules</term>
<term>Séquestosome-1</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Autophagosomes</term>
<term>Neuroblastoma</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>AMP-Activated Protein Kinases</term>
<term>Autophagosomes</term>
<term>Bécline-1</term>
<term>Complexe-1 cible mécanistique de la rapamycine</term>
<term>Homologue de la protéine-1 associée à l'autophagie</term>
<term>Neuroblastome</term>
<term>Protéine O3 à motif en tête de fourche</term>
<term>Protéines associées aux microtubules</term>
<term>Protéines et peptides de signalisation intracellulaire</term>
<term>Récepteurs du N-méthyl-D-aspartate</term>
<term>Séquestosome-1</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neuroblastoma</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Acide iboténique</term>
<term>Mémantine</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Ibotenic Acid</term>
<term>Memantine</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Glutamic Acid</term>
</keywords>
<keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Acide glutamique</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term>
<term>Humans</term>
<term>Necrosis</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Nécrose</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">We investigated the role of autophagy, a controlled lysosomal degradation of cellular macromolecules and organelles, in glutamate excitotoxicity during nutrient deprivation in vitro. The incubation in low-glucose serum/amino acid-free cell culture medium synergized with glutamate in increasing AMP/ATP ratio and causing excitotoxic necrosis in SH-SY5Y human neuroblastoma cells. Glutamate suppressed starvation-triggered autophagy, as confirmed by diminished intracellular acidification, lower LC3 punctuation and LC3-I conversion to autophagosome-associated LC3-II, reduced expression of proautophagic beclin-1 and ATG5, increase of the selective autophagic target NBR1, and decreased number of autophagic vesicles. Similar results were observed in PC12 rat pheochromocytoma cells. Both glutamate-mediated excitotoxicity and autophagy inhibition in starved SH-SY5Y cells were reverted by NMDA antagonist memantine and mimicked by NMDA agonists D-aspartate and ibotenate. Glutamate reduced starvation-triggered phosphorylation of the energy sensor AMP-activated protein kinase (AMPK) without affecting the activity of mammalian target of rapamycin complex 1, a major negative regulator of autophagy. This was associated with reduced mRNA levels of autophagy transcriptional activators (FOXO3, ATF4) and molecules involved in autophagy initiation (ULK1, ATG13, FIP200), autophagosome nucleation/elongation (ATG14, beclin-1, ATG5), and autophagic cargo delivery to autophagosomes (SQSTM1). Glutamate-mediated transcriptional repression of autophagy was alleviated by overexpression of constitutively active AMPK. Genetic or pharmacological AMPK activation by AMPK overexpression or metformin, as well as genetic or pharmacological autophagy induction by TFEB overexpression or lithium chloride, reduced the sensitivity of nutrient-deprived SH-SY5Y cells to glutamate excitotoxicity. These data indicate that transcriptional inhibition of AMPK-dependent cytoprotective autophagy is involved in glutamate-mediated excitotoxicity during nutrient deprivation in vitro.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31720741</PMID>
<DateCompleted><Year>2020</Year>
<Month>08</Month>
<Day>21</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>08</Month>
<Day>21</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1420-9071</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>77</Volume>
<Issue>17</Issue>
<PubDate><Year>2020</Year>
<Month>Sep</Month>
</PubDate>
</JournalIssue>
<Title>Cellular and molecular life sciences : CMLS</Title>
<ISOAbbreviation>Cell Mol Life Sci</ISOAbbreviation>
</Journal>
<ArticleTitle>Transcriptional block of AMPK-induced autophagy promotes glutamate excitotoxicity in nutrient-deprived SH-SY5Y neuroblastoma cells.</ArticleTitle>
<Pagination><MedlinePgn>3383-3399</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1007/s00018-019-03356-2</ELocationID>
<Abstract><AbstractText>We investigated the role of autophagy, a controlled lysosomal degradation of cellular macromolecules and organelles, in glutamate excitotoxicity during nutrient deprivation in vitro. The incubation in low-glucose serum/amino acid-free cell culture medium synergized with glutamate in increasing AMP/ATP ratio and causing excitotoxic necrosis in SH-SY5Y human neuroblastoma cells. Glutamate suppressed starvation-triggered autophagy, as confirmed by diminished intracellular acidification, lower LC3 punctuation and LC3-I conversion to autophagosome-associated LC3-II, reduced expression of proautophagic beclin-1 and ATG5, increase of the selective autophagic target NBR1, and decreased number of autophagic vesicles. Similar results were observed in PC12 rat pheochromocytoma cells. Both glutamate-mediated excitotoxicity and autophagy inhibition in starved SH-SY5Y cells were reverted by NMDA antagonist memantine and mimicked by NMDA agonists D-aspartate and ibotenate. Glutamate reduced starvation-triggered phosphorylation of the energy sensor AMP-activated protein kinase (AMPK) without affecting the activity of mammalian target of rapamycin complex 1, a major negative regulator of autophagy. This was associated with reduced mRNA levels of autophagy transcriptional activators (FOXO3, ATF4) and molecules involved in autophagy initiation (ULK1, ATG13, FIP200), autophagosome nucleation/elongation (ATG14, beclin-1, ATG5), and autophagic cargo delivery to autophagosomes (SQSTM1). Glutamate-mediated transcriptional repression of autophagy was alleviated by overexpression of constitutively active AMPK. Genetic or pharmacological AMPK activation by AMPK overexpression or metformin, as well as genetic or pharmacological autophagy induction by TFEB overexpression or lithium chloride, reduced the sensitivity of nutrient-deprived SH-SY5Y cells to glutamate excitotoxicity. These data indicate that transcriptional inhibition of AMPK-dependent cytoprotective autophagy is involved in glutamate-mediated excitotoxicity during nutrient deprivation in vitro.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vucicevic</LastName>
<ForeName>Ljubica</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Neurophysiology, Institute for Biological Research "Sinisa Stankovic", University of Belgrade, Belgrade, Serbia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Misirkic</LastName>
<ForeName>Maja</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Neurophysiology, Institute for Biological Research "Sinisa Stankovic", University of Belgrade, Belgrade, Serbia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ciric</LastName>
<ForeName>Darko</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Faculty of Medicine, Institute of Histology and Embryology, University of Belgrade, Belgrade, Serbia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Martinovic</LastName>
<ForeName>Tamara</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Faculty of Medicine, Institute of Histology and Embryology, University of Belgrade, Belgrade, Serbia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jovanovic</LastName>
<ForeName>Maja</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Faculty of Medicine, Institute of Medical and Clinical Biochemistry, University of Belgrade, Belgrade, Serbia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Isakovic</LastName>
<ForeName>Aleksandra</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Faculty of Medicine, Institute of Medical and Clinical Biochemistry, University of Belgrade, Belgrade, Serbia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Markovic</LastName>
<ForeName>Ivanka</ForeName>
<Initials>I</Initials>
<AffiliationInfo><Affiliation>Faculty of Medicine, Institute of Medical and Clinical Biochemistry, University of Belgrade, Belgrade, Serbia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Saponjic</LastName>
<ForeName>Jasna</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Neurobiology, Institute for Biological Research "Sinisa Stankovic", University of Belgrade, Belgrade, Serbia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Foretz</LastName>
<ForeName>Marc</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Inserm U1016, Institut Cochin, Paris, France.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>CNRS UMR8104, Paris, France.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Université Paris Descartes, Sorbonne Paris cité, Paris, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rabanal-Ruiz</LastName>
<ForeName>Yoana</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Regional Center for Biomedical Research, University of Castilla-La Mancha, Ciudad Real, Spain.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Korolchuk</LastName>
<ForeName>Viktor I</ForeName>
<Initials>VI</Initials>
<AffiliationInfo><Affiliation>Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Trajkovic</LastName>
<ForeName>Vladimir</ForeName>
<Initials>V</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0002-8061-2968</Identifier>
<AffiliationInfo><Affiliation>Faculty of Medicine, Institute of Microbiology and Immunology, University of Belgrade, Dr. Subotica 1, 11000, Belgrade, Serbia. vladimir.trajkovic@med.bg.ac.rs.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>CA15138</GrantID>
<Agency>COST TRANSAUTOPHAGY</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>Start up for Science</GrantID>
<Agency>Phillip Morris and Center for Leadership Development</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>173053</GrantID>
<Agency>Ministarstvo Prosvete, Nauke i Tehnološkog Razvoja</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>173022</GrantID>
<Agency>Ministarstvo Prosvete, Nauke i Tehnološkog Razvoja</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>41025</GrantID>
<Agency>Ministarstvo Prosvete, Nauke i Tehnološkog Razvoja</Agency>
<Country></Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2019</Year>
<Month>11</Month>
<Day>12</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Switzerland</Country>
<MedlineTA>Cell Mol Life Sci</MedlineTA>
<NlmUniqueID>9705402</NlmUniqueID>
<ISSNLinking>1420-682X</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071186">Beclin-1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C499517">FOXO3 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071316">Forkhead Box Protein O3</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D047908">Intracellular Signaling Peptides and Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D008869">Microtubule-Associated Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016194">Receptors, N-Methyl-D-Aspartate</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C099718">SQSTM1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071456">Sequestosome-1 Protein</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>2552-55-8</RegistryNumber>
<NameOfSubstance UI="D007051">Ibotenic Acid</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>3KX376GY7L</RegistryNumber>
<NameOfSubstance UI="D018698">Glutamic Acid</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D000071189">Autophagy-Related Protein-1 Homolog</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D000076222">Mechanistic Target of Rapamycin Complex 1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="C484754">ULK1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.31</RegistryNumber>
<NameOfSubstance UI="D055372">AMP-Activated Protein Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>W8O17SJF3T</RegistryNumber>
<NameOfSubstance UI="D008559">Memantine</NameOfSubstance>
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<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D055372" MajorTopicYN="N">AMP-Activated Protein Kinases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071182" MajorTopicYN="N">Autophagosomes</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071189" MajorTopicYN="N">Autophagy-Related Protein-1 Homolog</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071186" MajorTopicYN="N">Beclin-1</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004734" MajorTopicYN="N">Energy Metabolism</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071316" MajorTopicYN="N">Forkhead Box Protein O3</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018698" MajorTopicYN="N">Glutamic Acid</DescriptorName>
<QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007051" MajorTopicYN="N">Ibotenic Acid</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D047908" MajorTopicYN="N">Intracellular Signaling Peptides and Proteins</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000076222" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 1</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008559" MajorTopicYN="N">Memantine</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008869" MajorTopicYN="N">Microtubule-Associated Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009336" MajorTopicYN="N">Necrosis</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009447" MajorTopicYN="N">Neuroblastoma</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000078622" MajorTopicYN="N">Nutrients</DescriptorName>
<QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016194" MajorTopicYN="N">Receptors, N-Methyl-D-Aspartate</DescriptorName>
<QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071456" MajorTopicYN="N">Sequestosome-1 Protein</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014158" MajorTopicYN="N">Transcription, Genetic</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Brain</Keyword>
<Keyword MajorTopicYN="N">Energy stress</Keyword>
<Keyword MajorTopicYN="N">Ischemia</Keyword>
<Keyword MajorTopicYN="N">Neurodegeneration</Keyword>
<Keyword MajorTopicYN="N">Neurotoxicity</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year>
<Month>05</Month>
<Day>20</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2019</Year>
<Month>10</Month>
<Day>28</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2019</Year>
<Month>10</Month>
<Day>16</Day>
</PubMedPubDate>
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<Month>11</Month>
<Day>14</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PubMedPubDate PubStatus="medline"><Year>2020</Year>
<Month>8</Month>
<Day>22</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2019</Year>
<Month>11</Month>
<Day>14</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">31720741</ArticleId>
<ArticleId IdType="doi">10.1007/s00018-019-03356-2</ArticleId>
<ArticleId IdType="pii">10.1007/s00018-019-03356-2</ArticleId>
</ArticleIdList>
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</pubmed>
<affiliations><list><country><li>Espagne</li>
<li>France</li>
<li>Royaume-Uni</li>
<li>Serbie</li>
</country>
<region><li>Île-de-France</li>
</region>
<settlement><li>Paris</li>
</settlement>
<orgName><li>Université Paris-Descartes</li>
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</list>
<tree><country name="Serbie"><noRegion><name sortKey="Vucicevic, Ljubica" sort="Vucicevic, Ljubica" uniqKey="Vucicevic L" first="Ljubica" last="Vucicevic">Ljubica Vucicevic</name>
</noRegion>
<name sortKey="Ciric, Darko" sort="Ciric, Darko" uniqKey="Ciric D" first="Darko" last="Ciric">Darko Ciric</name>
<name sortKey="Isakovic, Aleksandra" sort="Isakovic, Aleksandra" uniqKey="Isakovic A" first="Aleksandra" last="Isakovic">Aleksandra Isakovic</name>
<name sortKey="Jovanovic, Maja" sort="Jovanovic, Maja" uniqKey="Jovanovic M" first="Maja" last="Jovanovic">Maja Jovanovic</name>
<name sortKey="Markovic, Ivanka" sort="Markovic, Ivanka" uniqKey="Markovic I" first="Ivanka" last="Markovic">Ivanka Markovic</name>
<name sortKey="Martinovic, Tamara" sort="Martinovic, Tamara" uniqKey="Martinovic T" first="Tamara" last="Martinovic">Tamara Martinovic</name>
<name sortKey="Misirkic, Maja" sort="Misirkic, Maja" uniqKey="Misirkic M" first="Maja" last="Misirkic">Maja Misirkic</name>
<name sortKey="Saponjic, Jasna" sort="Saponjic, Jasna" uniqKey="Saponjic J" first="Jasna" last="Saponjic">Jasna Saponjic</name>
<name sortKey="Trajkovic, Vladimir" sort="Trajkovic, Vladimir" uniqKey="Trajkovic V" first="Vladimir" last="Trajkovic">Vladimir Trajkovic</name>
</country>
<country name="France"><region name="Île-de-France"><name sortKey="Foretz, Marc" sort="Foretz, Marc" uniqKey="Foretz M" first="Marc" last="Foretz">Marc Foretz</name>
</region>
<name sortKey="Foretz, Marc" sort="Foretz, Marc" uniqKey="Foretz M" first="Marc" last="Foretz">Marc Foretz</name>
<name sortKey="Foretz, Marc" sort="Foretz, Marc" uniqKey="Foretz M" first="Marc" last="Foretz">Marc Foretz</name>
</country>
<country name="Royaume-Uni"><noRegion><name sortKey="Rabanal Ruiz, Yoana" sort="Rabanal Ruiz, Yoana" uniqKey="Rabanal Ruiz Y" first="Yoana" last="Rabanal-Ruiz">Yoana Rabanal-Ruiz</name>
</noRegion>
<name sortKey="Korolchuk, Viktor I" sort="Korolchuk, Viktor I" uniqKey="Korolchuk V" first="Viktor I" last="Korolchuk">Viktor I. Korolchuk</name>
</country>
<country name="Espagne"><noRegion><name sortKey="Rabanal Ruiz, Yoana" sort="Rabanal Ruiz, Yoana" uniqKey="Rabanal Ruiz Y" first="Yoana" last="Rabanal-Ruiz">Yoana Rabanal-Ruiz</name>
</noRegion>
</country>
</tree>
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</record>

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   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:31720741
   |texte=   Transcriptional block of AMPK-induced autophagy promotes glutamate excitotoxicity in nutrient-deprived SH-SY5Y neuroblastoma cells.
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	Serveur d'exploration sur la rapamycine et les champignons
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Serveur d'exploration sur la rapamycine et les champignons

Transcriptional block of AMPK-induced autophagy promotes glutamate excitotoxicity in nutrient-deprived SH-SY5Y neuroblastoma cells.

Transcriptional block of AMPK-induced autophagy promotes glutamate excitotoxicity in nutrient-deprived SH-SY5Y neuroblastoma cells.

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