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  1. Article ; Online: Should evidence of an autolysosomal de-acidification defect in Alzheimer and Parkinson diseases call for caution in prescribing chronic PPI and DMARD?

    Giuliano, Sandy / Montemagno, Christopher / Domdom, Marie-Angela / Teisseire, Manon / Brest, Patrick / Klionsky, Daniel J / Hofman, Paul / Pagès, Gilles / Mograbi, Baharia

    Autophagy

    2023  Volume 19, Issue 10, Page(s) 2800–2806

    Abstract: Nearly fifty million older people suffer from neurodegenerative diseases, including Alzheimer (AD) and Parkinson (PD) disease, a global burden expected to triple by 2050. Such an imminent "neurological pandemic" urges the identification of environmental ... ...

    Abstract Nearly fifty million older people suffer from neurodegenerative diseases, including Alzheimer (AD) and Parkinson (PD) disease, a global burden expected to triple by 2050. Such an imminent "neurological pandemic" urges the identification of environmental risk factors that are hopefully avoided to fight the disease. In 2022, strong evidence in mouse models incriminated defective lysosomal acidification and impairment of the autophagy pathway as modifiable risk factors for dementia. To date, the most prescribed lysosomotropic drugs are proton pump inhibitors (PPIs), chloroquine (CQ), and the related hydroxychloroquine (HCQ), which belong to the group of disease-modifying antirheumatic drugs (DMARDs). This commentary aims to open the discussion on the possible mechanisms connecting the long-term prescribing of these drugs to the elderly and the incidence of neurodegenerative diseases.
    MeSH term(s) Mice ; Animals ; Autophagy/physiology ; Alzheimer Disease/drug therapy ; Alzheimer Disease/metabolism ; Parkinson Disease/drug therapy ; Parkinson Disease/metabolism ; Amyloid Precursor Protein Secretases/metabolism ; Antirheumatic Agents/pharmacology ; Amyloid beta-Peptides/metabolism ; Hydroxychloroquine/adverse effects ; Aspartic Acid Endopeptidases/metabolism ; Aspartic Acid Endopeptidases/pharmacology ; Neurodegenerative Diseases/metabolism ; Lysosomes/metabolism ; Class III Phosphatidylinositol 3-Kinases/metabolism ; Chloroquine/pharmacology ; Hydrogen-Ion Concentration
    Chemical Substances Amyloid Precursor Protein Secretases (EC 3.4.-) ; Antirheumatic Agents ; Amyloid beta-Peptides ; Hydroxychloroquine (4QWG6N8QKH) ; Aspartic Acid Endopeptidases (EC 3.4.23.-) ; Class III Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; Chloroquine (886U3H6UFF)
    Language English
    Publishing date 2023-07-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2023.2214960
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: KRAS and NRAS Translation Is Increased upon MEK Inhibitors-Induced Processing Bodies Dissolution.

    Vidal-Cruchez, Olivia / Nicolini, Victoria J / Rete, Tifenn / Jacquet, Karine / Rezzonico, Roger / Lacoux, Caroline / Domdom, Marie-Angela / Roméo, Barnabé / Roux, Jérémie / Hubstenberger, Arnaud / Mari, Bernard / Mograbi, Baharia / Hofman, Paul / Brest, Patrick

    Cancers

    2023  Volume 15, Issue 12

    Abstract: Overactivation of the mitogen-activated protein kinase (MAPK) pathway is a critical driver of many human cancers. However, therapies directly targeting this pathway lead to cancer drug resistance. Resistance has been linked to compensatory RAS ... ...

    Abstract Overactivation of the mitogen-activated protein kinase (MAPK) pathway is a critical driver of many human cancers. However, therapies directly targeting this pathway lead to cancer drug resistance. Resistance has been linked to compensatory RAS overexpression, but the mechanisms underlying this response remain unclear. Here, we find that MEK inhibitors (MEKi) are associated with an increased translation of the KRAS and NRAS oncogenes through a mechanism involving dissolution of processing body (P-body) biocondensates. This effect is seen across different cell types and is extremely dynamic since removal of MEKi and ERK reactivation result in reappearance of P-bodies and reduced RAS-dependent signaling. Moreover, we find that P-body scaffold protein levels negatively impact RAS expression. Overall, we describe a new feedback loop mechanism involving biocondensates such as P-bodies in the translational regulation of RAS proteins and MAPK signaling.
    Language English
    Publishing date 2023-06-06
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers15123078
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: A multifactorial score including autophagy for prognosis and care of COVID-19 patients.

    Domdom, Marie-Angela / Brest, Patrick / Grosjean, Iris / Roméo, Barnabé / Landi, Maria Teresa / Gal, Jocelyn / Klionsky, Daniel J / Hofman, Paul / Mograbi, Baharia

    Autophagy

    2020  Volume 16, Issue 12, Page(s) 2276–2281

    Abstract: In less than eleven months, the world was brought to a halt by the COVID-19 outbreak. With hospitals becoming overwhelmed, one of the highest priorities concerned critical care triage to ration the scarce resources of intensive care units. Which patient ... ...

    Abstract In less than eleven months, the world was brought to a halt by the COVID-19 outbreak. With hospitals becoming overwhelmed, one of the highest priorities concerned critical care triage to ration the scarce resources of intensive care units. Which patient should be treated first? Based on what clinical and biological criteria? A global joint effort rapidly led to sequencing the genomes of tens of thousands of COVID-19 patients to determine the patients' genetic signature that causes them to be at risk of suddenly developing severe disease. In this commentary, we would like to consider some points concerning the use of a multifactorial risk score for COVID-19 severity. This score includes macroautophagy (hereafter referred to as autophagy), a critical host process that controls all steps harnessed by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus.
    MeSH term(s) Animals ; Autophagy/genetics ; Autophagy/physiology ; Autophagy-Related Proteins/analysis ; Autophagy-Related Proteins/genetics ; Biomarkers/analysis ; Biomarkers/metabolism ; COVID-19/diagnosis ; COVID-19/genetics ; COVID-19/pathology ; COVID-19/therapy ; Genetic Predisposition to Disease ; Humans ; Infectious bronchitis virus/physiology ; Mice ; Middle East Respiratory Syndrome Coronavirus/physiology ; Molecular Diagnostic Techniques/methods ; Prognosis ; Research Design ; Risk Factors ; SARS-CoV-2/physiology ; Severity of Illness Index ; Transcriptome/physiology
    Chemical Substances Autophagy-Related Proteins ; Biomarkers
    Language English
    Publishing date 2020-11-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2020.1844433
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6741: Show issues Location:
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  4. Article ; Online: Autophagopathies: from autophagy gene polymorphisms to precision medicine for human diseases.

    Grosjean, Iris / Roméo, Barnabé / Domdom, Marie-Angela / Belaid, Amine / D'Andréa, Grégoire / Guillot, Nicolas / Gherardi, Romain K / Gal, Jocelyn / Milano, Gérard / Marquette, Charles Hugo / Hung, Rayjean J / Landi, Maria Teresa / Han, Younghun / Brest, Patrick / Von Bergen, Martin / Klionsky, Daniel J / Amos, Christopher I / Hofman, Paul / Mograbi, Baharia

    Autophagy

    2022  Volume 18, Issue 11, Page(s) 2519–2536

    Abstract: At a time when complex diseases affect globally 280 million people and claim 14 million lives every year, there is an urgent need to rapidly increase our knowledge into their underlying etiologies. Though critical in identifying the people at risk, the ... ...

    Abstract At a time when complex diseases affect globally 280 million people and claim 14 million lives every year, there is an urgent need to rapidly increase our knowledge into their underlying etiologies. Though critical in identifying the people at risk, the causal environmental factors (microbiome and/or pollutants) and the affected pathophysiological mechanisms are not well understood. Herein, we consider the variations of autophagy-related (
    MeSH term(s) Humans ; Autophagy/genetics ; Precision Medicine ; Genome-Wide Association Study ; Carcinoma, Hepatocellular ; Carcinoma, Non-Small-Cell Lung ; Amyotrophic Lateral Sclerosis ; Frontotemporal Dementia ; Liver Neoplasms ; Lung Neoplasms ; Squamous Cell Carcinoma of Head and Neck ; Head and Neck Neoplasms ; Polymorphism, Genetic
    Language English
    Publishing date 2022-04-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2022.2039994
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6741: Show issues Location:
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  5. Article ; Online: Targeting the Proteasome-Associated Deubiquitinating Enzyme USP14 Impairs Melanoma Cell Survival and Overcomes Resistance to MAPK-Targeting Therapies.

    Didier, Robin / Mallavialle, Aude / Ben Jouira, Rania / Domdom, Marie Angela / Tichet, Mélanie / Auberger, Patrick / Luciano, Frédéric / Ohanna, Mickael / Tartare-Deckert, Sophie / Deckert, Marcel

    Molecular cancer therapeutics

    2018  Volume 17, Issue 7, Page(s) 1416–1429

    Abstract: Advanced cutaneous melanoma is one of the most challenging cancers to treat because of its high plasticity, metastatic potential, and resistance to treatment. New targeted therapies and immunotherapies have shown remarkable clinical efficacy. However, ... ...

    Abstract Advanced cutaneous melanoma is one of the most challenging cancers to treat because of its high plasticity, metastatic potential, and resistance to treatment. New targeted therapies and immunotherapies have shown remarkable clinical efficacy. However, such treatments are limited to a subset of patients and relapses often occur, warranting validation of novel targeted therapies. Posttranslational modification of proteins by ubiquitin coordinates essential cellular functions, including ubiquitin-proteasome system (UPS) function and protein homeostasis. Deubiquitinating enzymes (DUB) have been associated to multiple diseases, including cancer. However, their exact involvement in melanoma development and therapeutic resistance remains poorly understood. Using a DUB trap assay to label cellular active DUBs, we have observed an increased activity of the proteasome-associated DUB, USP14 (Ubiquitin-specific peptidase 14) in melanoma cells compared with melanocytes. Our survey of public gene expression databases indicates that high expression of
    MeSH term(s) Animals ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Survival/drug effects ; Deubiquitinating Enzymes/antagonists & inhibitors ; Deubiquitinating Enzymes/genetics ; Drug Resistance, Neoplasm/genetics ; GTP Phosphohydrolases/genetics ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; MAP Kinase Kinase 1/genetics ; Melanocytes/drug effects ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/pathology ; Membrane Proteins/genetics ; Mice ; Molecular Targeted Therapy ; Proteasome Inhibitors/pharmacology ; Proto-Oncogene Proteins B-raf/genetics ; Reactive Oxygen Species/metabolism ; Tumor Suppressor Protein p53/genetics ; Ubiquitin Thiolesterase/antagonists & inhibitors ; Ubiquitin Thiolesterase/genetics ; Xenograft Model Antitumor Assays
    Chemical Substances Membrane Proteins ; Proteasome Inhibitors ; Reactive Oxygen Species ; TP53 protein, human ; Tumor Suppressor Protein p53 ; USP14 protein, human ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; MAP Kinase Kinase 1 (EC 2.7.12.2) ; Deubiquitinating Enzymes (EC 3.4.19.12) ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; GTP Phosphohydrolases (EC 3.6.1.-) ; NRAS protein, human (EC 3.6.1.-)
    Language English
    Publishing date 2018-04-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2063563-1
    ISSN 1538-8514 ; 1535-7163
    ISSN (online) 1538-8514
    ISSN 1535-7163
    DOI 10.1158/1535-7163.MCT-17-0919
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5750: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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