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http://purl.uniprot.org/citations/34925009http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/34925009http://www.w3.org/2000/01/rdf-schema#comment"The autophagy-lysosomal pathway is an essential cellular mechanism that degrades aggregated proteins and damaged cellular components to maintain cellular homeostasis. Here, we identified HEXA-018, a novel compound containing a catechol derivative structure, as a novel inducer of autophagy. HEXA-018 increased the LC3-I/II ratio, which indicates activation of autophagy. Consistent with this result, HEXA-018 effectively increased the numbers of autophagosomes and autolysosomes in neuronal cells. We also found that the activation of autophagy by HEXA-018 is mediated by the AMPK-ULK1 pathway in an mTOR-independent manner. We further showed that ubiquitin proteasome system impairment- or oxidative stress-induced neurotoxicity was significantly reduced by HEXA-018 treatment. Moreover, oxidative stress-induced mitochondrial dysfunction was strongly ameliorated by HEXA-018 treatment. In addition, we investigated the efficacy of HEXA-018 in models of TDP-43 proteinopathy. HEXA-018 treatment mitigated TDP-43 toxicity in cultured neuronal cell lines and Drosophila. Our data indicate that HEXA-018 could be a new drug candidate for TDP-43-associated neurodegenerative diseases."xsd:string
http://purl.uniprot.org/citations/34925009http://purl.org/dc/terms/identifier"doi:10.3389/fphar.2021.747975"xsd:string
http://purl.uniprot.org/citations/34925009http://purl.uniprot.org/core/author"Han S."xsd:string
http://purl.uniprot.org/citations/34925009http://purl.uniprot.org/core/author"Lee S."xsd:string
http://purl.uniprot.org/citations/34925009http://purl.uniprot.org/core/author"Kim H.J."xsd:string
http://purl.uniprot.org/citations/34925009http://purl.uniprot.org/core/author"Kim S."xsd:string
http://purl.uniprot.org/citations/34925009http://purl.uniprot.org/core/author"Woo J."xsd:string
http://purl.uniprot.org/citations/34925009http://purl.uniprot.org/core/author"Kwon Y."xsd:string
http://purl.uniprot.org/citations/34925009http://purl.uniprot.org/core/author"Lee H.E."xsd:string
http://purl.uniprot.org/citations/34925009http://purl.uniprot.org/core/author"Mun J.Y."xsd:string
http://purl.uniprot.org/citations/34925009http://purl.uniprot.org/core/author"Jo M."xsd:string
http://purl.uniprot.org/citations/34925009http://purl.uniprot.org/core/author"Jeon Y.M."xsd:string
http://purl.uniprot.org/citations/34925009http://purl.uniprot.org/core/date"2021"xsd:gYear
http://purl.uniprot.org/citations/34925009http://purl.uniprot.org/core/name"Front Pharmacol"xsd:string
http://purl.uniprot.org/citations/34925009http://purl.uniprot.org/core/pages"747975"xsd:string
http://purl.uniprot.org/citations/34925009http://purl.uniprot.org/core/title"HEXA-018, a Novel Inducer of Autophagy, Rescues TDP-43 Toxicity in Neuronal Cells."xsd:string
http://purl.uniprot.org/citations/34925009http://purl.uniprot.org/core/volume"12"xsd:string
http://purl.uniprot.org/citations/34925009http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/34925009
http://purl.uniprot.org/citations/34925009http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/34925009
http://purl.uniprot.org/uniprot/#_P14199-mappedCitation-34925009http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34925009
http://purl.uniprot.org/uniprot/#_Q9W2S2-mappedCitation-34925009http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34925009
http://purl.uniprot.org/uniprot/#_X2JEE0-mappedCitation-34925009http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34925009
http://purl.uniprot.org/uniprot/#_X2JJA8-mappedCitation-34925009http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34925009
http://purl.uniprot.org/uniprot/X2JEE0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/34925009