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http://purl.uniprot.org/citations/23164509http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23164509http://www.w3.org/2000/01/rdf-schema#comment"As differentiated cells, hepatocytes primarily metabolize glucose for ATP production through oxidative phosphorylation of glycolytic pyruvate, whereas proliferative hepatocellular carcinoma (HCC) cells undergo a metabolic shift to aerobic glycolysis despite oxygen availability. Keratins, the intermediate filament (IF) proteins of epithelial cells, are expressed as pairs in a lineage/differentiation manner. Hepatocyte and HCC (hepatoma) cell IFs are made solely of keratins 8/18 (K8/K18), thus providing models of choice to address K8/K18 IF functions in normal and cancerous epithelial cells. Here, we demonstrate distinctive increases in glucose uptake, glucose-6-phosphate formation, lactate release, and glycogen formation in K8/K18 IF-lacking hepatocytes and/or hepatoma cells versus their respective IF-containing counterparts. We also show that the K8/K18-dependent glucose uptake/G6P formation is linked to alterations in hexokinase I/II/IV content and localization at mitochondria, with little effect on GLUT1 status. In addition, we find that the insulin-stimulated glycogen formation in normal hepatocytes involves the main PI-3 kinase-dependent signaling pathway and that the K8/K18 IF loss makes them more efficient glycogen producers. In comparison, the higher insulin-dependent glycogen formation in K8/K18 IF-lacking hepatoma cells is associated with a signaling occurring through a mTOR-dependent pathway, along with an augmentation in cell proliferative activity. Together, the results uncover a key K8/K18 regulation of glucose metabolism in normal and cancerous hepatic cells through differential modulations of mitochondrial HK status and insulin-mediated signaling."xsd:string
http://purl.uniprot.org/citations/23164509http://purl.org/dc/terms/identifier"doi:10.1016/j.yexcr.2012.11.011"xsd:string
http://purl.uniprot.org/citations/23164509http://purl.uniprot.org/core/author"Gilbert S."xsd:string
http://purl.uniprot.org/citations/23164509http://purl.uniprot.org/core/author"Mathew J."xsd:string
http://purl.uniprot.org/citations/23164509http://purl.uniprot.org/core/author"Faure R."xsd:string
http://purl.uniprot.org/citations/23164509http://purl.uniprot.org/core/author"Loranger A."xsd:string
http://purl.uniprot.org/citations/23164509http://purl.uniprot.org/core/author"Marceau N."xsd:string
http://purl.uniprot.org/citations/23164509http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23164509http://purl.uniprot.org/core/name"Exp Cell Res"xsd:string
http://purl.uniprot.org/citations/23164509http://purl.uniprot.org/core/pages"474-486"xsd:string
http://purl.uniprot.org/citations/23164509http://purl.uniprot.org/core/title"Keratin 8/18 regulation of glucose metabolism in normal versus cancerous hepatic cells through differential modulation of hexokinase status and insulin signaling."xsd:string
http://purl.uniprot.org/citations/23164509http://purl.uniprot.org/core/volume"319"xsd:string
http://purl.uniprot.org/citations/23164509http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23164509
http://purl.uniprot.org/citations/23164509http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23164509
http://purl.uniprot.org/uniprot/#_A0A994J753-mappedCitation-23164509http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23164509
http://purl.uniprot.org/uniprot/#_B4DG62-mappedCitation-23164509http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23164509
http://purl.uniprot.org/uniprot/#_A8K7J7-mappedCitation-23164509http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23164509
http://purl.uniprot.org/uniprot/#_B1AR62-mappedCitation-23164509http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23164509
http://purl.uniprot.org/uniprot/#_B3KRA9-mappedCitation-23164509http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23164509
http://purl.uniprot.org/uniprot/#_B3KXY9-mappedCitation-23164509http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23164509
http://purl.uniprot.org/uniprot/#_B2RA03-mappedCitation-23164509http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23164509
http://purl.uniprot.org/uniprot/#_P78542-mappedCitation-23164509http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23164509
http://purl.uniprot.org/uniprot/#_Q71V75-mappedCitation-23164509http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23164509
http://purl.uniprot.org/uniprot/#_I6L965-mappedCitation-23164509http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23164509