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http://purl.uniprot.org/citations/31885214http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31885214http://www.w3.org/2000/01/rdf-schema#comment"The dedicator of cytokinesis 5 (DOCK5) is associated with obesity. However, the mechanism by which DOCK5 contributes to obesity remains completely unknown. Here, we show that hepatic DOCK5 expression significantly decreases at a state of insulin resistance (IR). Deletion of DOCK5 in mice reduces energy expenditure, promotes obesity, augments IR, dysregulates glucose metabolism, and activates the mTOR (Raptor)/S6K1 pathway under a high-fat diet (HFD). The overexpression of DOCK5 in hepatocytes inhibits gluconeogenic gene expression and increases the level of insulin receptor (InsR) and Akt phosphorylation. DOCK5 overexpression also inhibits mTOR/S6K1 phosphorylation and decreases the level of raptor protein expression. The opposite effects were observed in DOCK5-deficient hepatocytes. Importantly, in liver-specific Raptor knockout mice and associated hepatocytes, the effects of an adeno-associated virus (AAV8)- or adenovirus-mediated DOCK5 knockdown on glucose metabolism and insulin signaling are largely eliminated. Additionally, DOCK5-Raptor interaction is indispensable for the DOCK5-mediated regulation of hepatic glucose production (HGP). Therefore, DOCK5 acts as a regulator of Raptor to control hepatic insulin activity and glucose homeostasis."xsd:string
http://purl.uniprot.org/citations/31885214http://purl.org/dc/terms/identifier"doi:10.15252/embr.201949473"xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/author"Li L."xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/author"Liu C."xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/author"Liu D."xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/author"Li S."xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/author"Lai Y."xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/author"Lin Y."xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/author"Song J."xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/author"Yang G."xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/author"Tan M."xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/author"Yang M."xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/author"Zheng H."xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/author"Zhu Z."xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/author"Zhao A."xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/name"EMBO Rep"xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/pages"e49473"xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/title"DOCK5 regulates energy balance and hepatic insulin sensitivity by targeting mTORC1 signaling."xsd:string
http://purl.uniprot.org/citations/31885214http://purl.uniprot.org/core/volume"21"xsd:string
http://purl.uniprot.org/citations/31885214http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31885214
http://purl.uniprot.org/citations/31885214http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31885214
http://purl.uniprot.org/uniprot/#_D0FZQ3-mappedCitation-31885214http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31885214
http://purl.uniprot.org/uniprot/#_A0A991EQV1-mappedCitation-31885214http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31885214