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http://purl.uniprot.org/citations/29474739http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29474739http://www.w3.org/2000/01/rdf-schema#comment"Bone formation and bone homeostasis are energy-expensive processes. How they are being regulated by energy needs is not completely understood. This is of high clinical importance because diabetic-induced bone loss is common whereas the underlying mechanisms are unclear. Here, we show that Mst1/2 are important regulators for glucose uptake during osteoblast differentiation. Genetically removal of both Mst1/2 kinases simultaneously in mice in early and mature osteoblasts inhibits bone formation and bone remodeling, respectively. We found that the activity of Mst1/2 kinases is sensitive to glucose levels, and in turn, regulates glucose uptake by stabilizing key glucose transporter Glut1. In the absence of Mst1/2 kinases, Glut1 expression is loss and results in AMP-dependent protein kinase (AMPK) activation and subsequent proteasomal degradation of Runx2. The streptozotocin (STZ)-induced diabetic mouse model also recapitulates similar changes in the bone tissues. In addition, Glut1 expression regulated by Mst1/2 kinases is independent of Yap/Taz expression. Our results unravel new mechanistic insights into the orchestration of glucose level and bone homeostasis. © 2018 American Society for Bone and Mineral Research."xsd:string
http://purl.uniprot.org/citations/29474739http://purl.org/dc/terms/identifier"doi:10.1002/jbmr.3413"xsd:string
http://purl.uniprot.org/citations/29474739http://purl.uniprot.org/core/author"Deng Y."xsd:string
http://purl.uniprot.org/citations/29474739http://purl.uniprot.org/core/author"Li W."xsd:string
http://purl.uniprot.org/citations/29474739http://purl.uniprot.org/core/author"Feng B."xsd:string
http://purl.uniprot.org/citations/29474739http://purl.uniprot.org/core/author"Mak K.K."xsd:string
http://purl.uniprot.org/citations/29474739http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/29474739http://purl.uniprot.org/core/name"J Bone Miner Res"xsd:string
http://purl.uniprot.org/citations/29474739http://purl.uniprot.org/core/pages"1183-1195"xsd:string
http://purl.uniprot.org/citations/29474739http://purl.uniprot.org/core/title"Mst1/2 Kinases Modulate Glucose Uptake for Osteoblast Differentiation and Bone Formation."xsd:string
http://purl.uniprot.org/citations/29474739http://purl.uniprot.org/core/volume"33"xsd:string
http://purl.uniprot.org/citations/29474739http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/29474739
http://purl.uniprot.org/citations/29474739http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/29474739
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http://purl.uniprot.org/uniprot/#_D6RHQ9-mappedCitation-29474739http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29474739
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http://purl.uniprot.org/uniprot/#_P26928-mappedCitation-29474739http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29474739
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