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http://purl.uniprot.org/citations/17952062http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17952062http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17952062http://www.w3.org/2000/01/rdf-schema#comment"Histone modifications induced by activated signalling cascades are crucial to cell-lineage decisions. Osteoblast and adipocyte differentiation from common mesenchymal stem cells is under transcriptional control by numerous factors. Although PPAR-gamma (peroxisome proliferator activated receptor-gamma) has been established as a prime inducer of adipogenesis, cellular signalling factors that determine cell lineage in bone marrow remain generally unknown. Here, we show that the non-canonical Wnt pathway through CaMKII-TAK1-TAB2-NLK transcriptionally represses PPAR-gamma transactivation and induces Runx2 expression, promoting osteoblastogenesis in preference to adipogenesis in bone marrow mesenchymal progenitors. Wnt-5a activates NLK (Nemo-like kinase), which in turn phosphorylates a histone methyltransferase, SETDB1 (SET domain bifurcated 1), leading to the formation of a co-repressor complex that inactivates PPAR-gamma function through histone H3-K9 methylation. These findings suggest that the non-canonical Wnt signalling pathway suppresses PPAR-gamma function through chromatin inactivation triggered by recruitment of a repressing histone methyltransferase, thus leading to an osteoblastic cell lineage from mesenchymal stem cells."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.org/dc/terms/identifier"doi:10.1038/ncb1647"xsd:string
http://purl.uniprot.org/citations/17952062http://purl.org/dc/terms/identifier"doi:10.1038/ncb1647"xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Kitagawa H."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Kitagawa H."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Kato S."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Kato S."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Minami Y."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Minami Y."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Nakamura T."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Nakamura T."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Matsumoto K."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Matsumoto K."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Kobayashi S."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Kobayashi S."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Takada S."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Takada S."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Igarashi M."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Igarashi M."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Takada I."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Takada I."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Shibuya H."xsd:string
http://purl.uniprot.org/citations/17952062http://purl.uniprot.org/core/author"Shibuya H."xsd:string