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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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http://www.tkuhn.ch/bel2nanopub/RAU1LHn5KTiMEYE66h6qCwj5c8x20Ne7sEGSElvY40iNk#_1
http://purl.obolibrary.org/obo/RO_0002204
http://www.informatics.jax.org/marker/MGI:102469
http://www.tkuhn.ch/bel2nanopub/RAU1LHn5KTiMEYE66h6qCwj5c8x20Ne7sEGSElvY40iNk#_1
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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http://www.w3.org/1999/02/22-rdf-syntax-ns#object
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p(MGI:Nfatc1) -> bp(GOBP:"osteoclast differentiation")
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http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel
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BEL Framework Large Corpus Document
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http://www.w3.org/ns/prov#value
Exogenous overexpression of a constitutively active form of NFATc1 in bone marrow-derived monocyte/macrophage cells (BMMs) induces formation of multinucleated osteoclasts as well as the expression of fusion-mediating molecules such as the d2 isoform of vacuolar ATPase V(o) domain (Atp6v0d2) and the dendritic cell-specific transmembrane protein (DC-STAMP). Moreover, inactivation of NFATc1 by cyclosporin A treatment attenuates expression of Atp6v0d2 and DC-STAMP and subsequent fusion process of osteoclasts. We show that NFATc1 binds to the promoter regions of Atp6v0d2 and DC-STAMP in osteoclasts and directly induces their expression.
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http://www.w3.org/ns/prov#wasQuotedFrom
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http://www.w3.org/2000/01/rdf-schema#label
Selventa
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2014-07-03T14:33:12.528+02:00
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