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All Rights Reserved." } ], "http://purl.org/dc/elements/1.1/title" : [ { "@value" : "BEL Framework Small Corpus Document" } ], "http://purl.org/dc/terms/license" : [ { "@value" : "Creative Commons Attribution-Non-Commercial-ShareAlike 3.0 Unported License" } ], "http://purl.org/pav/authoredBy" : [ { "@id" : "http://www.tkuhn.ch/bel2nanopub/RA1FtKvkgumU8hWoq27bs1espLPZgdMtBphKCgxpi8Tho#_7" } ], "http://purl.org/pav/version" : [ { "@value" : "20131211" } ] }, { "@id" : "http://www.tkuhn.ch/bel2nanopub/RA1FtKvkgumU8hWoq27bs1espLPZgdMtBphKCgxpi8Tho#_6", "http://www.w3.org/ns/prov#value" : [ { "@value" : "We next examined whether mutations of this MEF2 site affects MEF2 activity on the\nPGC-1α promoter. The mutated 2-kb promoter (called ΔMEF2; see Fig. 3A) is no longer\nable to mediate MEF2C or MEF2D induction alone, when activated by CnA or coactivated\nby PGC-1α, suggesting that this site is responsible for the MEF2 action\n(Fig. 3B). Moreover, electrophoretic mobility-shift assays revealed binding of\nMEF2C to this MEF-binding site but not the mutated ΔMEF site in the PGC-1α promoter\n(Fig. 3C). 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