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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAHiArzQCYHcgfr5wMQFCYRsWzte4ZWW2VdMxNRVm4F5A#_7 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAHiArzQCYHcgfr5wMQFCYRsWzte4ZWW2VdMxNRVm4F5A#_6 http://www.w3.org/ns/prov#value PGC-1{alpha} can also interact directly with and coactivate NRF-1 on the Tfam gene promoter. Third, studies in primary cardiac myocytes in culture and in the hearts of transgenic mice have demonstrated that overexpression of PGC-1{alpha} up-regulates the expression of genes involved in mitochondrial fatty acid oxidation, most of which are PPAR{alpha} targets, in addition to NRF-1 targets (Lehman et al. 2000Go). Cardiac-specific overexpression of PGC-1{alpha} in transgenic mice leads to massive mitochondrial proliferation, ultimately resulting in cardiomyopathy and death (Lehman et al. 2000Go). Interestingly, in neonatal cardiac myocytes in culture, PGC-1{alpha} induces mitochondria that support largely coupled respiration consistent with the known ATP-generating function of this organelle in heart (Lehman et al. 2000Go). Lastly, forced expression of PGC-1{alpha} in skeletal muscle of transgenic mice triggers mitochondrial proliferation and the formation of mitochondrial-rich type I, oxidative (\"slow-twitch\") muscle fibers (Lin et al. 2002bGo). 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