sub:provenance {
  beldoc: dce:description "Approximately 61,000 statements." ;
    dce:rights "Copyright (c) 2011-2012, Selventa. All rights reserved." ;
    dce:title "BEL Framework Large Corpus Document" ;
    pav:authoredBy sub:_7 ;
    pav:version "20131211" .
  sub:_6 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). Collectively, these results indicate that PGC-1{alpha} is capable of promoting mitochondrial biogenesis through its coactivating effects on key factors such as NRF-1." ;
    prov:wasQuotedFrom pubmed:15004004 .
  sub:_7 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:15004004 ;
    prov:wasDerivedFrom beldoc: , sub:_6 .
}