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MEF2C — MYOG

Pathways - manually collected, often from reviews:

• FastForward regulation: MEF2C → MYOG (transcriptional regulation, unknown) Nersesian et al., J Maine Med Assoc 1977*
  Evidence: DNABINDING
• Reactome Reaction: MEF2C → MYOG (indirect_complex) Black et al., Mol Cell Biol 1998*
• Reactome Reaction: MEF2C → MYOG (reaction) Black et al., Mol Cell Biol 1998*

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: MYOG — MEF2C (direct interaction, pull down) Molkentin et al., Cell 1995*

Text-mined interactions from Literome

Ridgeway et al., J Biol Chem 2000 (Carcinoma, Embryonal) : To examine whether MEF2C can differentially regulate MyoD or myogenin expression, P19 cell lines overexpressing MEF2C were analyzed ... MEF2C induced myogenesis in P19 cells and up-regulated the expression of myogenin with 25-fold greater efficiency than that of MyoD
Rogerson et al., FEBS Lett 2002 : Previously, using aggregated P19 cells, we have shown that myogenin upregulates MEF2C expression while MyoD does not [ Ridgeway et al., J. Biol. Chem. 275 ( 2000 ) 41-46 ]
Wilson et al., Mol Biol Cell 2004 : Inhibition of PI3-kinase did not prevent accumulation of muscle differentiation-specific proteins ( myogenin, troponin T, or myosin heavy chain ), did not block transcriptional activation of E-box containing muscle reporter genes by MyoD or myogenin , and did not inhibit the expression or function of endogenous MEF2C or MEF2D