Gα_i2 Signaling Promotes Skeletal Muscle Hypertrophy, Myoblast Differentiation, and Muscle Regeneration

Giulia C. Minetti, Jerome N. Feige, Antonia Rosenstiel, Florian Bombard, Viktor Meier, Annick Werner, Frederic Bassilana, Andreas W. Sailer, Peter Kahle, Christian Lambert, David J. Glass,* Mara Fornaro*

*To whom correspondence should be addressed. E-mail: mara.fornaro{at}novartis.com (M.F.); david.glass{at}novartis.com (D.J.G.)

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• Fig. S1. LPA and constitutively active Gα_i2 inhibit the cAMP-CREB pathway.
• Fig. S2. Abundance of Gα_i2, PGC-1α, and PPARβ/σ in tibialis muscle infected with AAV-Gα_i2 (Q205L) or AAV-EV.
• Fig. S3. Rapamycin but not LY294002 blocks hypertrophy induced by expression of constitutively active Gai2 in C2C12 myotubes.
• Fig. S4. LPA and Gα_i2 (Q205L) induce skeletal myotube hypertrophy of HuSkMC myotubes through a PKC-mediated pathway.
• Fig. S5. Gα_i2 promotes satellite cell activation and differentiation.
• Fig. S6. Expression of constitutively active Gα_i2 promotes nuclear export of HDAC4.
  

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