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I'd like to block a percentage of PGC-1β or Sod2 expression. According to the following paper's figure beta-blockers inhibit some expression of PGC-1α. Are there any medicines/chemicals which safely and temporarily block 50%-60% expression of PGC-1β or Sod2 in fully developed mice or humans? Thank you

http://jap.physiology.org/content/107/1/8.full

Fig. 1. Interactions of β-blockers and mitochondrial biogenesis. Aerobic exercise activates β2-adrenergic receptors (β-AR) on skeletal muscle and induces peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) transcription, a regulator of mitochondrial biogenesis. Selective and nonselective β-blockers can blunt β2-AR signaling, which restricts the expected PGC-1α response following exercise and can impair adaptations to mitochondria and aerobic capacity. V̇O2max, maximum oxygen consumption.

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Perhaps there is a transgenic mouse model available that uses a conditional knock-down approach? –  leonardo Nov 3 '12 at 1:47
    
@leonardo there is a transgenic mouse and there is a vector based method of depleting Sod2 and PGC-1β but it wont help me because the transition needs to be reversible –  caseyr547 Nov 3 '12 at 2:01
    
right, that's why I qualified the "conditional" knock-down. Not knowing these lines, vector based sounds like it could be reversible (eg, stop delivering the vector). The transgenic mouse might be a knock-out rather than a knock-down/conditional knock-out. –  leonardo Nov 3 '12 at 16:34
    
@leonardo yeah that is right the only thing is viral vectors cause leukemia in the long run; cell penetrating peptides are safe and fda aproved but they can only carry one cargo at a time as best i know –  caseyr547 Nov 3 '12 at 17:05
    
Maybe you can design a new transgenic model then. ;) –  leonardo Nov 3 '12 at 17:28
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Dexamethasone can be used to regulate PGC-1β http://www.ncbi.nlm.nih.gov/pubmed/20647557

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