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. Author manuscript; available in PMC: 2014 Apr 21.
Published in final edited form as: Diabetes Metab Res Rev. 2014 Jan;30(1):23–30. doi: 10.1002/dmrr.2451

Figure 3.

Figure 3

(A) Representative immunoblot of phospho-adenosine monophosphate-activated protein kinase (P-AMPK) and total AMPK using protein extracted from murine embryonic stem cells (mESC) that were untreated or treated for 1 h with 1 mmol/L AICAR (A) or 1 mmol/L metformin (M) compared with time 0 (t0). (B) Quantitation of P-AMPK/total AMPK of three replicate culture dishes of mESC that were treated as in panel (A). Band intensity is expressed as arbitrary units (AU) relative to time 0. *p <0.05 versus t0. (C) Real-time RT-PCR of Pax3 in undifferentiated (UD) mESC, differentiating neuronal progenitors derived from mESC (D), differentiating neuronal progenitors treated with AICAR for 48 h (D + AICAR) or differentiating neuronal progenitors treated with metformin for 48 h (D + metformin). Pax3 mRNA was normalized to rRNA and expressed relative to that of differentiating neuronal progenitors. ***p <0.001 versus UD; *p <0.001 versus D. n = 4 replicate tissue culture dishes for each treatment