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. Author manuscript; available in PMC: 2014 Jan 10.
Published in final edited form as: Mol Cell. 2012 Nov 29;49(1):145–157. doi: 10.1016/j.molcel.2012.10.027

Figure 5. Stabilization of PGC-1α Protein by α-MSH.

Figure 5

(A) Time course of induction of PGC-1α and PGC-1β mRNA (top) and PGC-1α protein (bottom) in B16-F10 cells treated with forskolin and IBMX (Fsk + IBMX) for the indicated times. (B) Stabilization of PGC-1α by α-MSH. WB, western blot.

(C) The PKA inhibitor (H89) blocks stabilization of PGC-1α protein.

(D) PGC-1α protein stabilization in cells treated with the adenylate cyclase activator (forskolin). GFP (lower panel) is expressed by the same promoter (CMV).

(E) Half-life of PGC-1α in B16-F10 cells treated with forskolin + IBMX. CHX, cycloheximide.

(F) Schematic of murine PGC-1α and predicted PKA target sites. Sites mutated to alanine in the 7A mutant are indicated below.

(G) Absence of stabilization of PGC-1α mutated at PKA target sites. The quantification of five experiments is shown below. WT, wild-type.

(H) Stabilization of PGC-1β in B16-F10 cells treated with forskolin + IBMX or α-MSH.

NS, nonspecific band. *p < 0.05. Error bars represent mean ± SD.

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