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. Author manuscript; available in PMC: 2015 Aug 21.
Published in final edited form as: Cell Rep. 2014 Aug 14;8(4):991–998. doi: 10.1016/j.celrep.2014.07.027

Figure 3. NCOA6 is required for normal transcriptional activity of PPARδ.

Figure 3

(A and B) Transcript levels of PPARδ targets in the left ventricles of f/f (white; male, n = 1; female, n = 2) and Δ/Δ (black; male, n = 1; female, n = 2) mice. *P < 0.05; **P < 0.01.

(C) mRNA levels of PPARδ in the hearts of f/f and Δ/Δ mice (n = 3 per each genotype). Gapdh was used as a loading control. NS, not statistically significant.

(D) Semi-quantitative PCR analyses of Ncoa6 in primary cardiomyocytes, transduced with lentivirus encoding GFP or Cre constructs, isolated from the f/f mouse heart.

(E–G) Transcript levels of Cd36 (E), Fatp1 (F), and Pdk4 (G) in f/f primary cardiomyocytes containing GFP or Cre constructs. Treatment with GW501516 lasted 48 h. *P < 0.05.

(H-M) Transcript and protein levels of NCOA6 were examined by RT-qPCR (H) and Western blot (I). Parental, no transfection; shGFP, shRNA against GFP; shNCOA6 #3 and #5, independent shRNA constructs against NCOA6. (J) Relative PPRE- luciferase activity. Treatment with GW501516 lasted 24 h. (K-M) Transcript levels of CD36 (K), FATP1 (L), and MCPT-1 (M) were measured by RT-qPCR analyses after treatment with GW501516 for 48 h. Graphs show means ± s.d. See also Figure S3.