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. Author manuscript; available in PMC: 2019 Mar 2.
Published in final edited form as: Circ Res. 2018 Jan 22;122(5):701–711. doi: 10.1161/CIRCRESAHA.117.311814

Figure 2. E2F1 suppresses BM PC oxidative metabolism via PDK4/2 expression.

Figure 2

(A–B) qRT-PCR analyses for mRNA expression of representative glycolysis and mitochondrial genes (A) and PDK genes (B) in WT and E2F1−/− BM PCs. The expression levels of individual genes were normalized to the β-actin mRNA and expressed relative to their levels in WT cells. n = 5 per group. (C–D) Western-blotting analyses (C) and quantification (D) of PDK2, PDK4 and phospho-PDH protein levels in BM PCs. n = 4 per group. (E–F) OCR measurements (E) and quantification (F, left panel, at basal condition; right panel, after FCCP injection) in WT and E2F1−/− PCs transduced with control-mCherry lentivirus and in E2F1−/− PCs transduced with PDK4-mCherry lentivirus. n = 5 per group. (G–H) ECAR measurements (G) and quantification (H, left panel, at basal condition; right panel, after Oligomycin treatment) in WT and E2F1−/− PCs transduced with control-mCherry lentivirus and in E2F1−/− PCs transduced with PDK4-mCherry lentivirus. n = 5 per group.