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. Author manuscript; available in PMC: 2016 Oct 1.
Published in final edited form as: Science. 2016 Feb 25;352(6281):54–61. doi: 10.1126/science.aad9642

Figure 2. Genetic or small molecule activation of the HIF response is protective against multiple forms of RC inhibition, in multiple cell types.

Figure 2

(A) Schematic for HIF degradation during normoxia. (B) Schematic for induction of hypoxia transcriptional program during hypoxia. (C) Growth curves for K562 VHL-knockout cells (cyan, blue) or non-targeting sgRNA cells (black, red) for untreated or disease conditions (mean shown). Disease conditions correspond to inhibition of Complex I (piericidin), Complex III (antimycin) or Complex V (oligomycin). Growth curves for (D) K562 cells, (E) HEK293T cells and (F) HT-29 cells ± FG-4592, in combination with untreated or disease conditions (inhibition of complex I, III and V). All time points were measured in duplicate and all growth curves are representative of 2-3 independent experiments (mean shown). All final cell counts of FG-treated rescue (or VHL-KO rescue in 2A) in presence of RC inhibitor were statistically significant (one-sided t-test p-value < 0.05).