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. Author manuscript; available in PMC: 2020 Sep 1.
Published in final edited form as: Biochem J. 2012 May 1;443(3):655–661. doi: 10.1042/BJ20120118

Figure 5. GCN5L1 knockdown increases mitochondrial respiration.

Figure 5.

(A) Steady-state GCN5L1 levels in HepG2 cells following control or GCN5L1 knockdown (KD). (B) Representative tracing of basal oxygen consumption and maximal oxygen consumption induced by the uncoupler dinitrophenol (2-DNP) comparing control and GCN5L1 KD HepG2 cells. (C) The absolute differences in basal oxygen consumption comparing control and GCN5L1 KD HepG2 cells, taken as a mean of the first three data points. (D) Relative differences in oxygen consumption in control and GCN5L1 KD cells following digitonin administration and the use of glutamate and malate as mitochondrial respiration substrates. (E) Differences in cellular ATP levels in control and GCN5L1 KD HepG2 cells. n ≥ 3 for all experiments. *p<0.05 and **p<0.01, compared to respective controls. Results are mean ± s.e.m.