Fig. 2: Respiratory complex I expression and activity are regulated in a MEK/ERK-dependent fashion. | Cell Death & Differentiation

Fig. 2: Respiratory complex I expression and activity are regulated in a MEK/ERK-dependent fashion.

From: Tumor growth of neurofibromin-deficient cells is driven by decreased respiration and hampered by NAD+ and SIRT3

Fig. 2

WB analyses of Complex I subunits upon modulation of ERK activity through expression of the constitutively-active or dominant-negative form of the upstream MEK1 kinase (MEK1-CA and MEK1-DN, respectively; A) or by treatment with the MEK inhibitor PD98059 (40 µM, 3 days; B). NDUFS1, GRIM19, NDUFS3 and NDUFB8 were used as complex I markers, subunits α, UQCRC2 and SDHA/B as complex V, complex III and complex II markers, respectively. pERK1/2 indicates phosphorylated, active ERK1/2. TRAP1 and calnexin were used as loading controls. C Complex I activity with or without PD98059 treatment (40 µM, 3 days) was analyzed as in Fig. 1C. D, E BN-PAGE of respiratory complexes performed on digitonized mitochondria from Nf1+/+ and Nf1−/− MEFs. The MEK-ERK pathway is modulated by expression of the constitutively-active or of the dominant-negative form of the upstream MEK1 kinase (MEK1-CA and MEK1-DN, respectively; D) or by treatment with the MEK inhibitor PD98059 (40 µM, 3 days; E). All experiments in the Figure were carried out on Nf1+/+ and Nf1−/− MEFs. Data are reported as mean ± SD values (n ≥ 3); ***p < 0.001; **p < 0.01 and *p < 0.05 with a Student’s t test analysis.

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