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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: ATAD3A mediates activation of RAS-independent mitochondrial ERK1/2 signaling, favoring head and neck cancer development

Fig. 5

ATAD3A interacts with mitochondrial ERK1/2 in a VDAC1-dependent manner. A The interaction between ATAD3A and ERK12 proteins in HN12 cells determined by IP. B The presence of VDAC1 in the ATAD3A-ERK1/2 immunocomplex in HN12 cell mitochondria. C The binding of ATAD3A N-terminus (Nter, 1-287 aa) and C-terminus (Cter, 258-586 aa) to VDAC1 protein in HN12 cells. D The necessity of the ATPase activity of ATAD3A for ATAD3A-ERK1/2 interaction in HN12 cells. E The effect of ATAD3A KO on the interaction between VDAC1 and ERK1/2. F The effect of VDAC1 knockdown on ERK1/2 activation in HN12 cells. G The effect of VDAC1 knockdown on the interaction between ATAD3A and ERK1/2 proteins in ATAD3A-overexpressing HN12 cells. The immunoprecipitates were pulled down using an anti-Flag antibody. H The effect of VDAC1 knockdown on the levels of mitochondrial ERK1/2 in HN12 cells. I The effect of VDAC1 on the cytosolic and mitochondrial ERK1/2 protein levels in HN12 cells. The purity of the mitochondrial fractions was indicated by the mitochondrial COXIV protein and the absence of the cytosolic GAPDH protein. Representative results and quantitative data from three independent experiments are shown in the upper and lower panels, respectively. *p < 0.05; **p < 0.01

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