Skip to main content


Springer Nature is making SARS-CoV-2 and COVID-19 research free. View research | View latest news | Sign up for updates

Figure 4 | Molecular Cancer

Figure 4

From: EGFR and EGFRvIII undergo stress- and EGFR kinase inhibitor-induced mitochondrial translocalization: A potential mechanism of EGFR-driven antagonism of apoptosis

Figure 4

Cancer cells expressing the mitochondrially enriched EGFRvIII mutant are more resistant to apoptosis. A, Generation of U87MG stable transfectant cell lines that express EGFRvIII-MTS1 and EGFRvIII-MTS2. Western blotting shows that the three isogenic cell lines express equivalent levels of the transgenes. B,C, The EGFRvIII-MTS1 mutant is enriched in the mitochondria as shown by immunofluorescence staining and confocal microscopy (B) and cell fractionation/western blotting (C). D, Stability of EGFRvIII and EGFRvIII-MTS1 proteins is similar. Protein half-life study using transcription inhibitor cycloheximide determined the two proteins to have similar degradation rates.

Back to article page