Skip to main content

Advertisement

Fig. 2 | Clinical Epigenetics

Fig. 2

From: ABT-737 and/or folate reverse the PDGF-induced alterations in the mitochondrial apoptotic pathway in low-grade glioma patients

Fig. 2

The apoptosis phenotype evasion is associated with the loss of Bax activation. a Effect of the folate or PDGFri (PDGFri 0.5 μM Calbiochem, France) treatment on the level of DNA methylation (i.e., on the 5methylcytosine number, 5mC) and on the UV-induced apoptosis. b Effect of the folate or PDGFri treatment on the cytochrome c release in cytosol (C) from mitochondria (M) via subcellular fractionation experiment. F1-ATPase is used as control of mitochondrial protein. c Effect of the folate or PDGFri treatment on the cytochrome c release in cytosol (C) from mitochondria (M) via confocal microscopy experiment. F1-ATPase is used as control of mitochondrial protein. CF represents the correlation factor or co-localization of F1-ATPase (i.e., mitochondria) with cytochrome c. The pictures are representative of at least 100 different cells. d Effect of the folate or PDGFri treatment on degree of Bax activation via the Bax6A7-immunoprecipitation (IP) method. Western blot (WB) is performed to analyze the effect of the folate or PDGFri treatment on the Bax expression. Actin is used as loading control. All experiments were done after 7 days of treatment as previously described (Hervouet et al. 2009)

Back to article page