Fig. 6: Restored autophagy program as a result of FOXO3a dysregulation by U2AF1S34F mutation. | Cell Death & Disease

Fig. 6: Restored autophagy program as a result of FOXO3a dysregulation by U2AF1S34F mutation.

From: U2AF1 mutation promotes tumorigenicity through facilitating autophagy flux mediated by FOXO3a activation in myelodysplastic syndromes

Fig. 6

A Biological process, molecular function, as well as cellular component are adopted to categorize GO. B, C Representative images of western blotting data. Quantitative analysis of the protein expression levels, and the LC3-II/ LC3-I ratio is demonstrated. Beclin 1, ATG5, ATG12, and ATG16 complex proteins were all up-regulated following S34F mutant U2AF1 treatment. These proteins were decreased after silencing of FOXO3a. D Representative transmission electron micrographs of autophagosomes ultrastructure. Scale bar, 5 µm. E Schematic representation of the potential role of U2AF1S34F mutation based on this study. The data represent at least two independent experiments with three samples per group in each. *p < 0.05, **p < 0.01, and ***p < 0.001. WT, wild-type, M mitochondria, AP autophagosome.

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