Fig. 4: CR8 attenuates activation of the p53-linked pro-apoptotic pathways following etoposide-induced DNA damage. | Cell Death & Disease

Fig. 4: CR8 attenuates activation of the p53-linked pro-apoptotic pathways following etoposide-induced DNA damage.

From: Comparing effects of CDK inhibition and E2F1/2 ablation on neuronal cell death pathways in vitro and after traumatic brain injury

Fig. 4

Neurons were treated with 50 μm of etoposide ± 1 μm CR8. Twenty-four hours later whole-cell lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against phospho-ATM, γ-H2A.X, p53, phospho-p53, Puma, Noxa, and p21. Protein levels were quantified by densitometry, normalized to β-actin, and presented as fold change compared with control untreated levels. Cell death occurs in all neurons treated with 50 μm etoposide (phospho-ATM and γ-H2A.X) including an increase in phospho-p53. However, 1 μm CR8 attenuates the etoposide-induced increase in downstream targets of p53 (Puma, Noxa, and p21). n = 3/group for all groups. Data represent mean ± SEM of one-way ANOVA and Tukey post hoc analysis, *p < 0.05 vs. control, &p < 0.05 vs. etoposide + CR8 at the same time point

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