Fig. 2: E2F2−/− and E2F1−/−/E2F2−/− mice show no attenuation in acute injury markers at the protein level in cortex. | Cell Death & Disease

Fig. 2: E2F2−/− and E2F1−/−/E2F2−/− mice show no attenuation in acute injury markers at the protein level in cortex.

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

Fig. 2: E2F2−/− and E2F1−/−/E2F2−/− mice show no attenuation in acute injury markers at the protein level in cortex.

Whole-tissue lysates from non-injured mouse cortices and 24 h after TBI were fractioned on SDS-polyacrylamide gel and immunobloted with antibodies against MCM2, E2F3, Mcl-1, p21, a-Fodrin, phospho-c-Jun (Ser63), c-Jun, and PSD95. Protein levels were quantified by densitometry, normalized to β-actin, and presented as fold change compared with non-injured mice. Non-injured controls include all the non-injured mice from all the genotypes, CCI group combines the B6 and FVB genotypes (WT CCI). B6 non-injured n = 4, CCI n = 5; FVB non-injured n = 3, CCI n = 5; E2F2−/− non-injured n = 4, CCI n = 11; E2F1−/−/E2F2−/− non-injured n = 4, CCI n = 12. Data represent mean ± SEM of one-way ANOVA and Tukey post hoc analysis, *p < 0.05 vs. non-injured control, ^p < 0.05 vs. E2F1−/−/E2F2−/−. For MCM2, Mcl-1, c-Jun, phospho-c-Jun, α-Fodrin, p21, and Jun data represent mean ± SEM of Kruskal-Wallis test with Dunn’s multiple comparisons post hoc test, *p < 0.05 vs. non-injured control, ^p < 0.05 vs. E2F1−/−/E2F2−/−

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