FIGURE 5.

Akap1 genetic deletion enhances ER stress-induced cell death after hyperoxic exposure: Wt and Akap1 mice were exposed to normoxia and hyperoxia for 48 h. After hyperoxia, the mice were killed, and protein was extracted from the lungs and subjected to Western blot analysis to evaluate the expression of CHOP and Erp57. β-actin was used as a loading control. Densitometry analysis of CHOP and Erp57 protein was followed by normalization to β-actin. Data are expressed as mean ± SEM (*p < 0.05, **p < 0.005) (n = 5 mice per group). NO, normoxia; HO, hyperoxia; AK, Akap1; KO: Knockout.