Fig 4.

Selectivity of the inhibitory effect of the AKAP-Lbc competitor fragment. (A) Transgenic mice overexpressing the competitor fragment of AKAP-Lbc (Comp.) and their WT littermates were subjected to TAC or a sham operation. The amounts of total and phosphorylated ERK1/2 and JNK, PKD, and Akt in heart lysates were determined by immunoblotting using specific antibodies, as indicated. (B) Cardiac overexpression of the AKAP-Lbc competitor fragment does not affect doxorubicin-induced p38 activation in the heart. Transgenic (Comp.) and WT mice were injected intraperitoneally with PBS or 20 mg/kg doxorubicin (DOX). The mice were sacrificed 5 days later, and the hearts were harvested. The amounts of total and phosphorylated p38, as well as the expression of the Flag-AKAP-Lbc-1570-1764 fragment in heart lysates, were determined by immunoblotting using specific antibodies, as indicated. (C) Quantitative analysis of phosphorylated p38 was performed by densitometry. The amount of phospho-p38 was normalized to the total amount of p38. Four mice were analyzed for each group. Values are presented as means and SEM. Statistical differences were analyzed using the Student t test. No statistically significant differences were found.