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. 2011 Oct 19;6(10):e26581. doi: 10.1371/journal.pone.0026581

Figure 6. Acute βAR stimulation induced increase in phosphorylation of Akt and ERK1/2 is β2AR-specific.

Figure 6

C57BL/6 mice were treated with vehicle control, dobutamine (Dob., 1.7 mg/kg, i.p.), or formoterol (For., 2.1 mg/kg, i.p.), for 30 min. (A) In vitro lipid kinase assay was performed as described except with higher amount of LV lysates (1 mg). PIP, the phosphorylated end-product. The bar graph shows the densitometric scanning results of the measurement of PI3K activities in the control, Dob.-treated and For.-treated mice (n = 4). (B) Representative Western blot analyses were performed on left ventricular lysates with antibodies against phospho-Akt (Thr308), phospho-Akt (Ser473), total Akt, phospho-ERK1/2 (Thr202/Tyr204) and total ERK1/2. The bar graphs show the densitometric scanning results from two seperate experiments (n = 5). Data are normalized with individual total protein levels and represent means ± S.E. of percent change in protein phosphorylation relative to that of vehicle control. *, p<0.05 versus vehicle control.