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. 2014 Nov 21;308(2):L208–L220. doi: 10.1152/ajplung.00242.2014

Fig. 2.

Fig. 2.

Deletion of Akt1 does not affect Akt2 expression in lung tissue, and LV hemodynamics are unaffected in Akt1−/− and Akt2−/− mice. A: genotyping characterization of Akt1−/−, Akt2−/−, and wild-type (WT) mice demonstrates the presence of only knockout (KO) alleles in the homozygous mice, whereas heterozygotes have both KO and WT alleles. Lung tissues were harvested from Akt1−/−, Akt2−/−, and WT mice. B: real-time quantitative RT-PCR detecting mRNA expression of Akt1 and Akt2 in the Akt1−/− and Akt2−/− mice. C and D: Western immunoblotting assessed Akt1 and Akt2 protein expression in lung tissue isolated from WT, Akt1+/−, and Akt+/− mice (C) as well as from WT, Akt1−/−, and Akt2−/− mice (D). *P < 0.05; ***P < 0.001 vs. WT. ND indicates not detectable. E and F: representative record of LV systolic pressures (LVSP, E) and systemic arterial pressures (SAP, F) with summarized data (means ± SE, left) in WT mice (n = 6), Akt1−/− mice (n = 3), and Akt2−/− mice (n = 3).