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. 2003 Jun 1;17(11):1352–1365. doi: 10.1101/gad.1089403

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Figure 1. — (A) RT–PCR analysis of Akt1, Akt2, and Akt3 RNA expression in mouse embryo fibroblasts (MEFs) of different genotypes derived from double-heterozygous matings. Complementary DNA was amplified by PCR with primers specific for mouse Akt1, Akt2, Akt3, and GAPDH (internal control). All PCR products were of the expected size. (Lane 1) Akt1^+/+/Akt2^+/- MEF. (Lane 2) Akt1^-/-/Akt2^+/+ MEF. (Lane 3) Akt1^-/-/Akt2^-/- MEF. (Lane 4) WT MEF. (Lane 5) Akt1^+/+/Akt2^-/- MEF. (B) Immunoblot showing expression of Akt1 and Akt2 proteins in skeletal muscles of WT and mutant E18.5 embryos, using anti-Akt1 and anti-Akt2. (C) Side views of E18.5 embryos and newborn littermates. WT, wild type; DHet, Akt1^+/-/Akt2^+/-; DKO, Akt1^-/-/Akt2^-/-. (D) Newborn body weight (BW) of WT and Akt1/Akt2 mutant mice. The relative average BW (percent of mutant to WT newborns) is shown in parentheses. Results are mean ± S.E.M. *, P < 0.05; ***, P < 0.001.

Figure 1. — (A) RT–PCR analysis of Akt1, Akt2, and Akt3 RNA expression in mouse embryo fibroblasts (MEFs) of different genotypes derived from double-heterozygous matings. Complementary DNA was amplified by PCR with primers specific for mouse Akt1, Akt2, Akt3, and GAPDH (internal control). All PCR products were of the expected size. (Lane 1) Akt1^+/+/Akt2^+/- MEF. (Lane 2) Akt1^-/-/Akt2^+/+ MEF. (Lane 3) Akt1^-/-/Akt2^-/- MEF. (Lane 4) WT MEF. (Lane 5) Akt1^+/+/Akt2^-/- MEF. (B) Immunoblot showing expression of Akt1 and Akt2 proteins in skeletal muscles of WT and mutant E18.5 embryos, using anti-Akt1 and anti-Akt2. (C) Side views of E18.5 embryos and newborn littermates. WT, wild type; DHet, Akt1^+/-/Akt2^+/-; DKO, Akt1^-/-/Akt2^-/-. (D) Newborn body weight (BW) of WT and Akt1/Akt2 mutant mice. The relative average BW (percent of mutant to WT newborns) is shown in parentheses. Results are mean ± S.E.M. *, P < 0.05; ***, P < 0.001.