Increased glucose tolerance and reduced adiposity in the absence of fasting hypoglycemia in mice with liver-specific G_sα deficiency
J. Clin. Invest. Min Chen, et al. 115:3217 doi:10.1172/JCI24196 [Go to this article.]

Figure 1
Generation of LGsKO mice. (A) The upstream portion of the wild-type Gnas allele (E1⁺) including alternative first exon 1A and G_sα exons 1, 2, and 3 is shown at the top, with the positions of the 5′ and 3′ probes used for Southern blot analysis shown above. The scale is in kilobases, with position 0 being the G_sα translational start site. The E1^neo-fl allele is shown below E1⁺, with loxP sites represented as triangles. E1^neo-fl mice were mated with EIIa-cre mice to generate mice with the E1^fl allele. Repeated mating of E1^fl and Alb-cre–transgenic mice produced LGsKO (E1^fl/flAlb-cre⁺) mice with liver-specific deletion of G_sα exon 1 (E1^–) in both alleles. S, SacI; Bg, BglII; Neo, neomycin resistance gene. (B) Southern blot analysis of founder mice (2 left lanes) or offspring of E1^neo-fl mice crossed with EIIa-cre mice (2 right lanes) after SacI digestion and hybridization with the 5′ probe. Genotypes are indicated above each lane. (C) Immunoblot analysis of protein extracts (60 μg/lane) of various tissues from E1^+/+, E1^fl/fl, and LGsKO mice, using a G_sα-specific antibody. The doublet represents the long and short forms of G_sα produced by alternative splicing of exon 3. (D) Immunoblot of liver (left) and kidney (right) extracts from control (C) and LGsKO mice (L) with anti–phospho-CREB (CREB-P; top row) and anti-CREB Abs (bottom row). Pairs are indicated by the lines above.