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. 2000 Nov;20(21):8035–8046. doi: 10.1128/mcb.20.21.8035-8046.2000

FIG. 10.

FIG. 10

Effect of expressing each regulatory isoform with or without p110α on GS and GSK3 activity (a and b) GS activity. One day after infection with the indicated adenoviruses at an MOI of 20, cells were starved for 20 h. They were treated with 100 nM insulin for 30 min and then subjected to GS assay as described in Materials and Methods. Each result was converted to the activity ratio determined by dividing the activity measured with 0.25 mM glucose-6-phosphate (ligand-dependent activity) by the activity measured with 10 mM glucose-6-phosphate (total activity). Each bar represents the mean ± SD of at least four independent experiments. (a) GS activity in the absence of p110α expression (∗, P < 0.01 LacZ versus p85; ∗∗, P < 0.05 LacZ versus AS53); (b) GS activity in the presence of p110α expression (∗, P < 0.01 LacZ versus p85; ∗∗, P < 0.01 LacZ versus AS53; ∗∗∗, P < 0.01 LacZ versus p50). (c) GSK3 kinase activity. One day after infection with the indicated adenoviruses at an MOI of 20, cells were starved for 20 h, then treated with 100 nM insulin for 20 min, and immunoprecipitated with αGSK3α. The immunoprecipitates were used for a kinase assay as described in Materials and Methods. The results are expressed as percentage of the maximum value for untreated cells expressing LacZ. Each bar represents the mean ± SD of at least four independent experiments (∗, P < 0.01 LacZ versus Lacz with p110; ∗∗, P < 0.01 LacZ with p110 versus AS53 with p110; ∗∗∗, P < 0.01 LacZ with p110 versus p50 with p110).