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. 2020 Jan 16;9:e52056. doi: 10.7554/eLife.52056

Figure 7. Gab1 binds to GSK3β and modulates its activity.

Figure 7.

(A) Precleared cortical lysates from wild-type mice (P21-23) were immunoprecipitated with mouse anti-Gab1 and anti-GSK3β antibodies. Immunoprecipitates were probed with antibodies to Gab1 (rabbit polyclonal antibody), GSK3β, Akt and GAPDH. The experiment was repeated three times. Rabbit IgG was used as the negative control. (B) The lysates of cultured OPCs and OLs were immunoprecipitated with mouse anti-Gab1 antibody. Immunoprecipitates were probed with antibodies to Gab1 (rabbit polyclonal antibody), GSK3β, PDGFRα, and GAPDH. The experiment was repeated three times. (C) The expression and phosphorylation of GSK3β, β-catenin and Akt in cerebral cortex from Gab1f/+;Olig1-cre and Gab1f/f;Olig1-cre mice at P21. GAPDH was the internal control. The increase of pGSK3β-S9 was 325 ± 16% (p=0.000077 vs control) in Gab1f/f;Olig1-cre mice. n = 3/group. t-test, df = t(5). (D) Expression and phosphorylation of GSK3β and β-catenin in myelin fractions from Gab1f/+;Olig1-cre and Gab1f/f;Olig1-cre mice at P60. GAPDH was the internal control. Percentage changes of pGSK3β-S9 and β-catenin were 216 ± 12% (p=0.00036 vs control) and 133 ± 8% (p=0.013 vs control) in Gab1f/f;Olig1-cre mice. n = 3/group. t-test, df = t(5). Gray dots indicate individual data points. *p<0.05. ***p<0.001.