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. Author manuscript; available in PMC: 2007 Nov 28.
Published in final edited form as: J Biol Chem. 2006 Apr 28;281(26):18081–18089. doi: 10.1074/jbc.M513640200

FIGURE 2. Dominant positive arrestin restores KSA-GFP mediated p38 MAPK activation.

FIGURE 2

KSA-GFP-expressing AtT-20 cells were transiently transfected with the dominant positive arrestin (R170E) and then exposed to U50,488 treatment. A, mean band intensities expressed as a percentage of basal-untreated control ± S.E. of KSA-GFP-expressing AtT-20 cells. Following 10 μM U50,488 treatment for 15 and 30 min (KSA U50 15, KSA U50 30), phospho-p38 levels were not significantly different from untreated controls. In KSA-GFP/R170E cells, 10 μM U50,488 treatment for 15 or 30 min (R170E U50 15, R170E U50 30) facilitated agonist-dependent p38 MAPK activation. n = 3, from separate transfections and experiments. *, significantly different from basal, p < 0.05, using the student’s t test. P-p38, phospho-p38 MAPK. B, representative Western blot data for phospho-p38 MAPK (P-p38) in KSA-GFP expressing A + T-20 cells.