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. Author manuscript; available in PMC: 2010 Apr 9.
Published in final edited form as: Sci Transl Med. 2009 Oct 7;1(1):1ra1. doi: 10.1126/scitranslmed.3000071

Fig. 1.

Fig. 1

PTH-βarr stimulates β-arrestin–mediated ERK1/2 activation, independent of G protein signaling, in osteoblasts. (A) cAMP activation in response to PTH(1–34) and PTH-βarr stimulation of endogenously expressed PTH1R in POBs isolated from β-arrestin2−/− and WT C57BL/6 mice. cAMP values were normalized to 10 μM forskolin–induced concentrations (2.24 ± 0.2 μM). Data correspond to the mean ± SEM from four independent experiments. ***P < 0.001 compared with the vehicle-stimulated WT POBs. †††P < 0.001; ††P < 0.01 compared with the vehicle-stimulated β-arrestin2−/− POBs; direct comparisons were made with two-tailed unpaired t test. Veh, vehicle. (B) PTH(1–34) and PTH-βarr stimulated ERK1/2 activation in POBs isolated from β-arrestin2−/− and WT C57BL/6 mice. Values presented are the fold ERK1/2 phosphorylation over vehicle-stimulated controls. Data represent the mean ± SEM from four independent experiments. **P < 0.01 compared with the vehicle-stimulated WT POBs. ††P < 0.01 compared with the vehicle-stimulated β-arrestin2−/− POBs; direct comparisons were made with two-tailed unpaired t test.