Fig. 6
From: Peroxiredoxin 6 mediates Gαi protein-coupled receptor inactivation by cJun kinase
PRDX6 mediates GPCR cross-tolerance. a MycKOR expressing or wild-type HEK293 cells transiently transfected with HA-D2DR(L) were pretreated with vehicle or MJ33 (10 µM) 30 min prior to being treated for 3-5 h with vehicle or norBNI (10 µM). Cells were then treated with 5 min with vehicle or quinpirole (100 nM) and cell lysates analyzed for phospho-ERK1/2 immunoreactivity. NorBNI reduced quinpirole-stimulated ERK1/2 phosphorylation; the norBNI inhibition of quinpirole response was blocked by MJ33 pretreatment and not observed in cells only expressing HA-D2DR(L). (Two-way ANOVA; significant interaction (P < 0.05), significant effect of norBNI (P < 0.01), and significant effect of KOR or MJ33 (P < 0.05), n = 5–8; **P < 0.01 Holm–Sidak post hoc analysis of norBNI vs. vehicle pretreatment; ## P < 0.01) Holm–Sidak post hoc analysis compared to KOR + D2DR without MJ33 pretreatment.). b Representative immunoblots for a. c EC50 values were calculated from concentration-response curves for quinpirole inhibition of dopamine release 5–7 h after vehicle, norBNI (10 mg kg−1, i.p.), or MJ33 (1.25 mg kg−1 i.p.) prior to norBNI. NorBNI treatment resulted in a significant increase in quinpirole EC50, which was reduced by MJ33 pretreatment (one-way ANOVA, P < 0.0001; *P < 0.05, **P < 0.01, ****P < 0.0001, Holm–Sidak post hoc). Error bars represent mean ± SEM
