Fig. 3: RhoA is necessary and sufficient for receptor-mediated PANX1 activation.
From: Deacetylation as a receptor-regulated direct activation switch for pannexin channels
a, b Effect of PE on whole-cell currents in HEK293T cells transfected with α1D-AR and mPanx1(TEV) alone (a) or when co-transfected with either C3 exoenzyme or dominant-negative RhoA(T19N) (b). c Grouped data (mean ± s.e.m) show that overexpression of C3 exoenzyme or RhoA(T19N) reduced PE-evoked Panx1 current. n = 12, 9, or 5 cells per group examined over 4 independent experiments. One-way ANOVA (F2,23 = 19.94, p < 0.0001) with Bonferroni’s multiple comparisons test. d–f Whole-cell currents in α1D-AR/hPANX1(TEV)-transfected cells co-expressing the constitutively-activated RhoA constructs: RhoA(G14V) (d), RhoA(G14V/T37Y), a control that cannot couple to downstream effectors (e), or RhoA(G14V/F39A) that only couples to mDia (f). g Summary data (mean ± s.e.m) reveal that the mDia-activating RhoA(G14V/F39A) construct can recapitulate increased basal hPANX1 currents and occluded PE effects observed with RhoA(G14V). n = 6, 6, or 11 cells per group examined over 5 independent experiments. Two-way ANOVA (F2,20 = 7.776, p = 0.0032) with Bonferroni’s multiple comparisons test. PE phenylephrine.
