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. 2021 Jan 8;296:100261. doi: 10.1016/j.jbc.2021.100261

Figure 2.

Figure 2

10C7 potentiates GPR56 activation of RhoA-mediated SRF signaling independent of receptor cleavage, but requires the STP domain.A, transient overexpression of GPR56 WT, ΔSTP, and T383A in 293T cells significantly enhances SRF-RE activity, which is blocked by pretreatment with Rho inhibitor I (2 μg/ml) for 3 h. Statistical significance determined by ANOVA, ∗∗∗∗p < 0.0001. Error bars, S.D. B, 10C7 induces a dose-dependent potentiation of SRF-RE in WT, T383A, and ΔPLL transfected cells. Error bars, S.E. C, western blot of GPR56 WT, T383A, and ΔPLL overexpression. D, 10C7 does not potentiate in ΔSTP transfected cells. Error bars, S.E. E, western blot of GPR56 WT and ΔSTP overexpression. F, effects of Rho inhibitor I and Src inhibitor (saracatinib) on 10C7 potentiation of GPR56-meditated SRF signaling. Error bars, S.E. All data represent at least three independent experiments.