Figure 2
Figure 2. EPCR occupancy induces β-arrestin-2 dependent translocation of Dvl-2 to the plasma membrane independent of β-catenin. (A-D) Western blot analysis of cytoplasmic and membrane fractions of Dvl-2 in cell lysates using an anti-Dvl-2 antibody. EA.hy926 cells were treated with 20 nM APC (A), 2 nM thrombin + 50 nM PC-S195A (B), 2 nM thrombin alone (C), or 50 nM PC-S195A alone (D) for different times, and cell lysates were fractionated and analyzed by anti-Dvl-2 as described in “Materials and methods.” In all panels, the protein level of actin was monitored by an anti-actin antibody as a control for the total and cytosolic fraction of Dvl-2, whereas the β-catenin level was monitored as a control for the membrane fraction of Dvl-2.

EPCR occupancy induces β-arrestin-2 dependent translocation of Dvl-2 to the plasma membrane independent of β-catenin. (A-D) Western blot analysis of cytoplasmic and membrane fractions of Dvl-2 in cell lysates using an anti-Dvl-2 antibody. EA.hy926 cells were treated with 20 nM APC (A), 2 nM thrombin + 50 nM PC-S195A (B), 2 nM thrombin alone (C), or 50 nM PC-S195A alone (D) for different times, and cell lysates were fractionated and analyzed by anti-Dvl-2 as described in “Materials and methods.” In all panels, the protein level of actin was monitored by an anti-actin antibody as a control for the total and cytosolic fraction of Dvl-2, whereas the β-catenin level was monitored as a control for the membrane fraction of Dvl-2.

Close Modal

or Create an Account

Close Modal
Close Modal