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. 2019 Jan 22;294(14):5604–5615. doi: 10.1074/jbc.RA118.004682

Figure 4.

Figure 4.

Effect of APD treatment specifically on the removal of cell-surface D2R from the plasma membrane examined via pulse-chase labeling with a membrane-impermeable biotinylation reagent. HaloTag-D2R, a D2R construct with an N-terminal extracellular HaloTag insertion, was transiently expressed in HEK293T cells, and the membrane-impermeable HaloTag-PEG-Biotin reagent was used to specifically biotinylate and pulse-label the cell-surface pool of HaloTag-D2R. After washing off unreacted HaloTag-PEG-Biotin reagent, cells were treated with the indicated APDs (10 μm, 24 h), and then the biotinylated HaloTag D2R remaining at the surface after APD treatment was quantified by probing the intact, nonpermeabilized cells with HRP-conjugated streptavidin. The levels of biotinylated receptor that remained at the surface after aripiprazole treatment were significantly lower (n = 8, Tukey) than that observed after vehicle (p < 0.0001), haloperidol (p < 0.005), or clozapine treatment (p < 0.001).