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. 2011 Oct 3;286(47):40464–40476. doi: 10.1074/jbc.M111.232009

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© 2011 by The American Society for Biochemistry and Molecular Biology, Inc.

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FIGURE 4. — Characterization of HA-GAT-1-mediated GABA transport. A, schematic representation of the localization of the HA tag, which was placed in EL2 of rat GAT-1; predicted N-glycosylation sites in the EL2 are indicated. B and C, saturation kinetics of GAT-1-mediated GABA uptake in HEK293 cells stably expressing HA-GAT-1 (B) or rGAT-1 (C). The K_m and V_max values are shown as an inset in the corresponding graph. D, [³H]GABA uptake through GAT-1 in HA-GAT-1-transduced (filled bars) and non-transduced (open bars) astrocytes. E, BDNF effects on GABA uptake in HA-rGAT-1-transduced (filled bars) and non-transduced (open bars) astrocytes from the same cell batch. The ordinates represent the [³H]GABA uptake as a percentage of the control value (no BDNF added) in the same experiment and in the same cell batch in similar conditions. In all panels, the results are expressed as mean ± S.E. (error bars) from three (B), two (C and D), or five (E) independent experiments. *, p < 0.05 (one-way ANOVA followed by Bonferroni's post-test) as compared with control (no drug added, first column on the left) in the same group of cells.