Increased glutamate permeability of EAAT2 anion channels cause epileptic encephalopathy

Kovermann, P. Kolobkova Y., Franzen, A., Fahlke, C.

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Figure 1 - dataset 1

Excel file: Membrane fluorescences of WT and variant EAAT2's.

Figure 1 - dataset 2

Excel file: Glykosylation ratios, protein expression, and transfection efficiencies.

Figure 2 - dataset 1

Excel file: L-glutamate uptake currents of WT and variant EAAT2's with D-gluconate currents.

Figure 3 - dataset 1 (WT) / Figure 3 - dataset 2 (G82R) / Figure 3 - dataset 3 (L85P)

Excel files: Anion currents of WT and variant EAAT2's (G82R, L85P) with internal and external Cl^-.

Figure 3 - dataset 5

Excel file: Correlations of single cell fluorescences and whole cell Cl^- currents from WT and variant EAAT2's.

Figure 4 - dataset 1

Excel file: IVs of WT and variant EAAT2's with internal L-glutamate and external Cl^- as main anions.

Figure 5 - dataset 1

Excel file: Anion currents of WT and P289R hEAAT2 with internal and external Cl^-.

Supplementary datasets

Supplementary Figure S1

Excel file: Transfection efficiencies and resulting protein expressions are provided in 'Figure 1 - dataset 2'.

Supplementary Figure S2

Excel file: Glutamate uptake currents at the reversal potential of D-gluconate.

Supplementary Figure S3

Excel file: Lists of reversal potentials with external Cl^- and internal D-gluconate or L-glutamate.