Reduced protein–protein interactions between BK and NMDAR containing disease-linked GluN2B subunits revealed by PLA. (A) Representative confocal microscopy images of PLA experiments in HEK293T cells co-expressing BK with NMDAR, including the GluN2B variants indicated on the left. Each column corresponds to an imaging channel (left, DAPI, 405 nm; middle, NMDAR-GFP, 488 nm; right, PLA, 540 nm); merged channels are shown at the far-right column. Scale bar is 20 μm. (B) Quantification of PLA signals normalized to cell area (µm2) for HEK293T cells non-transfected (NT) or transiently expressing the protein combinations indicated in the axis. Data points represent individual cells; horizontal bars correspond to mean values. n = 35–45 cell counts per experiment; four independent experiments. ****P < 0.0001 (Kruskal–Wallis/Dunn’s test).
Figure 7.

Reduced protein–protein interactions between BK and NMDAR containing disease-linked GluN2B subunits revealed by PLA. (A) Representative confocal microscopy images of PLA experiments in HEK293T cells co-expressing BK with NMDAR, including the GluN2B variants indicated on the left. Each column corresponds to an imaging channel (left, DAPI, 405 nm; middle, NMDAR-GFP, 488 nm; right, PLA, 540 nm); merged channels are shown at the far-right column. Scale bar is 20 μm. (B) Quantification of PLA signals normalized to cell area (µm2) for HEK293T cells non-transfected (NT) or transiently expressing the protein combinations indicated in the axis. Data points represent individual cells; horizontal bars correspond to mean values. n = 35–45 cell counts per experiment; four independent experiments. ****P < 0.0001 (Kruskal–Wallis/Dunn’s test).

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