Figure 5
From: Direct interaction between GluR2 and GAPDH regulates AMPAR-mediated excitotoxicity
Activation of AMPAR induces GluR2/GAPDH co-internalization. A, Quantification of GluR2 expression at the plasma membrane with/without glutamate treatment (100 μM, 30 minutes) in HEK-293 T cells expressing GluR1/2 subunits. *Significantly different from control group (P < 0.05, n = 9 per group), t-test. B, Quantification of cell surface-associated GAPDH with/without glutamate treatment in the presence/absence of the GluR2NT1-3–2 peptide in HEK-293 T cells expressing GluR1/2 subunits. *Significantly different from control group; #, significantly different from glutamate group (P < 0.05, n = 9 per group), ANOVA followed by post-hoc SNK test. C, Quantification of cell surface-associated GAPDH in non-transfected HEK-293 T cells with/without glutamate treatment (n = 9 per group). D, Quantification of cell surface-associated GAPDH with/without glutamate treatment in HEK-293 T cells expressing GluR1/3 subunits (n = 9 per group). Quantification of plasma membrane GluR2 (E) or cell surface-associated GAPDH (F) expression at the plasma membrane with/without glutamate treatment in HEK-293 T cells expressing GluR1/2 subunits with wild type dynamin (WT) or mutant K44E dynamin (K44E). *Significantly different from the corresponding control group (P < 0.05, n = 9 per group), t-test. G, Bar graph summarizing the quantitative measurements of PI fluorescence from HEK-293 T cells expressing GluR1/2 subunits with wild type dynamin (WT) or mutant K44E dynamin (K44E) with/without glutamate treatment. ***Significantly different from control WT group (P < 0.001, n = 9 per group); ##significantly different from control K44E group (P < 0.01, n = 9 per group), t-test. All assays in this figure were performed 3 times independently.