Fig. 6

STAT3 binds to NMDAR promoters and promotes the expression of NMDARs. a Overexpression of AAV-P301L decreased binding of STAT3 to the promoter regions of GluN1, GluN2A, and GluN2B genes in hippocampal CA3 extracts, as measured by chromatin immunoprecipitation assay (ChIP). Two-tailed Student’s t test, [GluN1] p = 0.002, [GluN2A] p = 0.002, [GluN2B] p = 0.041, n = 4. b Overexpression of wild-type STAT3 (WT-STAT3) ameliorated P301L-induced reduction of the transcription activity of NMDARs in HEK293 cells. Two-way analysis of variance (ANOVA) followed by the Bonferroni’ s post hoc test, [GluN1] ***p < 0.001, #p = 0.049; [GluN2A] ***p < 0.001, ##p = 0.006; [GluN2B] ***p < 0.001, ##p = 0.002; n = 4. c–h Diagrams show the predicted GAS promoter element (GASs) for STAT3 in the promoter (−2000 ± 298 bp) of GluN1 (c), GluN2B (e), and GluN2A (g). The GAS or the mutant (MUT) plasmids were co-transfected respectively with WT-STAT3 or its empty vector (Ctrl) into HEK293 cells for 24 h, and then the luciferase activity was measured (right panels, d, f, h). Two-tailed Student’s t test; d p = 0.004; f p = 0.035; h p < 0.001; n = 4. Data were presented as mean ± SEM