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. 2015 Sep 11;10(9):e0137432. doi: 10.1371/journal.pone.0137432

Fig 9. Luciferase reporter assays confirmed dme-miR-137 could inhibit the targets in neuroactive-ligand receptor interaction pathway.

Fig 9

(A) 3′UTRs of Nmdar2, D2R and GABA-B-R3 containing dme-miR-137-3p binding sites predicted by DIANA—microT (shown in square) were cloned into pGL3-promoter vectors. Arrows indicated the location of primers used for amplification. (B) The pGL3-promoter vector carrying Nmdar2, D2R and GABA-B-R3 3’UTR fragments flanking miR-137 targeting sites were co-transfected with Renilla plasmid pRL-TK as well as dme-miR-137-3p mimics into HEK 293 cells. The results showed that dme-miR-137-3p could inhibit the luciferase activities for all these vectors does dependently as compared with miR-negative control. (C) The inhibitory effects were abolished when all the miR-137 targeting sites within the amplified sequences in D2R 3’UTR were mutated. (* p<0.05, ** p<0.01).