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. 2017 Jan 27;13(3):1017–1024. doi: 10.3892/etm.2017.4091

Figure 5.

Figure 5.

(A) The predicted miR-138 binding site within the HIF-1α 3′UTR as well as its mutated version are indicated. (B) Representation of the WT- and MUT-HIF-1α vectors used in the Luciferase assay. (C) The repression of luciferase activity in a plasmid driven by the HIF-1α 3′UTR sequence was dependent on miR-138. Mutated HIF-1α 3′UTR abrogated miR-138 mediated repression of luciferase activity. **P<0.01 vs. control. PCT, probability of conserved targeting; WT, wild-type; MUT, mutant; NC, negative control; UTR, untranslated region; EPC, endothelial progenitor cells; miR-NC, scramble miR mimics; HIF-1α, hypoxia-inducible factor 1α; miR, microRNA; CMV, cytomegalovirus; hsa, Homo sapiens.