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. 2016 Jun 14;6:27945. doi: 10.1038/srep27945

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(A) Sequence alignment showing the relative position of the miR-16 binding site in the 3′UTR of BCL-2. (B) Expression of miR-16 decreased luciferase reporter gene activity in NRK-52 cells when linked to the targeted segment of the 3′UTR of BCL-2 and abolished miR-16 mediated decrease of luciferase activity after coinfected with antisense-miR16. (C) Time course of miRNA expression level of miR-16 in 293T cells after hypoxia/reoxygenization (H/R). (D) Time course of mRNA (reoxgenation period from 0 to 24 hrs) and protein level (reoxygenation period only 4 and 24 hrs) of BCL2 in 293T cells after hypoxia/reoxygenation (E) Real time polymerase chain reaction (qPCR) and protein expression levels detected marked induction of miR-16 which dramatically decreased BCL-2 levels in 293T cells after H/R (24 hrs/2 or 4 hrs) and abolished miR16-inhibited reaction by transfecting with antisense-miR16.