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

Figure 5. Gain of CCAAT enhancer binding protein beta (C/EBP-β) expression in renal epithelium cells upregulated the expression of microRNA(miR)-16 processing.

Figure 5

(A) Alignment of the C/EBP-β binding site on the promoter region of the miR-16 genome. Vertical arrow indicated C/EBP-β binding site. (B) The mRNA expression level of C/EBP-β and miR-16 in 293T cells, after hypoxia/reoxygenization (H/R). (C) Increased expression of miR-16 accompanied with decreased B cell lymphoma 2 (BCL-2) levels in 293T cells transfected with C/EBP-β following H/R by real time polymerase chain reaction (qPCR). (D) Chromatin derived from K562-C/EBP-p42-ER cells was immunoprecipitated with anti-C/EBPβ and IgG antibodies. Recovered DNA was polymerase chain reaction amplified with primers specific for C/EBPβ-binding and the internal control. (E) Schematic description of the wild-type miR-16b conserved regulatory element construct containing C/EBP-β binding sites and construct with the deletion sequences, which were designated as CNS-Luc and mCNS-Luc, respectively. Luciferase activity of the wild-type (CNS-Luc) or different deletion (CNS-Luc) reporter gene in HEK 293T cells transfected with empty vector pcDNA3.1 or expression vector pcDNA3-LAP2. Data were analyzed using Student’s t-test (P < 0.05).