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. Author manuscript; available in PMC: 2015 Jul 3.
Published in final edited form as: Leukemia. 2014 Aug 5;29(3):535–547. doi: 10.1038/leu.2014.231

Figure 3.

Figure 3

NF-κB (p65) binds to the miR-155 promoter and constitutively active STAT5 enhances transcriptional induction. (a) Scheme showing putative binding sites for NF-κB (p65) and STAT proteins in the miR-155 promoter. (b) Chromatin derived from MV4;11 cells was immunoprecipitated with anti-p65 or immunoglobulin G antibodies. Recovered DNA was PCR amplified with specific primers for p65 binding sites. (c) MV4;11 cells were treated for 24 h with the tyrosin kinase inhibitor CEP701 or control (dimethyl sulfoxide (DMSO)). Chromatin was immunoprecipitated with anti-p65 or immunglobulin G antibodies and DNA was amplified by PCR as described (b). (d) P65 and STAT5 show synergistic effects in miR-155 promoter activation. Luciferase activity assays were performed in 293 T cells. Cells were co-transfected with miR-155 promoter construct (pGL3-1783) or control (pGL3) and empty vector, p65, STAT5 and constitutively active STAT5. After 24 h Renilla luciferase activity was measured. Bars represent the average of three independent experiments ±s.d. All values were normalized to firefly luciferase and calculated to pGL3 (*P ≤ 0.05).