Figure 7
Figure 7. The BIM IGR functions as a dexamethasone-inducible enhancer of transcription. (A) The GR binding motif identified by GR ChIP-seq in in vivo dexamethasone-treated ALL-54 cells. (B) Two potential GREs at the BIM IGR were revealed by sequence analysis, both located within the first peak of the GR ChIP-seq signal. (C) Locations and sequences of the potential GREs, which were mutated as shown (mutated residues are underlined). (D) The effects of single or dual GRE mutations on dexamethasone-induced reporter gene activity in Nalm6 cells. Reporter plasmid with firefly luciferase and control plasmid with renilla luciferase were cotransfected into Nalm6 cells. Firefly luminescence was determined after 16-hour treatment of dexamethasone and normalized to the renilla luminescence signal. The fold inductions were then calculated by normalizing to pGL2P control. N = 5; *P < .05.

The BIM IGR functions as a dexamethasone-inducible enhancer of transcription. (A) The GR binding motif identified by GR ChIP-seq in in vivo dexamethasone-treated ALL-54 cells. (B) Two potential GREs at the BIM IGR were revealed by sequence analysis, both located within the first peak of the GR ChIP-seq signal. (C) Locations and sequences of the potential GREs, which were mutated as shown (mutated residues are underlined). (D) The effects of single or dual GRE mutations on dexamethasone-induced reporter gene activity in Nalm6 cells. Reporter plasmid with firefly luciferase and control plasmid with renilla luciferase were cotransfected into Nalm6 cells. Firefly luminescence was determined after 16-hour treatment of dexamethasone and normalized to the renilla luminescence signal. The fold inductions were then calculated by normalizing to pGL2P control. N = 5; *P < .05.

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