Figure 5
Figure 5. Involvement of BTG1 and PRMT1 in GC-dependent target gene regulation. (A) Association of PRMT1 with the promoter regions of BTG1 and GR in response to GC exposure is dependent on BTG1 expression. Quantitative ChIP analysis of PRMT1 binding to promoter sequences of BTG1 and NR3C1 in RS4;11 control vector-transduced cells versus BTG1-shRNA 1 cells treated with either 1 mg/mL prednisolone or mock treated for 8 hours. Error bars represent the SEM of 2 independent experiments. *Statistical significance (P < .05) was assessed with the Student t test compared with mock-treated cells. (B) Luciferase reporter assays were performed using MMTV-Luc in the presence of 20 ng of exogenous GR and increasing concentrations of HA-BTG1 (3-200 ng), with or without prednisolone treatment. Luciferase activity was normalized to Renilla values. Error bars represent the SEM of 2 independent experiments. *Statistical significance (P < .05) was assessed with Student t test compared with cells without HA-BTG1 expression. (C) Schematic representation explaining how BTG1 regulates expression of the GR and that of GR-target genes.

Involvement of BTG1 and PRMT1 in GC-dependent target gene regulation. (A) Association of PRMT1 with the promoter regions of BTG1 and GR in response to GC exposure is dependent on BTG1 expression. Quantitative ChIP analysis of PRMT1 binding to promoter sequences of BTG1 and NR3C1 in RS4;11 control vector-transduced cells versus BTG1-shRNA 1 cells treated with either 1 mg/mL prednisolone or mock treated for 8 hours. Error bars represent the SEM of 2 independent experiments. *Statistical significance (P < .05) was assessed with the Student t test compared with mock-treated cells. (B) Luciferase reporter assays were performed using MMTV-Luc in the presence of 20 ng of exogenous GR and increasing concentrations of HA-BTG1 (3-200 ng), with or without prednisolone treatment. Luciferase activity was normalized to Renilla values. Error bars represent the SEM of 2 independent experiments. *Statistical significance (P < .05) was assessed with Student t test compared with cells without HA-BTG1 expression. (C) Schematic representation explaining how BTG1 regulates expression of the GR and that of GR-target genes.

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