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. 2011 Apr;31(7):1409–1418. doi: 10.1128/MCB.00756-10

Fig. 3.

Fig. 3.

G-CSF restores the transcriptional potential of RA in APL cells (UF-1) with reduced sensitivity to RA. (A) RARα2 expression is induced in UF-1 cells treated for 24 h by G-CSF combined with RA or AM580 as assessed by quantitative real-time RT-PCR. (B) G-CSF enhanced RA-induced transactivation of a RARE element in UF-1 cells. (C) AM580, a selective RARα agonist, reproduced the differentiation obtained with RA alone or in combination with G-CSF in UF-1 cells. (D) ChIP analysis of PML-RARα, SMRT, and RARα recruitment at the RARα gene promoter in UF-1 cells treated for 1 h by RA and/or G-CSF. (E) ChIP analysis of histone H3 and H4 acetylation at the RARα gene promoter in UF-1 and NB4 cells treated for 1 h by RA and/or G-CSF. (F) ChIP experiments performed with NB4 and UF-1 cells treated for 1 h with RA and/or G-CSF and determining the recruitment of CBP/P300 to the RARα gene promoter. In all panels, values are the mean ± SD of duplicates performed with at least two separate experiments.