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Fig. 7 | Epigenetics & Chromatin

Fig. 7

From: CREBBP/EP300 bromodomains are critical to sustain the GATA1/MYC regulatory axis in proliferation

Fig. 7

Effects of three different CREBBP/EP300 inhibitors in K562. a Heat map showing the changes in gene expression of MYC, GATA1 and CCND1 at different time points during the treatment of K562 cells with 2 μM of three different CREBBP/EP300 inhibitors. Fold change to d0 is represented. b Changes in cell cycle distribution of K562 cells treated with 2 μM of the indicated CREBBP/EP300 inhibitors for 72 h. Significant differences in G0/G1 at p value ≤ 0.05 were found for all compounds compared to vehicle. c Western blot showing the levels of PARP and Caspase3 in K562 cells treated with 2 μM of the indicated CREBBP/EP300 inhibitors and for the indicated time points. d Proposed model for CBP30 action. CREBBP/EP300 is recruited to chromatin by transcription factors like GATA1 or MYC that recognize binding sites in the DNA (TFBS). Properly recruited CREBBP/EP300 is able to acetylate histones. CBP30 is able to displace CREBBP/EP300 from chromatin, and therefore, acetylation of histones is reduced, which might be resulting in reduced recruitment of bromodomain-containing proteins that transduce the acetylation signal. Our model predicts that both interaction with the transcription factor and binding of the bromodomain to acetylated histones is required for proper stabilization of CREBBP/EP300 in the chromatin and acetylation of histone tails

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