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. 2014 May 30;16(3):R56. doi: 10.1186/bcr3667

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Copyright © 2014 Li et al.; licensee BioMed Central Ltd.

This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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E2F and histone deacetylase (HDAC) are involved in the transcriptional inhibition of ARHI by JMJD2A. (A) Specific siRNAs against E2F1 and E2F4 were efficient to knockdown E2F1 and E2F4 expression level. (B) Effects of E2Fs knockdown on JMJD2A binding to the A2 site of the ARHI promoter. Both siRNAs could inhibit the binding of JMJD2A to the ARHI promoter. (C) Effects of JMJD2A-FL, JMJD2A mutants (H188A and M867) and trichostatin A (TSA) on ARHI promoter activity. *P <0.05, **P <0.01. ARHI, Aplasia Ras homolog member I.