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. 2004 Feb 19;23(5):1144–1154. doi: 10.1038/sj.emboj.7600109

Figure 7.

Figure 7

PML–RAR acts as an HDAC-dependent inhibitor of pathways regulated by wild-type PML and RAR. PML–RAR acts as a bifunctional protein: (i) it inhibits the transcription of RA target genes in the presence of physiological concentrations of ligand, thus blocking myeloid differentiation; and (ii) it inhibits p53 function (in a manner requiring wild-type PML), allowing enhanced survival of APL blasts. Both differentiation block and enhanced survival are mediated by recruitment of HDAC by the fusion protein.