<p>In quiescent cells, Fli1 forms a transcription repressor complex with p300 and HDAC1. HDAC1/p300 promotes deacetylation of Fli1, resulting in increased Fli1 DNA binding and a repressed chromatin state. After TGF-β stimulation, Fli1 phosphorylation by protein kinase C-δ induces disassembly of this transcription repressor complex and the acetylation of Fli1 by PCAF, leading to the loss of Fli1 DNA binding. Subsequently, the transcription activator complex consisting of Ets1 and p300 binds to the Ets binding site and activates transcription at least partially by promoting histone acetylation.</p
