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. Author manuscript; available in PMC: 2014 May 14.
Published in final edited form as: Curr Opin Rheumatol. 2009 Nov;21(6):623–629. doi: 10.1097/BOR.0b013e32833038ce

Figure 2. Regulation of collagen gene transcription by endogenous repressors.

Figure 2

Transcription factor Friend leukemia integration-1 (Fli1) functions as a constitutive repressor of collagen gene transcription by recruiting HDAC1 to the collagen promoter, which leads to reduced levels of histone acetylation (Asano, Kapanadze, and Trojanowska, unpublished observations). Activation of collagen gene transcription requires inactivation of Fli1. Transforming growth factor β (TGF-β) inactivates Fli1 through the mechanism that involves phosphorylation of Fli1 on threonine 312 by PKC-δ, subsequent acetylation of Fli1 on lysine 380 by PCAF, and dissociation of Fli1 from the DNA [28•,29]. perixosome proliferator-activated receptor-γ (PPAR-γ) functions as an inducible repressor of collagen gene transcription. In response to agonist stimulation PPAR-γ translocates to the nucleus in which it competes with other transcriptional activators, such as Smad2/3, for the limited amount of histone acetyltransferase p300.