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. 2009 May 22;37(13):4393–4406. doi: 10.1093/nar/gkp398

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© 2009 The Author(s)

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 7. — A schematic representation of proposed model for RFXB variants mediated antagonism between IFN-γ and TGF-β in collagen type I transcription. IFN-γ stimulates the production of RFXB, which interacts with RFX5 and recruits HDAC2 to the COL1A2 start site (in a specialized sub-nuclear ‘zone’) to repress transcription. Meanwhile, IFN-γ down-regulates the levels of RFXBSV, which does not interact with RFX5 and fails to bind to the COL1A2 start site, thus squelching HDAC2 away and alleviating the repression. TGF-β antagonizes IFN-γ induced COL1A2 repression by reshuffling the balance between RFXB and RFXBSV through differential regulation of their expression. In a separate ‘zone’ where SM22α gene is located, HDAC2 binds to the promoter more strongly and is immune from the squelching by RFXBSV.