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. 2010 Oct 19;39(4):1266–1279. doi: 10.1093/nar/gkq861

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© The Author(s) 2010. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 8. — Postulated model of SET9-mediated regulation of the AR. Our working model is that SET9 enhances AR activity by methylating the receptor and histone H3-K4. Step 1: SET9 is present at androgen response elements (AREs) in the absence of active AR to mono-methylate H3-K4. Step 2: Activation of the AR via dihydrotestosterone (DHT) binding enables interaction of SET9 and the AR followed by methylation of the receptor on lysine 632 that facilitates inter-domain interaction of the N- and C-termini of the AR. Step 3: Methylated AR associates with target genes and enhances transcription.

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