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. 2013 Jan 8;41(4):2255–2266. doi: 10.1093/nar/gks1454

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© The Author(s) 2013. 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/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 4. — A mutant ORE abolishes the hypoxic response. (A) The wild-type (top) and mutant (bottom) ORE used in this study. Two of the three mutations are in the consensus RBPJ binding site. (B) Activity of the mutant reporter in cells overexpressing the individual proteins that bind the ORE. The hypoxic effect is completely abolished in cells transfected with 1 µg each of the reporter alone or with overexpressed individual proteins. (C) Effect of RBPJ-VP16 on the mutant reporter. RBPJ-VP16 was tested for its ability to activate the mutant ORE under normoxia, a condition where this chimera activates the reporter (*P < 0.05).