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. 2008 Apr 3;36(9):2969–2980. doi: 10.1093/nar/gkn132

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© 2008 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 5. — TAp63γ mutants related to SHFM, EEC and ADULT human developmental syndromes show a functional difference in regulating S100A2 transcription. TAp63γ mutants originating from patients with developmental syndromes SHFM, EEC or ADULT differentially activate the S100A2 long reporter. Transfections and analyses were done as described above.