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. 2015 Dec 7;11:37. doi: 10.1186/s13223-015-0104-y

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© Zhang et al. 2015

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 5 — NF-κβ and AP1 mutation abolish TNF induced PTX3 promoter activity. HASMC were transiently transfected with WT PTX3 (−1200 bp), NF-κβ or AP1 mutated reporter luciferase construct (a) and stimulated with 10 ng/ml of TNF or vehicle for 12 h. b Values are presented as the mean fold increase of luciferase activity normalized to the mock renilla luciferase activity from 3 different HASMC (**P < 0.01)