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. 2016 Mar 5;7(5):338–350. doi: 10.1007/s13238-015-0241-6

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© The Author(s) 2016

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.

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IKKβ ablation leads to progressive activation of TGFβ and cell migration. The Ikkβ ^F/F fibroblasts were infected with Ad-GFP or Ad-Cre and the cells were maintained in culture for various days as indicated. The cells were examined for (A) IKKβ, α-SMA and β-actin protein, (B) mRNA for Tgfβ2 and SMAD-target genes, and (C) rate of wound healing. The Ikkβ ^F/F/Tgfbr2 ^F/F fibroblasts were infected with Ad-GFP or Ad-Cre. At 3 months after infection, the cells were examined for (D) IKKβ, α-SMA and β-actin protein and (E) rate of in vitro wound healing in the presence or absence of TGFβ1. Results represent the mean values ± SD from at least three independent experiments. *P < 0.05, **P < 0.01 and ***P < 0.001 were considered significantly different from the wild type or control samples