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. 2016 Sep 22;7(9):e2376. doi: 10.1038/cddis.2016.195

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Copyright © 2016 The Author(s)

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Compound 12 inhibits Hh signaling without affecting AP1/Jun and WNT/β-Catenin pathways. (a) The graphs show the Hh target genes expression levels in Ptch1^−/− MEFs treated for 48 h with 12 or DMSO as control. mRNA levels were determined by quantitative real-time PCR (qRT-PCR) normalized to endogenous control (β2-microglobulin and HPRT). Pfkfb3 gene was used as negative control. *P<0.05 versus CTR. (b and c) AP1/Jun and WNT/β-Catenin pathways activity were assayed in MEFs WT transfected with MMP1-luciferase reporter and c-Jun (b) or Top Flash-luciferase reporter and β-Catenin (c), respectively, in the presence or absence of increasing concentrations of compound 12. Treatment time was 24 h, and normalization was against Renilla luciferase. Data show the mean±S.D. of three independent experiments