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. 2021 May 10;4:544. doi: 10.1038/s42003-021-02054-9

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — a, b Relative ACTRT1, GLI1, and PTCH1 mRNA expression (a, b N = 6) and ARP-T1 expression (a N = 4; b N = 3) upon treatment with SAG in hTERT-RPE1 cells under proliferative (a) and differentiating (b) conditions. Actin is used as loading control for ARP-T1 expression. Numbers under the blots present the fold change expression of ARP-T1 compared to the vehicle (DMSO) treatment. c–e Relative ACTRT1 (c N = 7), GLI1 (d N = 4), PTCH1 (e N = 3) mRNA expression and ARP-T1 expression (c N = 4) upon treatment with purmorphamine (PUR) and/or vismodegib (VISMO) in differentiated hTERT-RPE1 cells. Tubulin is used as loading control for ARP-T1 expression. Numbers beneath the blots represent the fold change expression of ARP-T1 compared to the vehicle treatment. f, g Relative ACTRT1 mRNA expression upon treatment with different protein kinase inhibitors (f) or with PKC inhibitors (g) in differentiated NHEK (N = 3). h Relative ACTRT1 mRNA expression upon treatment with PKC inhibitors in differentiated HaCaT cells (N = 3). a–h Data are presented as means of the fold change compared to the value of vehicle-treated samples. Each open circle represents one independent experiment. i Schematic representation of ARP-T1 and ARP-T1 mutant (547_548insA) with predicted phosphorylation sites. j ARP-T1 and Phospho-Serine (P-Ser) PKC expression in NHEK transduced with lentiviral vectors, empty vector (V), ACTRT1 mutant (M), and ACTRT1 WT (WT), after immunoprecipitated (IP) with anti-FLAG monoclonal antibody M2-conjugated agarose.