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. 2017 Oct 3;7:12635. doi: 10.1038/s41598-017-12747-z

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© The Author(s) 2017

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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Downregulation of splice correction activity in a concentration-dependent manner by using small molecule ligands. (a,b) HeLa pLuc/705 cells treated for 24 h with PF14 and splice correction oligo (PF14/SCO) nano-complexes and splice correction suppressing ligands [CCG 203971 (CTGF inhibitor), PF 573228 (focal adhesion kinase (FAK) inhibitor), Atorvastatin LDL (HMG-CoA reductase inhibitor), Prostaglandin E2]. Splice correction activity is based on luminescence signal from splice corrected luciferase. Splice correction activity was normalized to the baseline signal of untreated cells, and 100% corresponds to treatment with PF14/SCO complexes (P < 0.0001).