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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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Upregulation of splice correction activity in 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 activating ligands [Pifithrin-μ (selective inhibitor of heat shock protein 70 (HSP70)), Alprenolol hydrochloride (β-adrenoceptor antagonist), CH-223191 (aryl hydrocarbon receptor (AHR) antagonist), Importazole (nuclear transport receptor importin-β inhibitor), TLR-4-IN-C34 (TLR4 inhibitor), MHY1485 (mTOR activator)]. 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 PF14/SCO complexes treatment (P < 0.0001).