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. 2019 Aug 1;10:3468. doi: 10.1038/s41467-019-11429-w

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© The Author(s) 2019

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. 3 — Degradation of NS3 contributes to antiviral activity. a NS3 degraders exhibit antiviral activity against HCV in cell culture. Huh7.5 cells were infected with HCV-JFH1-ad at a multiplicity of infection (MOI) of 0.1. The infected cells were treated from 24 to 48 h post-infection with a range of small molecule concentrations. The amount of infectious virus released to the supernatants at 48 h post-infection was measured using a 50% tissue infectious dose (TCID₅₀) assay. The concentration of compound that led to a 50% reduction in viral titers (IC₅₀) was determined by nonlinear regression. Data are presented as means ± standard error of n = 4 technical replicates. One representative experiment is shown, with IC₅₀ values averaged from n ≥ 2 independent experiments. Source data are provided as a Source Data file. b Mechanistic characterization of the antiviral activity of the NS3 degraders. Huh7.5-SGR cells stably replicating the HCV JFH1 subgenomic replicon were treated with 1000 nM of the indicated small molecules for 24 h. The abundance of intracellular HCV NS3 and GAPDH was analyzed by Western blot. Source data are provided as a Source Data file. NS3 abundance was normalized to the loading control (GAPDH) and is presented as a percentage of the DMSO-treated control samples. One representative experiment is shown from n = 2 independent experiments. c Degradation of NS3 contributes to the antiviral activity of the NS3 degraders. Wildtype Huh7.5 and Huh7.5 CRBN^−/− cells were infected with HCV-Jc1 at a MOI of 0.1. The infected cells were treated from 24 to 48 h post-infection with a range of small molecule concentrations (indicated in nM). The intracellular abundance of HCV NS3, CRBN, and GAPDH was analyzed by Western blot. Source data are provided as a Source Data file. One representative experiment is shown from n > 3 independent experiments. NS3 abundance was normalized to the loading control (GAPDH) and is presented as a percentage of the DMSO-treated control samples. Values represent the means of n = 3 independent experiments