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. 2018 Dec;28(12):1799–1811. doi: 10.1101/gr.233486.117

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© 2018 Kim et al.; Published by Cold Spring Harbor Laboratory Press

This article, published in Genome Research, is available under a Creative Commons License (Attribution 4.0 International), as described at http://creativecommons.org/licenses/by/4.0/.

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Figure 6. — Effect of selective inhibition of TNFSF10 by eRNA knockdown on virus-induced apoptosis. (A) Simplified representation of the TNFSF10 regulatory network. (B) Relative expression of TNFSF10 in eRNA knockdowns (#5, #30, and #38, triple eRNA KD) and control cells. Triple KD of eRNAs regulating the TNFSF10 results in loss of TNFSF10 expression. (C) Western blot using cleaved caspase 3 antibody to assess apoptosis. Stronger signal of cleaved caspase 3 indicates higher fraction of apoptotic cells. As an internal standard, beta actin was used. For an uncropped image of these blots, please see Supplemental Figure S8. (D) Cell viability by live cell counts (left panel) and apoptotic cell counts (right panel) for TNFSF10 eRNA KD and control cells are shown. (E) Regulation of apoptosis by TIC10- or virus-induced TNFSF10 expression. Possible mechanism through eRNA or direct gene activation is shown in the left panel. Cell viability by live cell counts (middle panel) for TIC10-treated cell, control cell, and apoptotic cell counts (right panel) for eRNA KD (triple KD) and control KD upon TIC10 treatment for 48 h. (F) TNFSF10 and its three eRNAs expression fold changes with or without TIC 10 treatment for 48 h (left panel), and with SeV or TIC10 treatment for 9 h (right panel).