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. 2010 Jul;2(7):275–288. doi: 10.1002/emmm.201000081

Figure 1. NF-κB pathway influences cellular susceptibility to EMCV-induced cytotoxicity.

Figure 1

  1. NEMO promotes susceptibility of MEFs to EMCV-induced death. Equal amounts of total cell lysates from WT and NEMO−/− MEFs were immunoblotted with anti-NEMO and anti-Vinculin antibodies (upper panel). WT and NEMO−/− MEFs were infected with EMCV (MOI = 0.1) and viable cells were counted at 2 h intervals post-infection by Annexin V-FITC/propidium iodide staining. Experiments were conducted in triplicate and error bars represent standard errors (lower graph). Two-way ANOVA was applied for statistical analysis between treatments and time points. * and *** denote p < 0.05 and p < 0.001, respectively.
  2. NEMO promotes susceptibility of 786-O CCRCC cells to EMCV-induced death. 786-O cells transfected with NEMO-specific siRNA (siNEMO) or scrambled non-targeting siRNA (siCON) (left panel) were infected with or without EMCV (MOI = 0.1), and viable cells counted 18 h post-infection by Trypan Blue exclusion assay (right graph).
  3. Activated NF-κB pathway promotes susceptibility of 786-O CCRCC cells to EMCV-induced death. 786-O cells were treated with or without JSH-23 (10 µM) in the presence or absence of LPS (10 µg/ml) and the level of nuclear NF-κB visualized by immunoblotting (left panel). 786-O cells treated with or without JSH-23 were challenged with EMCV (MOI = 0.1) and viable cells were counted 18 h post-infection by Trypan Blue exclusion assay (right graph). C1 + C2 denote two splice isoforms of nuclear restricted pre-mRNA binding protein hnRNP. Experiments were performed in triplicate and error bars represent standard errors, independent Student's t-test was used to analyse difference between groups.