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. 2019 Apr 12;20(6):e47227. doi: 10.15252/embr.201847227

Figure 2. cTAZ directly represses JAK‐STAT signaling.

Figure 2

  1. Cluster analysis of RNA expression of WT, cTAZ−/−, and cTAZ−/−/GFP‐cTAZ put‐back RKO cells. Genes down‐ and up‐regulated more than twofold (P < 0.05) in cTAZ KO cells were included in cluster analysis. Green and red indicate down‐ and up‐regulated genes, respectively.
  2. Gene ontology (GO) analysis identified differentially regulated pathway by cTAZ.
  3. cTAZ suppressed expression of ISGs. RNA levels of selected ISGs in WT, cTAZ−/−, and cTAZ−/−/GFP‐cTAZ RKO cells were quantified by qPCR. Error bars indicate SD, n = 3. **P < 0.01; ***P < 0.001; Student's t‐test.
  4. cTAZ repressed 5×ISRE‐luciferase activity induced by IFN‐α. HEK293A cells were transfected with 5×ISRE‐luciferase reporter along with the indicated plasmids, treated with or without IFN‐α (50 ng/ml) for 12 h. The expression of ectopic gene was determined by IB. Error bars indicate SD, n = 3. ***P < 0.001; one‐way ANOVA test was used for statistical analysis.
  5. Knockout of cTAZ promoted ISG expression in the presence of IFN‐α. WT and cTAZ −/− RKO cells were treated with or without of IFN‐α (50 ng/ml) for indicated time, and expression of selected genes was quantified by qPCR. WT or cTAZ −/− group was normalized by basal level, respectively. Error bars indicate SD, n = 3. *P < 0.05; **P < 0.01; Student's t‐test.

Source data are available online for this figure.