The Specificity of Innate Immune Responses Is Enforced by Repression of Interferon Response Elements by NF-κB p50

Christine S. Cheng, Kristyn E. Feldman, James Lee, Shilpi Verma, De-Bin Huang, Kim Huynh, Mikyoung Chang, Julia V. Ponomarenko, Shao-Cong Sun, Chris A. Benedict, Gourisankar Ghosh, Alexander Hoffmann*

*To whom correspondence should be addressed. E-mail: ahoffmann{at}ucsd.edu

This PDF file includes:

• Fig. S1. Expression profiling of IFN-β responses reveals the enhanced expression of some genes at early time points.
• Fig. S2. The gene expression phenotype observed in p50KO cells depends on the absence of p50 and not the absence of p105.
• Fig. S3. The DNA binding activities of transcriptional activators and the p50-p50 repressor in response to LPS.
• Fig. S4. STAT2 is recruited to IRE sequences irrespective of whether they are G-rich.
• Fig. S5. Increased expression of p50 protein reduced IRF-mediated activation of G-rich IRE–driven reporter gene, but not non–G-rich IRE–driven reporter gene.
• Fig. S6. G-rich IREs are more likely than non–G-rich IREs to exhibit enhanced basal expression in p50-deficient BMDMs.
• Fig. S7. IRF3 is not activated in response to CpG in either WT or p50KO BMDMs.
• Fig. S8. Assays of infection of cells by MCMV-GFP reveal IFN-β–mediated antiviral responses.
• Table S1. IFN response genes.
• Table S2. List of EMSA probes.
• Table S3. List of the primers used for ChIP assays.
• Table S4. List of the primers used for RT-qPCR assays.
  

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© 2011 American Association for the Advancement of Science