Supplementary Materials

Supplementary Materials for:

Distinct single-cell signaling characteristics are conferred by the MyD88 and TRIF pathways during TLR4 activation

Zhang Cheng, Brooks Taylor, Diana R. Ourthiague, Alexander Hoffmann*

*Corresponding author. E-mail: ahoffmann{at}ucla.edu

This PDF file includes:

  • Supplementary Text
  • Fig. S1. Fitting the model to biochemical measurements of BMDMs.
  • Fig. S2. Full schematic diagram of the TLR4–NF-κB model reaction network.
  • Fig. S3. Feed-forward loops from secreted TNF and IL-1 do not affect the dynamics of NF-κB signaling in response to LPS.
  • Fig. S4. Full range of the measured, single-cell NF-κB responses from live-cell imaging experiments.
  • Fig. S5. The model of Myddosome formation can be approached by Hill kinetics.
  • Fig. S6. Assay of the LPS concentration–dependent stimulation of the kinase activity of IKK.
  • Fig. S7. Robustness of the primary shuttling mode to parameter perturbation.
  • Fig. S8. Fitting and modeling of the endosomal maturation–induced degradation of TLR4 complexes.
  • Fig. S9. Endosomal maturation does not appear to be controlled by paracrine IFN signaling.
  • Fig. S10. RelA abundance is unrelated to the dynamics of NF-κB signaling.
  • Fig. S11. Predictions of the dynamics of NF-κB signaling based on varied degradation rates and protein abundances.
  • Fig. S12. Fitting extrinsic variability to aspects of NF-κB dynamics.
  • References (61–74)

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Citation: Z. Cheng, B. Taylor, D. R. Ourthiague, A. Hoffmann, Distinct single-cell signaling characteristics are conferred by the MyD88 and TRIF pathways during TLR4 activation. Sci. Signal. 8, ra69 (2015).

© 2015 American Association for the Advancement of Science