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)
Technical Details
Format: Adobe Acrobat PDF
Size: 2.2 MB
Other Supplementary Material for this manuscript includes the following:
- Table S1 (Microsoft Excel format). Model reactions and parameter values.
- Computational Model Files
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).
