Supplementary Materials

Supplementary Materials for:

The Receptor AXL Diversifies EGFR Signaling and Limits the Response to EGFR-Targeted Inhibitors in Triple-Negative Breast Cancer Cells

Aaron S. Meyer, Miles A. Miller, Frank B. Gertler, Douglas A. Lauffenburger*

*Corresponding author. E-mail: lauffen@mit.edu

This PDF file includes:

  • Fig. S1. Support vector classification to identify mechanisms of drug resistance.
  • Fig. S2. Single-cell EGFR and AXL expression with R428 treatment.
  • Fig. S3. RTK crosstalk occurs in TNBC cells.
  • Fig. S4. Receptor activation is similar in AXL knockdown cells.
  • Fig. S5. AXL signaling is required for EGF-elicited protrusion.
  • Fig. S6. A multivariate chemical cross-linking approach to study receptor colocalization.
  • Fig. S7. Cross-linking can predict receptor transactivation pairs.
  • Table S1. RTK genes significantly associated with both erlotinib and lapatinib resistance.
  • Table S2. Single phosphosite or condition analysis provides an incomplete perspective of the signaling effects upon AXL knockdown.
  • Table S3. Relative model goodness of fits based on the Akaike information criterion.

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Citation: A. S. Meyer, M. A. Miller, F. B. Gertler, D. A. Lauffenburger, The Receptor AXL Diversifies EGFR Signaling and Limits the Response to EGFR-Targeted Inhibitors in Triple-Negative Breast Cancer Cells. Sci. Signal. 6, ra66 (2013).

© 2013 American Association for the Advancement of Science