Supplementary Materials

Supplementary Materials for:

The Precise Sequence of FGF Receptor Autophosphorylation Is Kinetically Driven and Is Disrupted by Oncogenic Mutations

Erin D. Lew, Cristina M. Furdui, Karen S. Anderson, Joseph Schlessinger*

*To whom correspondence should be addressed. E-mail: joseph.schlessinger{at}yale.edu

This PDF file includes:

  • Fig. S1. Identification of tyrosine phosphorylation sites on kinase-dead mutants with ESI-MS and MS/MS.
  • Fig. S2. Identification of tyrosine phosphorylation sites of N546K glioblastoma with ESI-MS and MS/MS.
  • Fig. S3. Determination of Km for FGFR1-mediated substrate phosphorylation.
  • Fig. S4. 3T3 cells stably expressing wild-type or mutant FGFR1.
  • Table S1. Comparison of autophosphorylation kinetics of FGFR1 kinase (WT) and FGFR1 kinase mutant implicated in glioblastoma, N546K.

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Citation: E. D. Lew, C. M. Furdui, K. S. Anderson, J. Schlessinger, The precise sequence of FGF receptor autophosphorylation is kinetically driven and is disrupted by oncogenic mutations. Sci. Signal.2, ra6 (2009).

© 2009 American Association for the Advancement of Science