Supplementary Materials

EGFR Signals to mTOR Through PKC and Independently of Akt in Glioma

Qi-Wen Fan, Christine Cheng, Zachary A. Knight, Daphne Haas-Kogan, David Stokoe, C. David James, Frank McCormick,4 Kevan M. Shokat, William A. Weiss

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  • Fig. S1. Inhibition or knockdown of EGFR, Akt, PI3K, and mTOR in glioma; effects of serum.
  • Fig. S2. PMA interferes with the ability of erlotinib to decrease phosphorylation of rpS6 in PTENwt glioma cells regardless of EGFR status.
  • Fig. S3. Inhibition of PTEN leads to increased abundance of p-Akt in PTENwt LN229: EGFR cells.
  • Fig. S4. Knockdown of PKCα and PKCδ in LN229:EGFR glioma cells.
  • Fig. S5. Abundance of EGFR, p-PKCα, p-PKC (pan), p-rpS6, and p-Akt in normal brain and primary human glioblastoma tumors.
  • Fig. S6. A PKC inhibitor blocks proliferation in both PTENwt and PTENmt glioma cell lines.

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1Department of Neurology, University of California, 533 Parnassus Avenue, San Francisco, CA 94143, USA. 2Department of Pediatrics, University of California, San Francisco, CA 94143, USA. 3Department of Neurological Surgery and Brain Tumor Research Center, University of California, San Francisco, CA 94143, USA. 4Comprehensive Cancer Center, University of California, San Francisco, CA 94143, USA. 5Program in Chemistry and Chemical Biology, University of California, San Francisco, CA 94158, USA. 6Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94158, USA. 7Howard Hughes Medical Institute, University of California, San Francisco, CA 94158, USA.

*To whom correspondence should be addressed. E-mail, weiss{at}cgl.ucsf.edu

Citation: Q.-W. Fan, C. Cheng, Z. A. Knight, D. Haas-Kogan, D. Stokoe, C. D. James, F. McCormick, K. M. Shokat, W. A. Weiss, EGFR Signals to mTOR Through PKC and Independently of Akt in Glioma. Sci. Signal.2, ra4 (2009).

© 2009 American Association for the Advancement of Science