EGFR Signals to mTOR Through PKC and Independently of Akt in
Glioma
Qi-Wen Fan,1,2,3,4 Christine Cheng,1,2,3,4 Zachary A. Knight,5,6,7
Daphne Haas-Kogan,3,4 David Stokoe,3,4 C. David James,3,4 Frank McCormick,4
Kevan M. Shokat,5,6,7 William A. Weiss1,2,3,4,5*
This PDF file includes:
- 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
