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Akt demoted in glioblastoma

Academic Article
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Overview

authors

  • Vogt, Peter K.
  • Hart, J. R.

publication date

  • April 2009

journal

  • Science Signaling  Journal

abstract

  • In glioblastomas, an Akt-independent, PTEN (phosphatase and tensin homolog deleted on chromosome ten)-regulated signaling pathway links EGFR (epidermal growth factor receptor) to the phosphorylation of TOR (target of rapamycin) and of the ribosomal protein S6 and to the control of cell replication. Although PKCalpha (protein kinase Calpha) has been identified as an essential component, the detailed wiring of this previously unexplored noncanonical pathway remains to be worked out.

subject areas

  • Cell Line, Tumor
  • Cell Proliferation
  • Erlotinib Hydrochloride
  • Glioblastoma
  • Humans
  • Indoles
  • Maleimides
  • Models, Biological
  • PTEN Phosphohydrolase
  • Phosphorylation
  • Protein Kinase C-alpha
  • Protein Kinase Inhibitors
  • Protein Kinases
  • Proto-Oncogene Proteins c-akt
  • Quinazolines
  • Receptor, Epidermal Growth Factor
  • Ribosomal Protein S6
  • Signal Transduction
  • TOR Serine-Threonine Kinases
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Identity

International Standard Serial Number (ISSN)

  • 1937-9145

Digital Object Identifier (DOI)

  • 10.1126/scisignal.267pe26

PubMed ID

  • 19383977
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Additional Document Info

start page

  • pe26

volume

  • 2

issue

  • 67

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