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Linking L1CAM-mediated signaling to NF-κB activation.

Abstract
The cell adhesion molecule L1 (L1CAM) was originally identified as a neural adhesion molecule essential for neurite outgrowth and axon guidance. Many studies have now shown that L1CAM is overexpressed in human carcinomas and associated with poor prognosis. So far, L1CAM-mediated cellular signaling has been largely attributed to an association with growth factor receptors, referred to as L1CAM-'assisted' signaling. New data demonstrate that L1CAM can signal via two additional mechanisms: 'forward' signaling via regulated intramembrane proteolysis and 'reverse' signaling via the activation of the transcription factor nuclear factor (NF)-κB. Taken together, these findings lead to a new understanding of L1CAM downstream signaling that is fundamental for the development of anti-L1CAM antibody-mediated therapeutics in human tumor cells.
AuthorsHelena Kiefel, Marco Pfeifer, Sandra Bondong, John Hazin, Peter Altevogt
JournalTrends in molecular medicine (Trends Mol Med) Vol. 17 Issue 4 Pg. 178-87 (Apr 2011) ISSN: 1471-499X [Electronic] England
PMID21195665 (Publication Type: Journal Article, Review)
CopyrightCopyright © 2010 Elsevier Ltd. All rights reserved.
Chemical References
  • Interleukin-1beta
  • NF-kappa B
  • Neural Cell Adhesion Molecule L1
  • Transcription Factors
  • Receptor Protein-Tyrosine Kinases
Topics
  • Animals
  • Cell Adhesion
  • Cell Line, Tumor
  • Cell Nucleus (metabolism)
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Interleukin-1beta (metabolism)
  • MAP Kinase Signaling System
  • NF-kappa B (genetics, metabolism)
  • Neural Cell Adhesion Molecule L1 (genetics, metabolism)
  • Receptor Protein-Tyrosine Kinases (genetics, metabolism)
  • Signal Transduction
  • Transcription Factors (genetics, metabolism)

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