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.
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Authors | Helena Kiefel, Marco Pfeifer, Sandra Bondong, John Hazin, Peter Altevogt |
Journal | Trends in molecular medicine
(Trends Mol Med)
Vol. 17
Issue 4
Pg. 178-87
(Apr 2011)
ISSN: 1471-499X [Electronic] England |
PMID | 21195665
(Publication Type: Journal Article, Review)
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Copyright | Copyright © 2010 Elsevier Ltd. All rights reserved. |
Chemical References |
- Interleukin-1beta
- NF-kappa B
- Neural Cell Adhesion Molecule L1
- Transcription Factors
- Receptor Protein-Tyrosine Kinases
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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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