IMR Press / FBL / Volume 8 / Issue 4 / DOI: 10.2741/1014

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Cellular signalling mechanisms of neural cell adhesion molecules
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1 Department of Biochemistry Biophysics, 505 Mary Ellen Jones Bldg, CB#7260, University of North Carolina School of Medicine, Chapel Hill, NC 27599-7260, USA

Academic Editor: Michael Hortsch

Front. Biosci. (Landmark Ed) 2003, 8(4), 900–911; https://doi.org/10.2741/1014
Published: 1 May 2003
(This article belongs to the Special Issue Neural cell adhesion molecules)
Abstract

Neural cell adhesion molecules of the immunoglobulin superfamily are multidomain proteins involved in important cellular events pertinent to development and adult neurological function. This review attempts to give a concise overview of the complex intracellular signaling pathways enabling neural cell adhesion molecules NCAM and L1 to regulate axon growth, guidance, and synaptic plasticity. Recent research findings suggest that these molecules signal in part through integrins leading to cytoskeletal rearrangements locally in the growth cone or cell leading edge, and to MAP kinase, which has the potential to cause gene expression changes in the nucleus. Abnormal expression of NCAM on human chromosome 11q23 has been linked to schizophrenia in humans, a multigenic disease believed to be of neurodevelopmental origin. L1 at Xq28 is the target for mutation in a complex mental retardation disorder termed the L1 syndrome (also sometimes referred to as CRASH syndrome). Thus a full understanding of the mechanism of NCAM and L1 function will contribute to understanding both normal brain development and pathologies associated with cognitive dysfunction in schizophrenia and mental retardation.

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