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Reelin Glycoprotein pp 89–105Cite as

Reelin/Dab1 Signaling in the Developing Cerebral Cortex

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Abstract

Mice lacking the cytoplasmic adapter protein Dab1 (Disabled homolog-1) display histological defects in the central nervous system (CNS) that are essentially indistinguishable from those observed in the reeler mouse. Dab1 is expressed in virtually all Reelin-responsive cells and is rapidly phosphorylated in response to Reelin application. The finding of a near identity in phenotype, coupled with a direct biochemical response to Reelin, has raised great interest in understanding Dab1 function, both as an exemplar of an adapter protein with a profound phenotypic contribution, and as a means of decoding mechanisms of Reelin signaling. What has emerged from these studies is a surprisingly complex picture of Dab1 at the genomic, mRNA, protein, and functional levels. This chapter will summarize some of the key features of Dab1, and its role as a transducer of the Reelin signal in the developing cerebral cortex.

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Authors and Affiliations

  1. Department of Neuroscience and Physiology, SUNY Upstate Medical University, 750 E. Adams Street, Syracuse, NY, 13035

    Eric C. Olson

  2. Howard Hughes Medical Institute, BIDMC, Division of Genetics, Boston Children’s Hospital, Harvard Medical School, NRB 266, 77 Avenue Louis Pasteur, Boston, MA, 02115

    Christopher A. Walsh

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  1. Eric C. Olson
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Editors and Affiliations

  1. Medical School, University of Minnesota, Minneapolis, MN, USA

    S. Hossein Fatemi M.D., Ph.D. (Professor of Psychiatry, Adjunct Professor of Pharmacology and Neuroscience) (Professor of Psychiatry, Adjunct Professor of Pharmacology and Neuroscience)

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Olson, E.C., Walsh, C.A. (2008). Reelin/Dab1 Signaling in the Developing Cerebral Cortex. In: Fatemi, S.H. (eds) Reelin Glycoprotein. Springer, New York, NY. https://doi.org/10.1007/978-0-387-76761-1_7

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