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Protein Kinases and Signaling Pathways that Are Activated by Reelin

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Reelin Glycoprotein

Defects in the cortex, hippocampus, inferior olive, and cerebellum of Reeler mutant mice were first detected many decades ago (Caviness and Rakic, 1978; Rice and Curran, 2001). Recently, a plethora of other developmental and adult phenotypes have been detected in mutant mice, including misplacement of olfactory interneurons (Hack et al., 2002), facial motor neurons (FMNs) (Ohshima et al., 2002; Rössel et al., 2005), sympathetic preganglionic neurons (SPNs) (Yip et al., 2000), and gonadotropin-releasing hormone (GnRH) neurons (Cariboni et al., 2005), reduced dendrite outgrowth in the hippocampus (Niu et al., 2004), and defective long-term potentiation (LTP) and memory (Weeber et al., 2002). In some genetic backgrounds, the Reeler mutation also causes neurodegeneration and early death, but these phenotypes are not detected in other backgrounds and are likely to be indirect (Brich et al., 2003; Goffinet, 1990).How Reelin, the Reeler gene product, creates these different phenotypes is still incompletely understood.

The purpose of this chapter is to briefly review the core components and signaling mechanism of the Reelin pathway, and then to present evidence on possible downstream components. Issues related to the first two questions, the timing and site of Reelin action and the possible changes in cell biology, are left for other chapters.

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Cooper, J.A., Allen, N.S., Feng, L. (2008). Protein Kinases and Signaling Pathways that Are Activated by Reelin. In: Fatemi, S.H. (eds) Reelin Glycoprotein. Springer, New York, NY. https://doi.org/10.1007/978-0-387-76761-1_13

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