Titlebook: Reelin Glycoprotein; Structure, Biology a S. Hossein Fatemi (Professor of Psychiatry, Adjunc Book 2008 Springer-Verlag New York 2008 Alzhei

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The C-Terminal Region of Reelin: Structure and Function,sequence (D’Arcangelo ., 1995): the N-terminal F-spondin-like domain, the eight tandem of Reelin repeat, and the short and highly basic C-terminal region (CTR). The N-terminal F-spondin-like domain is proposed to be necessary and sufficient for multimerization of Reelin (Utsunomiya-Tate ., 2000). Th

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Crystal Structure of Reelin Repeats, region, another region containing at least eight “reelin repeats,” and a C-terminal basic peptide of ∼30 residues (Fig. 5.1A). Each complete reelin repeat contains a central EGF module flanked by two subrepeats of 150–190 amino acids (Fig. 5.1A, inset). The central EGF module is relatively short in

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Comparative Anatomy and Evolutionary Roles of Reelin,ncipally due to the presence of some very large introns. It is composed of 65 exons, 51 of which encode the eight reelin repeats. At the 3′-terminal portion of the gene, alternative splicing involves the inclusion of a hexanucleotide AGTAAG encoding amino acids Val-Ser, which create a potential phos

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Reelin/Dab1 Signaling in the Developing Cerebral Cortex,tially indistinguishable from those observed in the . 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

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Ultrastructural Localization of Reelin,nd final protein forms. It is not, therefore, our intention to provide an extensive background about the features of the reelin gene and protein, but to emphasize some relevant features that will be helpful for a better understanding of the data reviewed in the present chapter.

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Reelin and Radial Glial Cells,n described (Caviness and Rakic, 1978; Caviness ., 1988; Pinto-Lord ., 1982). Based on these findings, it has been hypothesized that radial glial defects contribute to the malpositioning of radially migrating neurons. Experimental evidence that Reelin may directly influence the development of radial