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      A protein related to extracellular matrix proteins deleted in the mouse mutant reeler.

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          Abstract

          The autosomal recessive mouse mutation reeler leads to impaired motor coordination, tremors and ataxia. Neurons in affected mice fail to reach their correct locations in the developing brain, disrupting the organization of the cerebellar and cerebral cortices and other laminated regions. Here we use a previously characterized reeler allele (rl(tg)) to close a gene, reelin, deleted in two reeler alleles. Normal but not mutant mice express reelin in embryonic and postnatal neurons during periods of neuronal migration. The encoded protein resembles extracellular matrix proteins involved in cell adhesion. The reeler phenotype thus seems to reflect a failure of early events associated with brain lamination which are normally controlled by reelin.

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          Author and article information

          Journal
          Nature
          Nature
          Springer Science and Business Media LLC
          0028-0836
          0028-0836
          Apr 20 1995
          : 374
          : 6524
          Affiliations
          [1 ] Roche Institute of Molecular Biology, Hoffman La Roche, Nutley, New Jersey 07110, USA.
          Article
          10.1038/374719a0
          7715726
          24b34cf7-1ba3-4b18-9ec4-2d997d65e09a
          History

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