Doublecortin is a developmentally regulated, microtubule-associated protein expressed in migrating and differentiating neurons.
Fiona Francis,Annette Koulakoff,Dominique Boucher,Philippe Chafey,Bruce T. Schaar,M C Vinet,Gaëlle Friocourt,Nathalie McDonnell,Orly Reiner,Axel Kahn,Susan K. McConnell,Yoheved Berwald-Netter,Philippe Denoulet,Jamel Chelly +13 more
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TL;DR: It is shown that Doublecortin is expressed in the brain throughout the period of corticogenesis in migrating and differentiating neurons, and Immunohistochemical studies show its localization in the soma and leading processes of tangentially migrating neuron, and a strong axonal labeling is observed in differentiating neuron.
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About: This article is published in Neuron. The article was published on 01 Jun 1999. and is currently open access. The article focuses on the topics: Doublecortin & Corticogenesis.
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A protein related to extracellular matrix proteins deleted in the mouse mutant reeler
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TL;DR: Electron microscopic analysis of serial sections showed that during chain migration, neural precursors moved associated with each other and were not guided by radial glial or axonal fibers.
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doublecortin, a Brain-Specific Gene Mutated in Human X-Linked Lissencephaly and Double Cortex Syndrome, Encodes a Putative Signaling Protein
Joseph G. Gleeson,Joseph G. Gleeson,Kristina M. Allen,Jeremy W. Fox,Edward D Lamperti,Samuel F. Berkovic,Ingrid E. Scheffer,Edward C. Cooper,William B. Dobyns,Sharon R. Minnerath,M. Elizabeth Ross,Christopher A. Walsh +11 more
TL;DR: A novel 10 kb brain-specific cDNA interrupted by a balanced translocation in an XLIS patient that encodes a novel 40 kDa predicted protein named Doublecortin, which may define an Abl-dependent pathway regulating neuronal migration.
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Isolation of a Miller-Dieker lissencephaly gene containing G protein beta-subunit-like repeats
Orly Reiner,Romeo Carrozzo,Ying Shen,Manfred Wehnert,Fabrizia Faustinella,William B. Dobyns,C. Thomas Caskey,David H. Ledbetter +7 more
TL;DR: The cloning of a gene (LIS-1, lissencephaly-1) in 17p13.3 that is deleted in Miller–Dieker patients is reported, identifying LIS-l as the disease gene and the deduced amino-acid sequence shows significant homology to β-subunits of heterotrimeric G proteins, suggesting that it could possibly be involved in a signal transduction pathway crucial for cerebral development.
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