Genes and Development

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

GENES & DEVELOPMENT 21:2850-2854, 2007
©2007 by Cold Spring Harbor Laboratory Press; ISSN 0890-9369/ $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kerjan, G.
Right arrow Articles by Gleeson, J. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kerjan, G.
Right arrow Articles by Gleeson, J. G.
Related Content
Right arrow Neurobiology
Right arrow Signal Transduction
Right arrowRelated Article
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

PERSPECTIVE

A missed exit: Reelin sets in motion Dab1 polyubiquitination to put the break on neuronal migration

Géraldine Kerjan and Joseph G. Gleeson1

Neurogenetics Laboratory, Department of Neurosciences, University of California at San Diego, La Jolla, California 92093, USA

The first 100 words of the full text of this article appear below.

In 1951, Douglas Scott Falconer first described the reeler spontaneous mutant mouse (Falconer 1951Go). In those mice, cortical neurons are generated normally but migrate abnormally, resulting in an inversion of the cortical laminar organization, with later-born neurons remaining in the deeper layers of the cortex. Forty-four years later, D’Arcangelo et al. (1995)Go identified the causative gene Rln and the encoded protein Reelin. Reelin pathway mutants, and particularly mice with mutations of its intracellular effector Dab1 (Disabled-1), probably represent the most-studied phenotype of altered neuronal migration. The observations that mutations of Dab1 phenocopy the Rln mutation, and that Dab1 is . . . [Full Text of this Article]


   The known side of Reelin/Dab1 signaling
 

   Down-regulating Dab1
 

   Overmigration: when Dab1 down-regulation fails to occur
 

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

Related Article

Cullin 5 regulates Dab1 protein levels and neuron positioning during cortical development
Libing Feng, Nathaniel S. Allen, Sergi Simo, and Jonathan A. Cooper
Genes & Dev. 2007 21: 2717-2730. [Abstract] [Full Text] [PDF]





Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Genome Res. Learn. Mem.
Protein Science RNA Genes Dev.
Copyright © 2007 by Cold Spring Harbor Laboratory Press.