@article{8c11d621603e4b61bb039d595f106a31,
title = "Reeler/disabled-like disruption of neuronal migration in knockout mice lacking the VLDL receptor and ApoE receptor 2",
abstract = "Layering of neurons in the cerebral cortex and cerebellum requires Reelin, an extracellular matrix protein, and mammalian Disabled (mDab1), a cytosolic protein that activates tyrosine kinases. Here, we report the requirement for two other proteins, cell surface receptors termed very low density lipoprotein receptor (VLDLR) and apolipoprotein E receptor 2 (ApoER2). Both receptors can bind mDab1 on their cytoplasmic tails and are expressed in cortical and cerebellar layers adjacent to layers that express Reelin- mDab1 expression is upregulated in knockout mice that lack both VLDLR and ApoER2. Inversion of cortical layers and absence of cerebellar foliation in these animals precisely mimic the phenotype of mice lacking Reelin or mDab1. These findings suggest that VLDLR and ApoER2 participate in transmitting the extracellular Reelin signal to intracellular signaling processes initiated by mDab1.",
author = "M. Trommsdorff and M. Gotthardt and T. Hiesberger and J. Shelton and W. Stockinger and J. Nimpf and Hammer, {Robert E} and Richardson, {James A} and Joachim Herz",
note = "Funding Information: The authors thank Mike Brown, Jon Cooper, Robert Farese, Joe Goldstein, Jane Johnson, Steve McKnight, David Russell, Thomas S{\"u}dhof, and Masashi Yanagisawa for reading of the manuscript and critical suggestions. We are indebted to Wen-Ling Niu, Shana Maika, Jeff Stark, and Laura Quinlivan for invaluable technical support, to Roger Janz for kindly providing GST-SVOP fusion protein, and to Dwight German for the calbindin probe. This work was supported by grants from the National Institutes of Health (HL20948, AG12300), the Keck Foundation, the Perot Family Foundation, the Human Frontiers Science Program, the Austrian Science Foundation (P11692), and the Howard Hughes Medical Institute. M. T. was supported by a fellowship from the Max-Kade Foundation; T. H. and W. S. are supported by the Austrian Science Foundation. J. H. is an Established Investigator of the American Heart Association and Parke-Davis. ",
year = "1999",
doi = "10.1016/S0092-8674(00)80782-5",
language = "English (US)",
volume = "97",
pages = "689--701",
journal = "Cell",
issn = "0092-8674",
publisher = "Cell Press",
number = "6",
}