LGI1 is a Nogo receptor 1 ligand that antagonizes myelin-based growth inhibition

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DOIResolve DOI: http://doi.org/10.1523/JNEUROSCI.5147-09.2010
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TypeArticle
Journal titleJ Neurosci
Volume30
Issue19
Pages66076612; # of pages: 6
Subjectbio; Brain; Cell Enlargement; Cell Line; Cercopithecus aethiops; Chick Embryo; Cos Cells; Ganglia,Spinal; growth&development; Growth Cones; Human; Humans; In Vitro; Ligands; metabolism; Mutation; Myelin Proteins; Myelin Sheath; Nerve Tissue Proteins; Neurons; physiology; Protein; Proteins; rat; Rats; Rats,Sprague-Dawley; Receptors,Cell Surface; Vitro; ADAM Proteins; Animals
AbstractMutations in leucine-rich glioma inactivated (LGI1) are a genetic cause of autosomal dominant temporal lobe epilepsy with auditory features. LGI1 is a secreted protein that shares homology with members of the SLIT family, ligands that direct axonal repulsion and growth cone collapse, and we therefore considered the possibility that LGI1 may regulate neuronal process extension or growth cone collapse. Here we report that LGI1 does not affect growth directly but instead enhances neuronal growth on myelin-based inhibitory substrates and antagonizes myelin-induced growth cone collapse. We show that LGI1 mediates this effect by functioning as a specific Nogo receptor 1 (NgR1) ligand that antagonizes the action of myelin-based inhibitory cues. Finally, we demonstrate that NgR1 and ADAM22 physically associate to form a receptor complex in which NgR1 facilitates LGI1 binding to ADAM22
Publication date
LanguageEnglish
AffiliationNational Research Council Canada (NRC-CNRC); NRC Biotechnology Research Institute
Peer reviewedYes
NRC number52761
NPARC number16225329
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Record identifier491239d6-4ce9-41ef-9307-d6329c4c4d01
Record created2010-11-05
Record modified2016-05-09
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