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rdf:type |
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lifeskim:mentions |
umls-concept:C0007603,
umls-concept:C0033414,
umls-concept:C0033684,
umls-concept:C0085103,
umls-concept:C0271510,
umls-concept:C0344329,
umls-concept:C0596632,
umls-concept:C1413393,
umls-concept:C1414477,
umls-concept:C1514562,
umls-concept:C1514873,
umls-concept:C1546857,
umls-concept:C1556066,
umls-concept:C1619636
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pubmed:issue |
3
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pubmed:dateCreated |
2008-1-17
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pubmed:abstractText |
Close homolog of L1 (CHL1) is a transmembrane cell adhesion molecule with unique developmental functions in cortical neuronal positioning and dendritic projection within the L1 family, as well as shared functions in promotion of integrin-dependent neurite outgrowth and semaphorin3A (Sema3A)-mediated axon repulsion. The molecular mechanisms by which CHL1 mediates these diverse functions are obscure. Here it is demonstrated using a cytofluorescence assay that CHL1 is able to recruit ezrin, a member of the ezrin-radixin-moesin (ERM) family of filamentous actin binding proteins to the plasma membrane, and that this requires a membrane-proximal motif (RGGKYSV) in the CHL1 cytoplasmic domain. This sequence in CHL1 is shown to have novel functions necessary for Sema3A-induced growth cone collapse and CHL1-dependent neurite outgrowth and branching in cortical embryonic neurons. In addition, stimulation of haptotactic cell migration and cellular adhesion to fibronectin by CHL1 depends on the CHL1/ERM recruitment motif. These findings suggest that a direct or indirect interaction between CHL1 and ERM proteins mediates Sema3A-induced growth cone collapse as well as neurite outgrowth and branching, which are essential determinants of axon guidance and connectivity in cortical development.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cell Adhesion Molecules,
http://linkedlifedata.com/resource/pubmed/chemical/Chl1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cytoskeletal Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Etv5 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Fibronectins,
http://linkedlifedata.com/resource/pubmed/chemical/Green Fluorescent Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Semaphorin-3A,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/ezrin
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1471-4159
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
104
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
731-44
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pubmed:meshHeading |
pubmed-meshheading:17995939-Animals,
pubmed-meshheading:17995939-Cell Adhesion,
pubmed-meshheading:17995939-Cell Adhesion Molecules,
pubmed-meshheading:17995939-Cell Membrane,
pubmed-meshheading:17995939-Cell Movement,
pubmed-meshheading:17995939-Cells, Cultured,
pubmed-meshheading:17995939-Cerebral Cortex,
pubmed-meshheading:17995939-Cytoskeletal Proteins,
pubmed-meshheading:17995939-DNA-Binding Proteins,
pubmed-meshheading:17995939-Embryo, Mammalian,
pubmed-meshheading:17995939-Fibronectins,
pubmed-meshheading:17995939-Green Fluorescent Proteins,
pubmed-meshheading:17995939-Growth Cones,
pubmed-meshheading:17995939-Humans,
pubmed-meshheading:17995939-Mice,
pubmed-meshheading:17995939-Mice, Inbred C57BL,
pubmed-meshheading:17995939-Mice, Transgenic,
pubmed-meshheading:17995939-Neurites,
pubmed-meshheading:17995939-Neurons,
pubmed-meshheading:17995939-Rats,
pubmed-meshheading:17995939-Semaphorin-3A,
pubmed-meshheading:17995939-Transcription Factors,
pubmed-meshheading:17995939-Transfection
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pubmed:year |
2008
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pubmed:articleTitle |
CHL1 promotes Sema3A-induced growth cone collapse and neurite elaboration through a motif required for recruitment of ERM proteins to the plasma membrane.
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pubmed:affiliation |
Department of Biochemistry and Biophysics, School of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599-7260, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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