Abstract
Myelin inhibitory ligands of the Nogo-66 receptor (NgR1) limit axon regeneration in the adult CNS. Recent findings have identified additional co-receptors (functional homologues) of the trimeric NgR1 complex, post-translational modifications of the co-receptors within the cell membrane and novel Ca(2+)-dependent cytoplasmic-protein phosphorylation mechanisms. Such unique signalling pathways provide the potential to transduce myelin-derived growth inhibitory signals to the axonal cytoskeleton, and have been areas of intense investigation in recent years. Here, we summarize current understanding of the molecular basis of myelin-derived axon-growth inhibition in the CNS.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amyloid Precursor Protein Secretases
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Animals
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Aspartic Acid Endopeptidases
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Axons / chemistry
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Axons / physiology*
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Endopeptidases / metabolism
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ErbB Receptors / metabolism
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GPI-Linked Proteins
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Humans
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Membrane Proteins / metabolism
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Myelin Proteins / metabolism*
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Myelin Sheath / metabolism*
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Nerve Regeneration
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Nerve Tissue Proteins / metabolism
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Nogo Receptor 1
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Nogo Receptor 2
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Nogo Receptors
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Protein Processing, Post-Translational
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Receptors, Cell Surface / metabolism*
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Receptors, Nerve Growth Factor / metabolism
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Receptors, Tumor Necrosis Factor / metabolism
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Second Messenger Systems
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Signal Transduction
Substances
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GPI-Linked Proteins
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LINGO1 protein, human
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Membrane Proteins
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Myelin Proteins
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NGFR protein, human
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Nerve Tissue Proteins
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Nogo Receptor 1
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Nogo Receptor 2
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Nogo Receptors
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RTN4R protein, human
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RTN4RL1 protein, human
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RTN4RL2 protein, human
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Receptors, Cell Surface
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Receptors, Nerve Growth Factor
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Receptors, Tumor Necrosis Factor
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TNFRSF19 protein, human
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ErbB Receptors
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Amyloid Precursor Protein Secretases
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Endopeptidases
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Aspartic Acid Endopeptidases
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BACE1 protein, human