Identification of a receptor mediating Nogo-66 inhibition of axonal regeneration

@article{Fournier2001IdentificationOA,
  title={Identification of a receptor mediating Nogo-66 inhibition of axonal regeneration},
  author={Alyson E. Fournier and Tadzia Grandpr{\'e} and Stephen M. Strittmatter},
  journal={Nature},
  year={2001},
  volume={409},
  pages={341-346}
}
Nogo has been identified as a component of the central nervous system (CNS) myelin that prevents axonal regeneration in the adult vertebrate CNS. Analysis of Nogo-A has shown that an axon-inhibiting domain of 66 amino acids is expressed at the extracellular surface and at the endoplasmic reticulum lumen of transfected cells and oligodendrocytes. The acidic amino terminus of Nogo-A is detected at the cytosolic face of cellular membranes and may contribute to inhibition of axon regeneration at… 

Localization of Nogo-A and Nogo-66 Receptor Proteins at Sites of Axon–Myelin and Synaptic Contact

Data confirm the apposition of Nogo ligand and NgR receptor in situations of limited axonal regeneration and support the hypothesis that this system regulates CNS axonal plasticity and recovery from injury.

Nogo-66 receptor antagonist peptide promotes axonal regeneration

The Nogo-66(1–40) antagonist peptide (NEP1-40) blocks Nogo or CNS myelin inhibition of axonal outgrowth in vitro, demonstrating that NgR mediates a significant portion of axon outgrowth inhibition by myelin.

Oligodendrocyte-myelin glycoprotein is a Nogo receptor ligand that inhibits neurite outgrowth

It is shown that a glycosylphosphatidylinositol-anchored CNS myelin protein, oligodendrocyte-myelin glycoprotein (OMgp), is a potent inhibitor of neurite outgrowth in cultured neurons and that Interfering with the OMgp/NgR pathway may allow lesioned axons to regenerate after injury in vivo.

Nogos and the Nogo‐66 receptor: Factors inhibiting CNS neuron regeneration

Together, these proteins provide new molecular handles for the design of therapeutic interventions for CNS injuries and neurodegenerative diseases, as well as possible leads to anticancer strategies.

Soluble Nogo Receptor Down-regulates Expression of Neuronal Nogo-A to Enhance Axonal Regeneration*

The results indicate that neuronal Nogo-A is an important intermediate in neurite growth dynamics and its expression is regulated by signals related to axonal injury and regeneration, that CNS myelin appears to activate signaling events that mimicAxonal injury, and that NgSR released from QHNgSR may be used to improve recovery after injury.

Genetic deletion of the Nogo receptor does not reduce neurite inhibition in vitro or promote corticospinal tract regeneration in vivo.

NgR is not essential for mediating inhibitory signals from CNS myelin, at least in the neurons tested, whereas p75(NTR) plays a central role in this response.

Inhibition of Retinal Ganglion Cell Axonal Outgrowth Through the Amino-Nogo-A Signaling Pathway

The results suggest that Amino-Nogo inhibits RGC axonal outgrowth primarily through the integrin αv signaling pathway.
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