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

  title={Identification of a receptor mediating Nogo-66 inhibition of axonal regeneration},
  author={Alyson E. Fournier and Tadzia Grandpr{\'e} and Stephen M. Strittmatter},
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.



Identification of the Nogo inhibitor of axon regeneration as a Reticulon protein

The IN-1 antibody, which recognizes NI35 and NI250(Nogo), allows moderate degrees of axonal regeneration and functional recovery after spinal cord injury, and provides a molecular basis to assess the contribution of Nogo to the failure ofAxonal regeneration in the adult CNS.

Nogo-A is a myelin-associated neurite outgrowth inhibitor and an antigen for monoclonal antibody IN-1

Cl cloning of nogo A, the rat complementary DNA encoding NI-220/250 is reported, showing that Nogo-A is a potent inhibitor of neurite growth and an IN-1 antigen produced by oligodendrocytes, and may allow the generation of new reagents to enhance CNS regeneration and plasticity.

Axonal regeneration in the rat spinal cord produced by an antibody against myelin-associated neurite growth inhibitors

The capacity for CNS axons to regenerate and elongate within differentiated CNS tissue after the neutralization of myelin-associated neurite growth inhibitors is demonstrated.

Neurobiology: Inhibitor of neurite outgrowth in humans

This work has used this bovine sequence to identify the human Nogo gene and has isolated complementary DNA clones encoding three different Nogo isoforms that are potent inhibitors of neurite outgrowth and which may help block the regeneration of the central nervous system in adults.

Application of Neutralizing Antibodies against NI-35/250 Myelin-Associated Neurite Growth Inhibitory Proteins to the Adult Rat Cerebellum Induces Sprouting of Uninjured Purkinje Cell Axons

Functional neutralization of NI-35/250 proteins induces outgrowth from uninjured Purkinje neurites in the adult cerebellum, which suggests that these molecules regulate axonal plasticity to maintain the proper targeting of terminal arbors within specific gray matter regions.

Oligodendrocytes and CNS myelin are nonpermissive substrates for neurite growth and fibroblast spreading in vitro

  • M. SchwabP. Caroni
  • Biology, Chemistry
    The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 1988
To study the interaction of neurons with CNS glial cells, dissociated sympathetic or sensory ganglion cells or fetal retinal cells were plated onto cultures of dissociated optic nerve glial cells of

Two membrane protein fractions from rat central myelin with inhibitory properties for neurite growth and fibroblast spreading

The data presented demonstrate the existence of membrane proteins with potent nonpermissive substrate properties and suggest that these proteins might play a crucial inhibitory role during development and regeneration in CNS white matter.

Collapsin-induced growth cone collapse mediated by an intracellular protein related to UNC-33

A Xenopus laevis oocyte expression system is used to identify molecules involved in collapsin signalling, which appears to be an intracellular component of a signalling cascade initiated by an unidentified transmembrane collapsin-binding protein.