The p75 receptor mediates axon growth inhibition through an association with PIR-B

Cell Death Dis. 2011 Sep 1;2(9):e198. doi: 10.1038/cddis.2011.85.

Abstract

The Nogo receptor and paired immunoglobulin-like receptor B (PIR-B) are receptors for three myelin-derived axon-growth inhibitors, including myelin-associated glycoprotein (MAG). In this study, we report that the p75 receptor is required for the signal transduction of PIR-B, which interacted with p75 upon ligand binding. In addition, p75 was required for activation of Src homology 2-containing protein tyrosine phosphatase (SHP), which is induced by MAG binding to PIR-B. Mice carrying a mutation in the p75 gene showed promotion of axonal regeneration after optic nerve injury. Thus, our results indicate that p75 has a critical role in axon growth inhibition in specific neuronal tracts.

MeSH terms

  • Animals
  • Axons / physiology*
  • COS Cells
  • Chlorocebus aethiops
  • Mice
  • Mice, Inbred C57BL
  • Mutation
  • Myelin-Associated Glycoprotein / metabolism
  • Protein Binding
  • Protein Tyrosine Phosphatases / chemistry
  • Protein Tyrosine Phosphatases / metabolism
  • Receptor, Nerve Growth Factor / genetics
  • Receptor, Nerve Growth Factor / metabolism*
  • Receptor, trkB / metabolism
  • Receptors, Immunologic / metabolism*
  • Signal Transduction
  • src Homology Domains

Substances

  • Myelin-Associated Glycoprotein
  • Pirb protein, mouse
  • Receptor, Nerve Growth Factor
  • Receptors, Immunologic
  • Receptor, trkB
  • Protein Tyrosine Phosphatases