p75NTR and apoptosis: Trk-dependent and Trk-independent effects

Trends Neurosci. 1997 Jul;20(7):287-90. doi: 10.1016/s0166-2236(96)01049-1.


The ongoing dissection of the roles of p75NTR and TrkA, -B and -C in neurotrophin signaling has generated a number of apparent paradoxes. Limiting consideration to the role of p75NTR in cell death, a theory is proposed that is based on the following postulates: (1) that p75NTR displays a pro-apoptotic intrinsic (ligand-independent, Trk-independent) receptor effect (IRE), which is inhibited by ligand binding; (2) that p75NTR and TrkA exhibit mutual repression of signaling; and (3) that p75NTR and TrkA are required for the efficient generation of high-affinity NGF binding sites.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Apoptosis / physiology*
  • Humans
  • Models, Neurological*
  • Proto-Oncogene Proteins / physiology*
  • Receptor Protein-Tyrosine Kinases / physiology*
  • Receptor, Nerve Growth Factor
  • Receptor, trkA
  • Receptors, Nerve Growth Factor / physiology*


  • Proto-Oncogene Proteins
  • Receptor, Nerve Growth Factor
  • Receptors, Nerve Growth Factor
  • Receptor Protein-Tyrosine Kinases
  • Receptor, trkA