Active killing of neurons during development and following stress: a role for p75(NTR) and Fas?

C Raoul; B Pettmann; C E Henderson

doi:10.1016/s0959-4388(99)00055-0

Active killing of neurons during development and following stress: a role for p75(NTR) and Fas?

Curr Opin Neurobiol. 2000 Feb;10(1):111-7. doi: 10.1016/s0959-4388(99)00055-0.

Authors

C Raoul¹, B Pettmann, C E Henderson

Affiliation

¹ INSERM U.382, Developmental Biology Institute of Marseille (CNRS-INSERM - Univ. Méditerranée - AP Marseille), Marseille, 13288, France. raoul@ibdm.univ-mrs.fr

PMID: 10679436
DOI: 10.1016/s0959-4388(99)00055-0

Abstract

Evidence for active triggering of neuronal death continues to accumulate. The transmembrane receptors p75(NTR) and Fas can trigger (and in some cases are required for) programmed cell death of the neurons that express them, through signalling pathways that are regulated by a variety of cytoplasmic effectors. Neuronal death induced by trophic deprivation often requires Fas signalling, further blurring the boundaries between naturally occurring and stress-induced neuronal death.

Publication types

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

MeSH terms

Animals
Apoptosis*
Fas Ligand Protein
Humans
Membrane Glycoproteins / metabolism
Nervous System / cytology
Nervous System / embryology
Nervous System / growth & development*
Nervous System / physiopathology
Neurons / cytology*
Neurons / metabolism
Receptors, Nerve Growth Factor / chemistry
Receptors, Nerve Growth Factor / metabolism*
Signal Transduction
Stress, Physiological / pathology
Stress, Physiological / physiopathology*
Up-Regulation
fas Receptor / metabolism*

Substances

FASLG protein, human
Fas Ligand Protein
Membrane Glycoproteins
Receptors, Nerve Growth Factor
fas Receptor