Active killing of neurons during development and following stress: a role for p75(NTR) and Fas?
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.
Raoul
C
C
INSERM U.382, Developmental Biology Institute of Marseille (CNRS-INSERM - Univ. Méditerranée - AP Marseille), Marseille, 13288, France. raoul@ibdm.univ-mrs.fr
Pettmann
B
B
Henderson
C E
CE
D000818:Animals; D017209:Apoptosis; D053222:Fas Ligand Protein; D006801:Humans; D008562:Membrane Glycoproteins / Q000378:metabolism; D009420:Nervous System / Q000166:cytology / Q000196:embryology / Q000254:growth & development* / Q000503:physiopathology; D009474:Neurons / Q000166:cytology* / Q000378:metabolism; D017475:Receptors, Nerve Growth Factor / Q000737:chemistry / Q000378:metabolism*; D015398:Signal Transduction; D013312:Stress, Physiological / Q000473:pathology / Q000503:physiopathology*; D015854:Up-Regulation; D019014:fas Receptor / Q000378:metabolism*
C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D017475:Receptors, Nerve Growth Factor; D019014:fas Receptor