Nerve growth factor (NGF)-mediated protection of neural crest cells from antimitotic agent-induced apoptosis: the role of the low-affinity NGF receptor.

Abstract

Prevention by nerve growth factor (NGF) of apoptotic death in neural cells has been variously ascribed to binding of NGF to its low-affinity (p75) or high-affinity (trkA) receptor or to a cooperative interaction between the two. In a series of studies using, in turn, neuroblastoma cell lines that express only p75, mutant NGF species that bind selectively to either p75 or trkA, and a polyclonal antibody that binds to the NGF-binding domain of p75, we demonstrate that NGF binding to p75 is both necessary and sufficient for the abrogation of apoptosis in neuroblastoma cells treated with antimitotic agents.

• Authors: M H Cortazzo, E S Kassis, K A Sproul, N F Schor
• Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience (J Neurosci) Vol. 16 Issue 12 Pg. 3895-9 (Jun 15 1996) ISSN: 0270-6474 [Print] United States
• PMID: 8656283 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Antineoplastic Agents
• Bacterial Proteins
• Biomarkers
• Nerve Growth Factors
• Neuroprotective Agents
• Receptors, Nerve Growth Factor
• Zinostatin
• Receptor, trkA

Topics

• Antineoplastic Agents (pharmacology)
• Apoptosis (physiology)
• Bacterial Proteins (drug effects, metabolism)
• Biomarkers
• Cell Adhesion (drug effects)
• Humans
• Mutagenesis, Site-Directed (physiology)
• Nerve Growth Factors (genetics, metabolism, pharmacology)
• Neural Crest (cytology)
• Neuroblastoma
• Neuroprotective Agents (metabolism, pharmacology)
• Receptor, trkA (drug effects, metabolism)
• Receptors, Nerve Growth Factor (drug effects, metabolism, physiology)
• Tumor Cells, Cultured (cytology, drug effects, physiology)
• Zinostatin (pharmacology)