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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Antineoplastic Agents / pharmacology
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Apoptosis / physiology
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Bacterial Proteins / drug effects
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Bacterial Proteins / metabolism
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Biomarkers
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Cell Adhesion / drug effects
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Humans
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Mutagenesis, Site-Directed / physiology
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Nerve Growth Factors / genetics
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Nerve Growth Factors / metabolism
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Nerve Growth Factors / pharmacology*
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Neural Crest / cytology*
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Neuroblastoma
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Neuroprotective Agents / metabolism
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Neuroprotective Agents / pharmacology
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Receptor, trkA / drug effects
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Receptor, trkA / metabolism
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Receptors, Nerve Growth Factor / drug effects
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Receptors, Nerve Growth Factor / metabolism
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Receptors, Nerve Growth Factor / physiology*
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Tumor Cells, Cultured / cytology
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Tumor Cells, Cultured / drug effects
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Tumor Cells, Cultured / physiology
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Zinostatin / pharmacology
Substances
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Antineoplastic Agents
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Bacterial Proteins
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Biomarkers
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Nerve Growth Factors
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Neuroprotective Agents
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Receptors, Nerve Growth Factor
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Zinostatin
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Receptor, trkA