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Nerve Growth Factor‐Induced Differentiation in Neuroblastoma Cells Expressing TrkA but Lacking p75 NGFR
Author(s) -
Hartman Deborah S.,
Hertel Cornelia
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.63041261.x
Subject(s) - nerve growth factor , tropomyosin receptor kinase a , low affinity nerve growth factor receptor , nerve cells , neuroblastoma , cellular differentiation , microbiology and biotechnology , neuroscience , biology , chemistry , endocrinology , medicine , cell culture , receptor , biochemistry , genetics , gene
Nerve growth factor (NGF) binds to two distinct cell surface receptors, TrkA, which is a receptor tyrosine kinase, and p75 NGFR , whose role in NGF‐induced signal transduction remains unclear. We have found that human neuroblastoma IMR‐32 cells express TrkA, but p75 NGFR expression was not detectable in these cells by northern blot analysis, immunoblotting, or chemical crosslinking experiments. Despite the lack of p75 NGFR expression, subnanomolar concentrations of recombinant human NGF induced neurite outgrowth, tyrosine phosphorylation, and immediate early gene expression in these cells. These results strongly suggest that NGF‐induced neuronal differentiation in IMR‐32 cells is initiated through TrkA in the absence of p75 NGFR . Thus, IMR‐32 cells may provide a model for studying neurotrophic effects of NGF on adult striatal cholinergic neurons, which also lack p75 NGFR expression.