ArticleThe Journal of cell biology1993
Ectopic trkA expression mediates a NGF survival response in NGF-independent sensory neurons but not in parasympathetic neurons.
Article in The Journal of cell biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 53 citations in OpenAlex.
- Sprouty2-a Novel Therapeutic Target in the Nervous System?Molecular neurobiology · 2019Review
- Differential cell death and Bcl-2 expression in the mouse retina after glutathione decrease by systemic D,L-buthionine sulphoximine administration.Molecules and cells · 2013Article
- Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons.Nature communications · 2012Article
- p75 neurotrophin receptor signaling regulates growth cone filopodial dynamics through modulating RhoA activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Receptors of the glial cell line-derived neurotrophic factor family of neurotrophic factors signal cell survival through the phosphatidylinositol 3-kinase pathway in spinal cord motoneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Bcl-2 accelerates the maturation of early sensory neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- Studies of neurotrophin biology in the developing trigeminal system.Journal of anatomy · 1997Review
- Mutational studies of conserved residues in the dimer interface of nerve growth factor.Protein science : a publication of the Protein Society · 1996Article
- Article
- Regulation of nerve growth factor receptor gene expression in sympathetic neurons during development.The Journal of cell biology · 1995Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We have investigated the role of trkA, the tyrosine kinase NGF receptor, in mediating the survival response of embryonic neurons to NGF. Embryonic trigeminal mesencephalic (TMN) neurons, which normally survive in the presence of brain-derived neurotrophic factor (BDNF) but not NGF, become NGF-responsive when microinjected with an expression vector containing trkA cDNA. In contrast, microinjection of ciliary neurotrophic factor (CNTF)-dependent embryonic ciliary neurons with the same construct does not result in the acquisition of NGF responsiveness by these neurons despite de novo expression of trkA mRNA and protein. The failure of trkA to result in an NGF-promoted survival response in ciliary neurons is not due to absence of the low-affinity NGF receptor, p75, in these neurons. Quantitative RT/PCR and immunocytochemistry showed that TMN and ciliary neurons both express p75 mRNA and protein. These findings not only provide the first direct experimental demonstration of trkA mediating a physiological response in an appropriate cell type, namely NGF-promoted survival of embryonic neurons, but indicate that not all neurons are able to respond to a trkA-mediated signal transduction event.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.