ArticleThe Journal of cell biology1997
NGF and neurotrophin-3 both activate TrkA on sympathetic neurons but differentially regulate survival and neuritogenesis.
Article in The Journal of cell biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
67 citing papers in PubMed, 173 citations in OpenAlex.
- Brown Adipose Tissue: Molecular Mechanisms of Regulation, Physiological Functions, and Therapeutic Targets.MedComm · 2026Review
- Mechanisms and Manifestations of Ligand Bias in Signaling: Focus on Receptor Tyrosine Kinases.Chemical reviews · 2026Review
- Small-Molecule Trk Agonists: Where Do We Go from Here?Journal of medicinal chemistry · 2025Review
- Selective, Intrinsically Fluorescent Trk Modulating Probes.ACS chemical neuroscience · 2024Article
- Vascular smooth muscle cell-derived nerve growth factor regulates sympathetic collateral branching to innervate blood vessels in embryonic skin.Biology open · 2024Article
- Lower Nerve Growth Factor Levels in Major Depression and Suicidal Behaviors: Effects of Adverse Childhood Experiences and Recurrence of Illness.Brain sciences · 2023Article
- Neuroprotective and Disease-Modifying Effects of the Triazinetrione ACD856, a Positive Allosteric Modulator of Trk-Receptors for the Treatment of Cognitive Dysfunction in Alzheimer's Disease.International journal of molecular sciences · 2023Article
- Neurotoxic Effect of Doxorubicin Treatment on Cardiac Sympathetic Neurons.International journal of molecular sciences · 2022Article
- Innervation in organogenesis.Current topics in developmental biology · 2022Article
- Crosstalk between adipose tissue and the microbiota-gut-brain axis in metabolic diseases.International journal of biological sciences · 2022Review
- Ligand bias in receptor tyrosine kinase signaling.The Journal of biological chemistry · 2020Review
- Exploring the Pathogenesis of Alzheimer Disease in Basal Forebrain Cholinergic Neurons: Converging Insights From Alternative Hypotheses.Frontiers in neuroscience · 2019Review
- Nicotine is neuroprotective to neonatal neurons of sympathetic ganglion in rat.Autonomic neuroscience : basic & clinical · 2019Article
- Going Too Far Is the Same as Falling ShortFrontiers in cellular neuroscience · 2019Review
- Recent advances in understanding context-dependent mechanisms controlling neurotrophin signaling and function.F1000Research · 2019Review
- Dimerization of the Trk receptors in the plasma membrane: effects of their cognate ligands.The Biochemical journal · 2018Article
- Neurotrophin Responsiveness of Sympathetic Neurons Is Regulated by Rapid Mobilization of the p75 Receptor to the Cell Surface through TrkA Activation of Arf6.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Delineating neurotrophin-3 dependent signaling pathways underlying sympathetic axon growth along intermediate targets.Molecular and cellular neurosciences · 2017Article
- Neurotrophin signaling endosomes: biogenesis, regulation, and functions.Current opinion in neurobiology · 2016Review
- Characterization of canine dental pulp cells and their neuroregenerative potential.In vitro cellular & developmental biology. Animal · 2015Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this report we examine the biological and molecular basis of the control of sympathetic neuron differentiation and survival by NGF and neurotrophin-3 (NT-3). NT-3 is as efficient as NGF in mediating neuritogenesis and expression of growth-associated genes in NGF-dependent sympathetic neurons, but it is 20-40-fold less efficient in supporting their survival. Both NT-3 and NGF induce similar sustained, long-term activation of TrkA, while NGF is 10-fold more efficient than NT-3 in mediating acute, short-term TrkA activity. At similar acute levels of TrkA activation, NT-3 still mediates neuronal survival two- to threefold less well than NGF. However, a mutant NT-3 that activates TrkC, but not TrkA, is unable to support sympathetic neuron survival or neuritogenesis, indicating that NT-3-mediated TrkA activation is necessary for both of these responses. On the basis of these data, we suggest that NGF and NT-3 differentially regulate the TrkA receptor both with regard to activation time course and downstream targets, leading to selective regulation of neuritogenesis and survival. Such differential responsiveness to two ligands acting through the same Trk receptor has important implications for neurotrophin function throughout the nervous system.
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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.