ArticleThe Journal of biological chemistry2001
The extracellular domain of p75NTR is necessary to inhibit neurotrophin-3 signaling through TrkA.
Article in The Journal of biological chemistry, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 92 citations in OpenAlex.
- Molecular determinants of signal transduction in tropomyosin receptor kinases.FEBS open bio · 2026Review
- Small-Molecule Trk Agonists: Where Do We Go from Here?Journal of medicinal chemistry · 2025Review
- Selective Modulation of Trk Receptors byACS chemical neuroscience · 2025Article
- Selective, Intrinsically Fluorescent Trk Modulating Probes.ACS chemical neuroscience · 2024Article
- Article
- The role of neurotrophic factors in novel, rapid psychiatric treatments.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Review
- Immune activation of the p75 neurotrophin receptor: implications in neuroinflammation.Frontiers in molecular neuroscience · 2023Article
- A, B, C's of Trk Receptors and Their Ligands in Ocular Repair.International journal of molecular sciences · 2022Review
- Human immunomodulatory ligand B7-1 mediates synaptic remodeling via the p75 neurotrophin receptor.The Journal of clinical investigation · 2022Article
- High-affinity TrkA and p75 neurotrophin receptor complexes: A twisted affair.The Journal of biological chemistry · 2022Review
- Swedish Nerve Growth Factor Mutation (NGFThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Targeting Neurotrophins to Specific Populations of Neurons: NGF, BDNF, and NT-3 and Their Relevance for Treatment of Spinal Cord Injury.International journal of molecular sciences · 2017Review
- The conundrum of the high-affinity NGF binding site formation unveiled?Biophysical journal · 2015Article
- Overexpression of NTRK1 Promotes Differentiation of Neural Stem Cells into Cholinergic Neurons.BioMed research international · 2015Article
- Molecular and genetic basis of depression.Journal of genetics · 2014Review
- Divergent roles of p75NTR and Trk receptors in BDNF's effects on dendritic spine density and morphology.Neural plasticity · 2012Article
- Dissecting the involvement of tropomyosin-related kinase A and p75 neurotrophin receptor signaling in NGF deficit-induced neurodegeneration.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Proneurotrophin-3 is a neuronal apoptotic ligand: evidence for retrograde-directed cell killing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- p75 and TrkA signaling regulates sympathetic neuronal firing patterns via differential modulation of voltage-gated currents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Expression of p75NTR in fetal brain and medulloblastomas: evidence of a precursor cell marker and its persistence in neoplasia.Journal of neuro-oncology · 2009Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
The TrkA receptor is activated primarily by nerve growth factor (NGF), but it can also be activated by high concentrations of neurotrophin 3 (NT-3). The pan-neurotrophin receptor p75(NTR) strongly inhibits activation of TrkA by NT-3 but not by NGF. To examine the role of p75(NTR) in regulating the specificity of TrkA signaling, we expressed both receptors in Xenopus oocytes. Application of NGF or NT-3 to oocytes expressing TrkA alone resulted in efflux of (45)Ca(2+) by a phospholipase C-gamma-dependent pathway. Coexpression of p75(NTR) with TrkA inhibited (45)Ca(2+) efflux in response to NT-3 but not NGF. The inhibitory effect on NT-3 activation of TrkA increased with increasing expression of p75(NTR). Coexpression of a truncated p75(NTR) receptor lacking all but the first 9 amino acids of the cytoplasmic domain inhibited NT-3 stimulation of (45)Ca(2+) efflux, whereas coexpression of an epidermal growth factor receptor/p75(NTR) chimera (extracellular domain of epidermal growth factor receptor with transmembrane and cytoplasmic domains of p75(NTR)) did not inhibit NT-3 signaling through TrkA. These studies demonstrated that the extracellular domain of p75(NTR) was necessary to inhibit NT-3 signaling through TrkA. Remarkably, p75(NTR) binding to NT-3 was not required to prevent signaling through TrkA, since occupying p75(NTR) with brain-derived neurotrophic factor or anti-p75 antibody (REX) did not rescue the ability of NT-3 to activate (45)Ca(2+) efflux. These data suggested a physical association between TrkA and p75(NTR). Documenting this physical interaction, we showed that p75(NTR) and TrkA could be coimmunoprecipitated from Xenopus oocytes. Our results suggest that the interaction of these two receptors on the cell surface mediated the inhibition of NT-3-activated signaling through TrkA.
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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.