ArticleMolecular biology of the cell1994
TrkA cross-linking mimics neuronal responses to nerve growth factor.
Article in Molecular biology of the cell, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
82 citing papers in PubMed, 222 citations in OpenAlex.
- Ndfip2 in TrkA-expressing sensory neurons regulates noxious mechanosensation through control of TrkA signaling and protein levels.Cell death & disease · 2026Article
- Utility of a commercial antibody against NTRK1 for western blotting and potential application to immunohistochemistry in adult mouse brain.Scientific reports · 2025Article
- From Gene to Protein: Unraveling the Reproductive Blueprint of Male Grey Squirrels via Nerve Growth Factor (NGF) and Cognate Receptors.Animals : an open access journal from MDPI · 2024Article
- Molecular Adaptations of BDNF/NT-4 Neurotrophic and Muscarinic Pathways in Ageing Neuromuscular Synapses.International journal of molecular sciences · 2024Article
- Enhanced TrkA signaling impairs basal forebrain-dependent behavior.Frontiers in molecular neuroscience · 2023Article
- Targeted viral vector transduction of relaxin-3 neurons in the ratIBRO reports · 2020Article
- Article
- Dimerization of the Trk receptors in the plasma membrane: effects of their cognate ligands.The Biochemical journal · 2018Article
- Nerve Growth Factor Signaling from Membrane Microdomains to the Nucleus: Differential Regulation by Caveolins.International journal of molecular sciences · 2017Article
- The TrkA receptor mediates experimental thermal hyperalgesia produced by nerve growth factor: Modulation by the p75 neurotrophin receptor.Neuroscience · 2017Article
- Article
- Hypofunctional TrkA Accounts for the Absence of Pain Sensitization in the African Naked Mole-Rat.Cell reports · 2016Article
- Noise-induced hearing loss: Neuropathic pain via Ntrk1 signaling.Molecular and cellular neurosciences · 2016Article
- Activity-Dependent Inhibitory Synaptogenesis in Cerebellar Cultures.Brain plasticity (Amsterdam, Netherlands) · 2016Review
- HBpF-proBDNF: A New Tool for the Analysis of Pro-Brain Derived Neurotrophic Factor Receptor Signaling and Cell Biology.PloS one · 2016Article
- Ligand-induced dynamics of neurotrophin receptors investigated by single-molecule imaging approaches.International journal of molecular sciences · 2015Review
- RabGEF1/Rabex-5 Regulates TrkA-Mediated Neurite Outgrowth and NMDA-Induced Signaling Activation in NGF-Differentiated PC12 Cells.PloS one · 2015Article
- The changeable nervous system: studies on neuroplasticity in cerebellar cultures.Neuroscience and biobehavioral reviews · 2014Review
- Novel small molecule activators of the Trk family of receptor tyrosine kinases.Biochimica et biophysica acta · 2013Review
- The effect of P75 on Trk receptors in neuroblastomas.Cancer letters · 2011Article
22 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
4 authors at 1 institution in 1 country.
Funding
Abstract
TrkA, a tyrosine kinase receptor, is an essential component of the nerve growth factor (NGF) response pathway. The binding of NGF to the receptor induces receptor autophosphorylation and activation of intracellular signaling pathways, resulting in diverse biological effects. We prepared polyclonal antibodies against the entire extracellular domain of rat trkA produced using a baculovirus expression system. These antibodies specifically recognize rat trkA on antigen blots and in immunoprecipitations. Both IgG and Fab fragments block binding of NGF to trkA expressed by the PC12 cell line. In NGF binding studies using anti-trkA and anti-low-affinity NGF receptor (LNGFR) immunoglobulin (Ig) G, essentially all binding of NGF can be inhibited. The results imply that > or = 97% of the NGF binding sites on PC12 cells are accounted for by trkA and the LNGFR. The binding data also argue that all low-affinity NGF binding sites on PC12 cells reflect interactions with the LNGFR, while all high-affinity sites are trkA dependent. A fraction of the high-affinity (or slow) binding sites seem to require both trkA and the LNGFR. Although the monovalent anti-trkA Fab fragments inhibited the biological effects of NGF, such as induction of tyrosine phosphorylation, and survival and neurite outgrowth of sympathetic neurons, the IgG preparation was not effective as an inhibitor. Instead, the IgG fraction by itself was almost as effective as NGF at stimulating receptor activation, cell survival, and neurite outgrowth. Thus, it appears oligomerization of trkA by antibody-induced cross-linking is sufficient to produce the known cellular effects of NGF.
Indexed as
Identifiers
What OpenQuestion holds
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.