ArticleNature2010
Neurotrophin receptors TrkA and TrkC cause neuronal death whereas TrkB does not.
Article in Nature, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
What it found
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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.
The trial behind it
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Who cites it
112 citing papers in PubMed, 210 citations in OpenAlex.
- Discovery of a sulfotyrosine-motif in the human TrkB extracellular domain required for agonist activation.bioRxiv : the preprint server for biology · 2026Article
- Targeted BDNF upregulation via upstream open reading frame disruption.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Motor Neuron Size-Dependent Differences in mRNA Expression of Tropomyosin-Related Kinase Receptor B in Adult Rats.Journal of neurochemistry · 2026Article
- Molecular determinants of signal transduction in tropomyosin receptor kinases.FEBS open bio · 2026Review
- Early life shifts in cortical inhibitory-excitatory balance underlies sensitive periods and skill development.Frontiers in cellular neuroscience · 2026Article
- Structural basis for the transmembrane signaling and antidepressant-induced activation of the receptor tyrosine kinase TrkB.Nature communications · 2024Article
- Atypical cellular responses mediated by intracellular constitutive active TrkB (NTRK2) kinase domains and a solely intracellular NTRK2-fusion oncogene.Cancer gene therapy · 2024Article
- The clustered gamma protocadherin PcdhγC4 isoform regulates cortical interneuron programmed cell death in the mouse cortex.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- Inflammation and Neurodegeneration in Glaucoma: Isolated Eye Disease or a Part of a Systemic Disorder? - Serum Proteomic Analysis.Journal of inflammation research · 2024Article
- Mutation in the TRKB Cholesterol Recognition Site that blocks Antidepressant Binding does not Influence the Basal or BDNF-Stimulated Activation of TRKB.Cellular and molecular neurobiology · 2023Article
- How Neuromembrane Lipids Modulate Membrane Proteins: Insights from G-Protein-Coupled Receptors (GPCRs) and Receptor Tyrosine Kinases (RTKs).Cold Spring Harbor perspectives in biology · 2023Review
- Exosome-sheathed ROS-responsive nanogel to improve targeted therapy in perimenopausal depression.Journal of nanobiotechnology · 2023Article
- Review
- Unique ligand and kinase-independent roles of the insulin receptor in regulation of cell cycle, senescence and apoptosis.Nature communications · 2023Article
- Brain-Derived Neurotropic Factor in Neurodegenerative Disorders.Biomedicines · 2022Review
- Innervation in organogenesis.Current topics in developmental biology · 2022Article
- Retinal Protection from LED-Backlit Screen Lights by Short Wavelength Absorption Filters.Cells · 2021Article
- Dependence receptors: new targets for cancer therapy.EMBO molecular medicine · 2021Review
- Activation of HERV-K(HML-2) disrupts cortical patterning and neuronal differentiation by increasing NTRK3.Cell stem cell · 2021Article
52 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 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurons of the peripheral nervous system have long been known to require survival factors to prevent their death during development. But why they selectively become dependent on secretory molecules has remained a mystery, as is the observation that in the central nervous system, most neurons do not show this dependency. Using engineered embryonic stem cells, we show here that the neurotrophin receptors TrkA and TrkC (tropomyosin receptor kinase A and C, also known as Ntrk1 and Ntrk3, respectively) instruct developing neurons to die, both in vitro and in vivo. By contrast, TrkB (also known as Ntrk2), a closely related receptor primarily expressed in the central nervous system, does not. These results indicate that TrkA and TrkC behave as dependence receptors, explaining why developing sympathetic and sensory neurons become trophic-factor-dependent for survival. We suggest that the expansion of the Trk gene family that accompanied the segregation of the peripheral from the central nervous system generated a novel mechanism of cell number control.
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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.