ArticlePhilosophical transactions of the Royal Society of London. Series B, Biological sciences2019
MNK-eIF4E signalling is a highly conserved mechanism for sensory neuron axonal plasticity: evidence from
Article in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- From nociception in aneural animals to human suffering: toward a comparative biology of pain.The Journal of experimental biology · 2025Review
- MicroRNA-1985 enhances the redox capability of scallop (Frontiers in immunology · 2025Article
- A nociceptor-specific RNAi screen inPeerJ · 2025Article
- Tomivosertib reduces ectopic activity in dorsal root ganglion neurons from patients with radiculopathy.Brain : a journal of neurology · 2024Article
- ephrin-B2 promotes nociceptive plasticity and hyperalgesic priming through EphB2-MNK-eIF4E signaling in both mice and humans.Pharmacological research · 2024Article
- Degenerative and regenerative peripheral processes are associated with persistent painful chemotherapy-induced neuropathies in males and females.Scientific reports · 2024Article
- Induction of long-term hyperexcitability by memory-related cAMP signaling in isolated nociceptor cell bodies.bioRxiv : the preprint server for biology · 2024Article
- The Emerging Translational Potential of MNK Inhibitors for the Treatment of Chronic Pain.Neuroscience · 2023Article
- Persistent nociceptor hyperactivity as a painful evolutionary adaptation.Trends in neurosciences · 2023Review
- MNK1 and MNK2 expression in the human dorsal root and trigeminal ganglion.bioRxiv : the preprint server for biology · 2023Article
- Exaptation and Evolutionary Adaptation in Nociceptor Mechanisms Driving Persistent Pain.Brain, behavior and evolution · 2023Review
- Depolarization-Dependent C-Raf Signaling Promotes Hyperexcitability and Reduces Opioid Sensitivity of Isolated Nociceptors after Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Evolution of mechanisms and behaviour important for pain.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Article
- Article
- Interleukin-6 induces nascent protein synthesis in human dorsal root ganglion nociceptors primarily via MNK-eIF4E signaling.Neurobiology of pain (Cambridge, Mass.)Article
- Induction of long-term hyperexcitability by memory-related cAMP signaling in isolated nociceptor cell bodies.Neurobiology of pain (Cambridge, Mass.)Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Injury to sensory neurons causes an increase in the excitability of these cells leading to enhanced action potential generation and a lowering of spike threshold. This type of sensory neuron plasticity occurs across vertebrate and invertebrate species and has been linked to the development of both acute and persistent pain. Injury-induced plasticity in sensory neurons relies on localized changes in gene expression that occur at the level of mRNA translation. Many different translation regulation signalling events have been defined and these signalling events are thought to selectively target subsets of mRNAs. Recent evidence from mice suggests that the key signalling event for nociceptor plasticity is mitogen-activated protein kinase-interacting kinase (MNK) -mediated phosphorylation of eukaryotic translation initiation factor (eIF) 4E. To test the degree to which this is conserved in other species, we used a previously described sensory neuron plasticity model in
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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.