ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017
The MNK-eIF4E Signaling Axis Contributes to Injury-Induced Nociceptive Plasticity and the Development of Chronic Pain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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89 citing papers in PubMed, 138 citations in OpenAlex.
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- From nociception in aneural animals to human suffering: toward a comparative biology of pain.The Journal of experimental biology · 2025Review
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- eEF2K regulates pain through translational control of BDNF.Molecular cell · 2025Article
- MNK: A Novel Promising Target for Cancer Immunotherapy.Current medicinal chemistry · 2025Review
- 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
- Persistent changes in nociceptor translatomes govern hyperalgesic priming in mouse models.bioRxiv : the preprint server for biology · 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
- Endoplasmic reticular stress as an emerging therapeutic target for chronic pain: a narrative review.British journal of anaesthesia · 2024Review
29 more citing papers are in PubMed but not listed here.
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18 authors at 6 institutions in 5 countries.
Funding
Abstract
Injury-induced sensitization of nociceptors contributes to pain states and the development of chronic pain. Inhibiting activity-dependent mRNA translation through mechanistic target of rapamycin and mitogen-activated protein kinase (MAPK) pathways blocks the development of nociceptor sensitization. These pathways convergently signal to the eukaryotic translation initiation factor (eIF) 4F complex to regulate the sensitization of nociceptors, but the details of this process are ill defined. Here we investigated the hypothesis that phosphorylation of the 5' cap-binding protein eIF4E by its specific kinase MAPK interacting kinases (MNKs) 1/2 is a key factor in nociceptor sensitization and the development of chronic pain. Phosphorylation of ser209 on eIF4E regulates the translation of a subset of mRNAs. We show that pronociceptive and inflammatory factors, such as nerve growth factor (NGF), interleukin-6 (IL-6), and carrageenan, produce decreased mechanical and thermal hypersensitivity, decreased affective pain behaviors, and strongly reduced hyperalgesic priming in mice lacking eIF4E phosphorylation (
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