ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2022
Inhibitions and Down-Regulation of Motor Protein Eg5 Expression in Primary Sensory Neurons Reveal a Novel Therapeutic Target for Pathological Pain.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Microtubule Cytoskeleton Dysfunction in Chronic Pain: Mechanisms of Transport Failure and Emerging Therapeutic Targets.International journal of molecular sciences · 2026Review
- Kinesins in Cancer Drug Resistance: Mechanisms, Therapeutic Targeting, and Translational Potential.Cancers · 2026Review
- Insights into KIF11 pathogenesis in microcephaly-lymphedema-chorioretinopathy syndrome from a lymphatic perspective.JCI insight · 2026Article
- Paclitaxel neurotoxicity is triggered by epidermal EG5-dependent microtubule fasciculation and X-ROS formation.Research square · 2025Article
- Mitotic Functions and Characters of KIF11 in Cancers.Biomolecules · 2024Review
- KIF11 promotes vascular smooth muscle cell proliferation by regulating cell cycle progression and accelerates neointimal formation after arterial injury in mice.Frontiers in pharmacology · 2024Article
- Kinesin-5 inhibition improves neural regeneration in experimental autoimmune neuritis.Journal of neuroinflammation · 2023Article
- Chemokine receptor CXCR2 in primary sensory neurons of trigeminal ganglion mediates orofacial itch.Frontiers in molecular neuroscience · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The motor protein Eg5, known as kif11 or kinesin-5, interacts with adjacent microtubules in the mitotic spindle and plays essential roles in cell division, yet the function of Eg5 in mature postmitotic neurons remains largely unknown. In this study, we investigated the contribution and molecular mechanism of Eg5 in pathological pain. Pharmacological inhibition of Eg5 and a specific shRNA-expressing viral vector reversed complete Freund's adjuvant (CFA)-induced pain and abrogated vanilloid receptor subtype 1 (VR1) expression in dorsal root ganglion (DRG) neurons. In the dorsal root, Eg5 inhibition promoted VR1 axonal transport and decreased VR1 expression. In the spinal cord, Eg5 inhibition suppressed VR1 expression in axon terminals and impaired synapse formation in superficial laminae I/II. Finally, we showed that Eg5 is necessary for PI3K/Akt signalling-mediated VR1 membrane trafficking and pathological pain. The present study provides compelling evidence of a noncanonical function of Eg5 in primary sensory neurons. These results suggest that Eg5 may be a potential therapeutic target for intractable pain.
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Registered trials
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