ArticleMolecular neurobiology2023
Posttranscriptional Regulation of Gene Expression Participates in the Myelin Restoration in Mouse Models of Multiple Sclerosis: Antisense Modulation of HuR and HuD ELAV RNA Binding Protein.
Article in Molecular neurobiology, 2023. 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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8 citing papers in PubMed, 14 citations in OpenAlex.
- RNA-binding proteins: a comprehensive review of multifaceted regulatory mechanisms in neuroinflammation and implications in the pathogenesis of neurological disorders.Journal of neuroinflammation · 2026Review
- Protection From Demyelination by the Novel Adenosine Dual AJournal of cellular and molecular medicine · 2025Article
- Outer radial glia promotes white matter regeneration after neonatal brain injury.Cell reports. Medicine · 2025Article
- Fluoride Exposure Increases the Activity of the Cystine/Glutamate Exchanger in Glia Cells.Neurochemical research · 2025Article
- The Antidepressant Effect of Resveratrol Is Related to Neuroplasticity Mediated by the ELAVL4-International journal of molecular sciences · 2025Article
- Temporal changes of spinal microglia in murine models of neuropathic pain: a scoping review.Frontiers in immunology · 2024Article
- Honokiol-RichAntioxidants (Basel, Switzerland) · 2023Article
- Nucleic acid-based therapeutics for the treatment of central nervous system disorders.Frontiers in genetics · 2023Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain is the most difficult-to-treat pain syndrome in multiple sclerosis. Evidence relates neuropathic pain to demyelination, which often originates from unresolved neuroinflammation or altered immune response. Posttranscriptional regulation of gene expression might play a fundamental role in the regulation of these processes. The ELAV RNA-binding proteins HuR and HuD are involved in the promotion of inflammatory phenomena and in neuronal development and maintenance, respectively. Thus, the aim of this study was to investigate the role of HuR and HuD in demyelination-associated neuropathic pain in the mouse experimental autoimmune encephalomyelitis (EAE) model. HuR resulted overexpressed in the spinal cord of MOG
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