ReviewInternational journal of molecular sciences2022
Emerging Roles for the RNA-Binding Protein HuD (ELAVL4) in Nervous System Diseases.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 17 citations in OpenAlex.
- ELAVL Proteins, miRNA Fate, and Extracellular RNA Communication in Brain Aging and Neurodegeneration.Cells · 2026Review
- The RNA-Binding Protein ELAVL4/HuD Promotes Stress-Associated Tumor Survival in Neuroendocrine Cancers.International journal of molecular sciences · 2026Review
- Transcriptomic Analysis ofInternational journal of molecular sciences · 2026Article
- Transcriptomic Analysis ofbioRxiv : the preprint server for biology · 2026Article
- Distinct proteomic CSF profiles in genetic frontotemporal lobar degeneration.Brain : a journal of neurology · 2026Article
- Article
- Protein Predictors of Worsening Cerebral Edema in Traumatic Brain Injury in Critically Ill Patients.bioRxiv : the preprint server for biology · 2026Article
- Playing both sides - Epstein-Barr Virus accumulates select cellular transcripts to counter virus-mediated host shut-off in lytic cells.PLoS pathogens · 2026Article
- MYCN inhibits TrkC-mediated differentiation in neuroblastoma cells via disruption of the PKA signalling pathway.Cell death discovery · 2026Article
- Article
- MicroRNAs and Long Non-Coding RNAs Affect the Mechanisms Involved in Age-Related Neurodegeneration in a Manner Depending on RNA-Binding Proteins.Molecular neurobiology · 2026Review
- Context-tuned strategies for marker selection precision in neuronal studies.Frontiers in neuroscience · 2026Review
- ELAV/Hu RNA-binding protein family: key regulators in neurological disorders, cancer, and other diseases.RNA biology · 2025Review
- Evidence of Involvement of the Calcitonin Gene-Related Peptide in Restless Legs Syndrome.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- The Role of Tau in Neuronal Function and Neurodegeneration.Neurology international · 2025Review
- The Antidepressant Effect of Resveratrol Is Related to Neuroplasticity Mediated by the ELAVL4-International journal of molecular sciences · 2025Article
- HuD impairs neuromuscular junctions and induces apoptosis in human iPSC and Drosophila ALS models.Nature communications · 2024Article
- Neurodegeneration: can metabolites fromFrontiers in pharmacology · 2024Article
- The molecular genetics of nELAVL in brain development and disease.European journal of human genetics : EJHG · 2023Review
- Short- and Long-Term Regulation of HuD: A Molecular Switch Mediated by Folic Acid?International journal of molecular sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The main goal of this review is to provide an updated overview of the involvement of the RNA-binding protein (RBP) HuD, encoded by the ELAVL4 gene, in nervous system development, maintenance, and function, and its emerging role in nervous system diseases. A particular focus is on recent studies reporting altered HuD levels, or activity, in disease models and patients. Substantial evidence suggests HuD involvement in Parkinson's disease (PD), Alzheimer's disease (AD), and amyotrophic lateral sclerosis (ALS). Interestingly, while possible disease-causing mutations in the ELAVL4 gene remain elusive, a common theme in these diseases seems to be the altered regulation of HuD at multiple steps, including post-transcriptional and post-translational levels. In turn, the changed activity of HuD can have profound implications for its target transcripts, which are overly stabilized in case of HuD gain of function (as proposed in PD and ALS) or reduced in case of decreased HuD binding (as suggested by some studies in AD). Moreover, the recent discovery that HuD is a component of pathological cytoplasmic inclusion in both familial and sporadic ALS patients might help uncover the common molecular mechanisms underlying such complex diseases. We believe that deepening our understanding of the involvement of HuD in neurodegeneration could help developing new diagnostic and therapeutic tools.
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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.