ArticleProceedings of the National Academy of Sciences of the United States of America2005
Neuronal ELAV proteins enhance mRNA stability by a PKCalpha-dependent pathway.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 128 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
- Neuronal protein Sex-lethal modulates tRNA synthesis via the polymerase III subunit Polr3E in male Drosophila neurons.PLoS biology · 2026Article
- Article
- HuD and alpha-crystallin A axis protects neuro-retinal cells in early diabetes.Molecular and cellular biochemistry · 2025Article
- ELAV/Hu RNA-binding protein family: key regulators in neurological disorders, cancer, and other diseases.RNA biology · 2025Review
- The quantitative impact of 3'UTRs on gene expression.Nucleic acids research · 2025Article
- Article
- Association of Apolipoprotein E4-related Microvascular Disease in the Alzheimer's Disease Hippocampal CA1 Stratum Radiatum.Neuroscience · 2023Article
- Short- and Long-Term Regulation of HuD: A Molecular Switch Mediated by Folic Acid?International journal of molecular sciences · 2023Article
- The Labyrinthine Landscape of APP Processing: State of the Art and Possible Novel Soluble APP-Related Molecular Players in Traumatic Brain Injury and Neurodegeneration.International journal of molecular sciences · 2023Article
- Bryostatin-1: a promising compound for neurological disorders.Frontiers in pharmacology · 2023Review
- Emerging Roles for the RNA-Binding Protein HuD (ELAVL4) in Nervous System Diseases.International journal of molecular sciences · 2022Review
- A critical developmental window for ELAV/Hu-dependent mRNA signatures at the onset of neuronal differentiation.Cell reports · 2022Article
- HIV Promotes Neurocognitive Impairment by Damaging the Hippocampal Microvessels.Molecular neurobiology · 2022Article
- Bryostatin Placebo-Controlled Trials Indicate Cognitive Restoration Above Baseline for Advanced Alzheimer's Disease in the Absence of Memantine1.Journal of Alzheimer's disease : JAD · 2022Article
- PKCε Activation Restores Loss of PKCε, Manganese Superoxide Dismutase, Vascular Endothelial Growth Factor, and Microvessels in Aged and Alzheimer's Disease Hippocampus.Frontiers in aging neuroscience · 2022Article
- Review
- ELAV Proteins Bind and Stabilize C/EBP mRNA in the Induction of Long-Term Memory inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Sovateltide (IRL-1620) activates neuronal differentiation and prevents mitochondrial dysfunction in adult mammalian brains following stroke.Scientific reports · 2020Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
More than 1 in 20 human genes bear in the mRNA 3' UTR a specific motif called the adenine- and uridine-rich element (ARE), which posttranscriptionally determines its expression in response to cell environmental signals. ELAV (embryonic lethal abnormal vision) proteins are the only known ARE-binding factors that are able to stabilize the bound mRNAs, thereby positively controlling gene expression. Here, we show that in human neuroblastoma SH-SY5Y cells, neuron-specific ELAV (nELAV) proteins (HuB, HuC, and HuD) are up-regulated and redistributed by 15 min of treatment with the activators of PKC phorbol esters and bryostatin-1. PKC stimulation also induces nELAV proteins to colocalize with the translocated PKCalpha isozyme preferentially on the cytoskeleton, with a concomitant increase of nELAV threonine phosphorylation. The same treatment promotes stabilization of growth-associated protein 43 (GAP-43) mRNA, a well known nELAV target, and induces an early increase in GAP-43 protein concentration, again only in the cytoskeletal cell fraction. Genetic or pharmacological inactivation of PKCalpha abolishes nELAV protein cytoskeletal up-regulation, GAP-43 mRNA stabilization, and GAP-43 protein increase, demonstrating the primary role of this specific PKC isozyme in the cascade of nELAV recruitment. Finally, in vivo PKC activation is associated with an up-regulation of nELAV proteins in the hippocampal rat brain. These findings suggest a model for gene expression regulation by nELAV proteins through a PKCalpha-dependent pathway that is relevant for the cellular programs in which ARE-mediated control plays a pivotal role.
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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.