ArticleNucleic acids research2012
Neuron-specific ELAV/Hu proteins suppress HuR mRNA during neuronal differentiation by alternative polyadenylation.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed.
- Change of guards: ELAVL proteins switch miRNA export responsibility to regulate differentiation of PC12 cells.RNA biology · 2026Article
- Regulation of gene expression by alternative polyadenylation in health and disease.Nature reviews. Genetics · 2026Review
- ELAV/Hu RNA-binding protein family: key regulators in neurological disorders, cancer, and other diseases.RNA biology · 2025Review
- One RNA-binding protein, many decisions: integrating the transcript life cycle into neuronal regulation.Frontiers in molecular neuroscience · 2025Article
- Dynamic mRNA Stability Buffer Transcriptional Activation During Neuronal Differentiation and Is Regulated by SAMD4A.Journal of cellular physiology · 2025Article
- Phylogenomic instructed target analysis reveals ELAV complex binding to multiple optimally spaced U-rich motifs.Nucleic acids research · 2024Article
- A developmental mechanism to regulate alternative polyadenylation in an adult stem cell lineage.Genes & development · 2024Article
- A Developmental Mechanism to Regulate Alternative Polyadenylation in an Adult Stem Cell Lineage.bioRxiv : the preprint server for biology · 2024Article
- Neuronal RNA processing: cross-talk between transcriptional regulation and RNA-binding proteins.Frontiers in molecular neuroscience · 2024Review
- Regulation of alternative splicing and polyadenylation in neurons.Life science alliance · 2023Review
- Long 3'UTRs predispose neurons to inflammation by promoting immunostimulatory double-stranded RNA formation.Science immunology · 2023Article
- Coordination of alternative splicing and alternative polyadenylation revealed by targeted long read sequencing.Nature communications · 2023Article
- Extension of mRNA poly(A) tails and 3'UTRs during neuronal differentiation exhibits variable association with post-transcriptional dynamics.Nucleic acids research · 2023Article
- 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.Molecular neurobiology · 2023Article
- Coordination of Alternative Splicing and Alternative Polyadenylation revealed by Targeted Long-Read Sequencing.bioRxiv : the preprint server for biology · 2023Article
- Regulation and function of alternative polyadenylation in development and differentiation.RNA biology · 2023Review
- A critical developmental window for ELAV/Hu-dependent mRNA signatures at the onset of neuronal differentiation.Cell reports · 2022Article
- Regulation of the Alternative Neural Transcriptome by ELAV/Hu RNA Binding Proteins.Frontiers in genetics · 2022Review
- Analysis of ROQUIN, Tristetraprolin (TTP), and BDNF/miR-16/TTP regulatory axis in late onset Alzheimer's disease.Frontiers in aging neuroscience · 2022Article
- Targeting the RNA-Binding Protein HuR as Potential Thera-Peutic Approach for Neurological Disorders: Focus on Amyo-Trophic Lateral Sclerosis (ALS), Spinal Muscle Atrophy (SMA) and Multiple Sclerosis.International journal of molecular sciences · 2021Review
5 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors.
Funding
Abstract
The ubiquitously expressed RNA-binding protein HuR increases the stability and translation of mRNAs encoding growth regulatory proteins that promote proliferation in a variety of cell types. However, the three neuron-specific ELAV/Hu proteins, HuB, HuC and HuD, while binding to the same types of mRNAs, are required instead for neuronal differentiation, and it becomes difficult to reconcile these contrary functions when all four Hu proteins are expressed in the same neuron. HuR mRNA exists as three alternatively polyadenylated variants, a 1.5-kb testes-specific mRNA isoform, a ubiquitous 2.4-kb isoform and a 6.0-kb isoform that we now show is induced during neuronal differentiation and appears to be neuron-specific. This 6.0-kb neuron-specific mRNA isoform is inherently less stable and produces less HuR protein than the ubiquitous 2.4-kb mRNA. Furthermore, we show that neuronal HuB, HuC and HuD, as well as HuR itself, can bind at the 2.4-kb mRNA polyadenylation site, and when overexpressed can affect alternative polyadenylation to generate an extended HuR 3'-UTR that is translationally suppressed. We propose that the regulation of HuR protein expression by alternative polyadenylation allows neurons to post-transcriptionally regulate mRNAs-encoding factors required for proliferation versus differentiation to facilitate neuronal differentiation.
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