ArticleFrontiers in molecular neuroscience2017
Regulation of Adult CNS Axonal Regeneration by the Post-transcriptional Regulator Cpeb1.
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- The RNA-binding protein CPEB1 marks healthy adult β cells in mice but is dispensable for β cell identity and function.Scientific reports · 2025Article
- Characterization of the Expressions and m6A Methylation Modification Patterns of mRNAs and lncRNAs in a Spinal Cord Injury Rat Model.Molecular neurobiology · 2025Article
- Disruption of Neuromuscular Junction Following Spinal Cord Injury and Motor Neuron Diseases.International journal of molecular sciences · 2024Review
- Clemastine in remyelination and protection of neurons and skeletal muscle after spinal cord injury.Neural regeneration research · 2023Review
- Long-Term Memory Formation inCells · 2023Article
- Insights into nervous system repair from the fruit fly.Neuronal signaling · 2022Review
- Heterozygous ANKRD17 loss-of-function variants cause a syndrome with intellectual disability, speech delay, and dysmorphism.American journal of human genetics · 2021Article
Corrections and comments
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Authors and funding
21 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adult mammalian central nervous system (CNS) neurons are unable to regenerate following axonal injury, leading to permanent functional impairments. Yet, the reasons underlying this regeneration failure are not fully understood. Here, we studied the transcriptome and translatome shortly after spinal cord injury. Profiling of the total and ribosome-bound RNA in injured and naïve spinal cords identified a substantial post-transcriptional regulation of gene expression. In particular, transcripts associated with nervous system development were down-regulated in the total RNA fraction while remaining stably loaded onto ribosomes. Interestingly, motif association analysis of post-transcriptionally regulated transcripts identified the cytoplasmic polyadenylation element (CPE) as enriched in a subset of these transcripts that was more resistant to injury-induced reduction at the transcriptome level. Modulation of these transcripts by overexpression of the CPE binding protein, Cpeb1, in mouse and
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