ArticleJournal of molecular histology2015
Expression profile of aminoacyl-tRNA synthetases in dorsal root ganglion neurons after peripheral nerve injury.
Article in Journal of molecular histology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed, 5 citations in OpenAlex.
- Quantitative BONCAT Allows Identification of Newly Synthesized Proteins after Optic Nerve Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Aminoacyl-tRNA Synthetases: On Anti-Synthetase Syndrome and Beyond.Frontiers in immunology · 2022Review
- A novel therapeutic target for peripheral nerve injury-related diseases: aminoacyl-tRNA synthetases.Neural regeneration research · 2015Article
- Aminoacyl tRNA synthetases and their relationships with peripheral nerve degeneration and regeneration.Neural regeneration research · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aminoacyl-tRNA synthetases (AminoARSs) are essential enzymes involved in acylating tRNA with amino acids. In addition to the typical functions of AminoARSs, various non-canonical functions have been reported, such as involvement in cellular regulatory processes and signal transduction. Here, to explore the cellular changes in sensory neurons after nerve injury, we evaluated AARS mRNA expression in rat dorsal root ganglia (DRG) neurons using AminoARS-specific primers. Of 20 AminoARSs, we found that expression of lysyl-tRNA synthetase (KARS) and glutaminyl-tRNA synthetase (QARS) was decreased in the DRG injured side. We observed decreased KARS and QARS expression in DRG neuronal cell bodies, but not in satellite cells. Therefore, we suggest the possibility that KARS and QARS may act as signaling molecules to transfer abnormal sensory signals to the spinal dorsal horn after peripheral nerve damage. Therefore, KARS and QARS may represent powerful pharmaceutical targets via control of their non-canonical functions.
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