ArticleRNA (New York, N.Y.)2023
Site-directed A → I RNA editing as a therapeutic tool: moving beyond genetic mutations.
Article in RNA (New York, N.Y.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- A-to-I RNA editing remodels 5'-UTR initiation codons to tune translational output.Scientific reports · 2026Article
- Improved RNA base editing with guide RNAs mimicking highly edited endogenous ADAR substrates.Nature biotechnology · 2026Article
- Discovery and Tuning of RNA Editing Guides via High-Throughput Screening and Chemical Modification.Chembiochem : a European journal of chemical biology · 2025Article
- Control of ADAR2 Dimerization and RNA Editing Efficiency by Site-Specific 2'-Fluoro Modification of Guide RNAs.ACS chemical biology · 2025Article
- Filamin A editing in myeloid cells reduces intestinal inflammation and protects from colitis.The Journal of experimental medicine · 2025Article
- Emerging clinical applications of ADAR based RNA editing.Stem cells translational medicine · 2025Review
- Harnessing RNA base editing for diverse applications in RNA biology and RNA therapeutics.Advanced biotechnology · 2025Review
- Precise in vivo RNA base editing with a wobble-enhanced circular CLUSTER guide RNA.Nature biotechnology · 2025Article
- En masse evaluation of RNA guides (EMERGe) for ADARs.Methods in enzymology · 2025Article
- LoDEI: a robust and sensitive tool to detect transcriptome-wide differential A-to-I editing in RNA-seq data.Nature communications · 2024Article
- Structural perspectives on adenosine to inosine RNA editing by ADARs.Molecular therapy. Nucleic acids · 2024Review
- Unveiling the A-to-I mRNA editing machinery and its regulation and evolution in fungi.Nature communications · 2024Article
- Structural and functional effects of inosine modification in mRNA.RNA (New York, N.Y.) · 2024Article
- The role of ADAR1 through and beyond its editing activity in cancer.Cell communication and signaling : CCS · 2024Review
- Engineered deaminases as a key component of DNA and RNA editing tools.Molecular therapy. Nucleic acids · 2023Review
- Chemical Modifications in RNA: Elucidating the Chemistry of dsRNA-Specific Adenosine Deaminases (ADARs).Accounts of chemical research · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Adenosine deamination by the ADAR family of enzymes is a natural process that edits genetic information as it passes through messenger RNA. Adenosine is converted to inosine in mRNAs, and this base is interpreted as guanosine during translation. Realizing the potential of this activity for therapeutics, a number of researchers have developed systems that redirect ADAR activity to new targets, ones that are not normally edited. These site-directed RNA editing (SDRE) systems can be broadly classified into two categories: ones that deliver an antisense RNA oligonucleotide to bind opposite a target adenosine, creating an editable structure that endogenously expressed ADARs recognize, and ones that tether the catalytic domain of recombinant ADAR to an antisense RNA oligonucleotide that serves as a targeting mechanism, much like with CRISPR-Cas or RNAi. To date, SDRE has been used mostly to try and correct genetic mutations. Here we argue that these applications are not ideal SDRE, mostly because RNA edits are transient and genetic mutations are not. Instead, we suggest that SDRE could be used to tune cell physiology to achieve temporary outcomes that are therapeutically advantageous, particularly in the nervous system. These include manipulating excitability in nociceptive neural circuits, abolishing specific phosphorylation events to reduce protein aggregation related to neurodegeneration or reduce the glial scarring that inhibits nerve regeneration, or enhancing G protein-coupled receptor signaling to increase nerve proliferation for the treatment of sensory disorders like blindness and deafness.
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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.