ReviewCellular and molecular life sciences : CMLS2020
Adenosine-to-inosine RNA editing in the immune system: friend or foe?
Review in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 56 citations in OpenAlex.
- Differential A-to-I editing of SINE B2 RNAs unveils an epitranscriptome response to Aβ neurotoxicity.Life science alliance · 2026Article
- Neuron-specific deletion of ADAR1 induces brain malformation and early postnatal lethality.Journal of neuroinflammation · 2026Article
- CDIN1-Codanin-1 complex defective in congenital dyserythropoietic anaemia type I is an RNA nuclease.Nature communications · 2026Article
- RNA Aptamers and Epitranscriptomics: Charting Unexplored Territories in RNA Biology.Molecular diagnosis & therapy · 2026Review
- New insight into RNA biomarkers in neuropathic pain: a clinician-neuroscientist roadmap to translational testing and treatment monitoring a clinical review.Frontiers in pain research (Lausanne, Switzerland) · 2026Review
- Deaminase Modulation Driving a New Era in Drug Development.International journal of molecular sciences · 2025Review
- Epitranscriptomic alterations induced by environmental toxins: implications for RNA modifications and disease.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025Review
- Deciphering the mechanistic roles of ADARs in cancer pathogenesis, tumor immune evasion, and drug resistance.Frontiers in immunology · 2025Review
- Advances in A-to-I RNA editing in cancer.Molecular cancer · 2024Review
- ADAR-Mediated A>I(G) RNA Editing in the Genotoxic Drug Response of Breast Cancer.International journal of molecular sciences · 2024Review
- RNA editing and immune control: from mechanism to therapy.Current opinion in genetics & development · 2024Review
- RNA editing enzymes: structure, biological functions and applications.Cell & bioscience · 2024Review
- Recent insights into crosstalk between genetic parasites and their host genome.Briefings in functional genomics · 2024Review
- Human TLR8 induces inflammatory bone marrow erythromyeloblastic islands and anemia in SLE-prone mice.Life science alliance · 2023Article
- Article
- Novel insight into RNA modifications in tumor immunity: Promising targets to prevent tumor immune escape.Innovation (Cambridge (Mass.)) · 2023Review
- Somatic A-to-I RNA-edited RHOA isoform 2 specific-R176G mutation promotes tumor progression in lung adenocarcinoma.Molecular carcinogenesis · 2023Article
- Adenosine deaminase acting on RNA 1 (ADAR1) as crucial regulators in cardiovascular diseases: structures, pathogenesis, and potential therapeutic approach.Frontiers in pharmacology · 2023Review
- The regulation of antiviral innate immunity through non-mFrontiers in immunology · 2023Review
- The involvement of ADAR1 in chronic unpredictable stress-induced cognitive impairment by targeting DARPP-32 with miR-874-3p in BALB/c mice.Frontiers in cell and developmental biology · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Our body expresses sensors to detect pathogens through the recognition of expressed molecules, including nucleic acids, lipids, and proteins, while immune tolerance prevents an overreaction with self and the development of autoimmune disease. Adenosine (A)-to-inosine (I) RNA editing, catalyzed by adenosine deaminases acting on RNA (ADARs), is a post-transcriptional modification that can potentially occur at over 100 million sites in the human genome, mainly in Alu repetitive elements that preferentially form a double-stranded RNA (dsRNA) structure. A-to-I conversion within dsRNA, which may induce a structural change, is required to escape from the host immune system, given that endogenous dsRNAs transcribed from Alu repetitive elements are potentially recognized by melanoma differentiation-associated protein 5 (MDA5) as non-self. Of note, loss-of-function mutations in the ADAR1 gene cause Aicardi-Goutières syndrome, a congenital autoimmune disease characterized by encephalopathy and a type I interferon (IFN) signature. However, the loss of ADAR1 in cancer cells with an IFN signature induces lethality via the activation of protein kinase R in addition to MDA5. This makes cells more sensitive to immunotherapy, highlighting the opposing immune status of autoimmune diseases (overreaction) and cancer (tolerance). In this review, we provide an overview of insights into two opposing aspects of RNA editing that functions as a modulator of the immune system in autoimmune diseases and cancer.
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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.