ArticleOncotarget2016
ADAR1 is vital for B cell lineage development in the mouse bone marrow.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 32 citations in OpenAlex.
- Two codes of RNA editing by deamination in human diseases.Experimental & molecular medicine · 2026Review
- A dynamic RNA editing landscape in porcine spleen highlights a post-transcriptional mechanism for immune maturation.Molecular genetics and genomics : MGG · 2026Article
- The context-dependent role of the dsRNA response in linking A-to-I editing and ADAR to normal hematopoiesis and leukemia.Frontiers in cell and developmental biology · 2026Review
- Increased interferon I signaling, DNA damage response and evidence of T-cell exhaustion in a patient with combined interferonopathy (Aicardi-Goutières Syndrome, AGS) and cohesinopathy (Cornelia de Lange Syndrome, CdLS).Pediatric rheumatology online journal · 2025Article
- RNA editing regulates host immune response and T cell homeostasis in SARS-CoV-2 infection.PloS one · 2024Article
- Do RNA modifications contribute to modulation of immune responses in allergic diseases?Frontiers in allergy · 2023Review
- RNA modifications: importance in immune cell biology and related diseases.Signal transduction and targeted therapy · 2022Review
- Review
- Epitranscriptomics in Normal and Malignant Hematopoiesis.International journal of molecular sciences · 2020Review
- Adenosine-to-inosine RNA editing in the immune system: friend or foe?Cellular and molecular life sciences : CMLS · 2020Review
- Epitranscriptomics in Hematopoiesis and Hematologic Malignancies.Blood cancer discovery · 2020Review
- An internal deletion of ADAR rescued by MAVS deficiency leads to a minute phenotype.Nucleic acids research · 2020Article
- Cell death following the loss of ADAR1 mediated A-to-I RNA editing is not effected by the intrinsic apoptosis pathway.Cell death & disease · 2019Article
- Hyper-Editing of Cell-Cycle Regulatory and Tumor Suppressor RNA Promotes Malignant Progenitor Propagation.Cancer cell · 2019Article
- ADAR1-mediated RNA editing is required for thymic self-tolerance and inhibition of autoimmunity.EMBO reports · 2018Article
- RNA editing by ADAR1 leads to context-dependent transcriptome-wide changes in RNA secondary structure.Nature communications · 2017Article
- RNA-editing enzymes ADAR1 and ADAR2 coordinately regulate the editing and expression of Ctn RNA.FEBS letters · 2017Article
- Gene regulation in the immune system by long noncoding RNAs.Nature immunology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenosine deaminase acting on RNA (ADAR) 1 is the master editor of the transcriptome, catalyzing the conversion of adenosine to inosine (A-to-I). RNA transcripts fold into a variety of secondary structures including long intramolecular RNA duplexes that are the major substrate of ADAR1. Most A-to-I editing sites occur within RNA duplexes formed by complementary pairing of inverted retrotransposable elements interspersed within noncoding regions of transcripts. This catalytic activity of ADAR1 most likely prevents the abnormal activation of cytosolic nucleic acid sensors by self-dsRNAs. Homozygous disruption of mouse Adar is embryonic lethal due to a toxic type-I interferons response and correspondingly biallelic missense mutations in human ADAR1 cause a severe congenital interferonopathy. Here, we report that Cd19-Cre-mediated Adar gene ablation in the mouse causes a significant defect in the final stages of B cell development with an almost complete absence of newly formed immature and CD23+ mature recirculating B cells in the BM. Adar ablation in pre-B cells induced upregulation of typical interferon-stimulated genes (ISGs) and apoptosis upon further maturation. ADAR1 deficiency also inhibited the in vitro, IL-7-mediated, differentiation of BM-derived B cell precursors. In summary, ADAR1 is required, non-redundantly, for normal B lymphopoiesis in the BM and peripheral maintenance.
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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.