Evidence map›Paper›PMID 28913566›Full record

ReviewHuman genetics2017

ADAR RNA editing in human disease; more to it than meets the I.

Angela Gallo, Dragana Vukic, David Michalík, Mary A O'Connell, Liam P Keegan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Human genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
7.5field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

82 citing papers in PubMed, 134 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Phylogenetic and structural analysis of Hydra ADAR.Archives of biochemistry and biophysics · 2025
    Article
  9. Article
  10. mRNA Transcript Variants Expressed in Mammalian Cells.International journal of molecular sciences · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. RNA-Based Therapeutic Technology.International journal of molecular sciences · 2023
    Review
  20. Review

22 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Angela GalloOncohaematology Department, Ospedale Pediatrico Bambino Gesù (IRCCS), Viale di San Paolo, 15, 00146, Rome, Italy.
Dragana VukicCEITEC, Masaryk University, Kamenice 753/5, Pavilion A35, Brno, 62 500, Czech Republic.
David MichalíkCEITEC, Masaryk University, Kamenice 753/5, Pavilion A35, Brno, 62 500, Czech Republic.
Mary A O'ConnellCEITEC, Masaryk University, Kamenice 753/5, Pavilion A35, Brno, 62 500, Czech Republic.
Liam P KeeganCEITEC, Masaryk University, Kamenice 753/5, Pavilion A35, Brno, 62 500, Czech Republic. liam.keegan@ceitec.muni.cz.
Central European Institute of Technology – Masaryk University · CZIstituti di Ricovero e Cura a Carattere Scientifico · ITMasaryk University · CZ

Funding

AIRC IG 17615EU 621368
6 · The paper itself

Abstract

We review the structures and functions of ADARs and their involvements in human diseases. ADAR1 is widely expressed, particularly in the myeloid component of the blood system, and plays a prominent role in promiscuous editing of long dsRNA. Missense mutations that change ADAR1 residues and reduce RNA editing activity cause Aicardi-Goutières Syndrome, a childhood encephalitis and interferonopathy that mimics viral infection and resembles an extreme form of Systemic Lupus Erythmatosus (SLE). In Adar1 mouse mutant models aberrant interferon expression is prevented by eliminating interferon activation signaling from cytoplasmic dsRNA sensors, indicating that unedited cytoplasmic dsRNA drives the immune induction. On the other hand, upregulation of ADAR1 with widespread promiscuous RNA editing is a prominent feature of many cancers and particular site-specific RNA editing events are also affected. ADAR2 is most highly expressed in brain and is primarily required for site-specific editing of CNS transcripts; recent findings indicate that ADAR2 editing is regulated by neuronal excitation for synaptic scaling of glutamate receptors. ADAR2 is also linked to the circadian clock and to sleep. Mutations in ADAR2 could contribute to excitability syndromes such as epilepsy, to seizures, to diseases involving neuronal plasticity defects, such as autism and Fragile-X Syndrome, to neurodegenerations such as ALS, or to astrocytomas or glioblastomas in which reduced ADAR2 activity is required for oncogenic cell behavior. The range of human disease associated with ADAR1 mutations may extend further to include other inflammatory conditions while ADAR2 mutations may affect psychiatric conditions.

Indexed as

Adenosine DeaminaseMental DisordersMutationNervous System DiseasesRNA-Binding ProteinsRNA, Double-StrandedAnimalsHumansMiceMice, Mutant StrainsRNA EditingADAR1 protein, mouseADAR2 protein, mouseADARB1 protein, humanADAR protein, humanAdenosine DeaminaseRNA-Binding ProteinsRNA, Double-Stranded

Identifiers

PMID28913566
OpenAlexW2756441483

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.