Evidence map›Paper›PMID 31815657›Full record

ArticleGenome biology2019

The majority of A-to-I RNA editing is not required for mammalian homeostasis.

Alistair M Chalk, Scott Taylor, Jacki E Heraud-Farlow, Carl R Walkley

Open access · goldAbstract read
In one paragraph

Article in Genome biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

73 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Two codes of RNA editing by deamination in human diseases.Experimental & molecular medicine · 2026
    Review
  7. Article
  8. Article
  9. Review
  10. Advances in RNA modification in myocardial fibrosis (Review).International journal of molecular medicine · 2025
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Phylogenetic and structural analysis of Hydra ADAR.Archives of biochemistry and biophysics · 2025
    Article
  17. Review
  18. Review
  19. Article
  20. Article

13 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

4 authors at 3 institutions in 1 country.

Alistair M ChalkSt. Vincent's Institute of Medical Research, 9 Princes St, Fitzroy, VIC, 3065, Australia.ORCID 0000-0002-9630-6236
Scott TaylorSt. Vincent's Institute of Medical Research, 9 Princes St, Fitzroy, VIC, 3065, Australia.
Jacki E Heraud-FarlowSt. Vincent's Institute of Medical Research, 9 Princes St, Fitzroy, VIC, 3065, Australia. jhfarlow@svi.edu.au.ORCID 0000-0002-3786-8474
Carl R WalkleySt. Vincent's Institute of Medical Research, 9 Princes St, Fitzroy, VIC, 3065, Australia. cwalkley@svi.edu.au.ORCID 0000-0002-4784-9031
The University of Melbourne · AUSt Vincent's Hospital Melbourne · AUSt Vincents Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAdenosine-to-inosine (A-to-I) RNA editing, mediated by ADAR1 and ADAR2, occurs at tens of thousands to millions of sites across mammalian transcriptomes. A-to-I editing can change the protein coding potential of a transcript and alter RNA splicing, miRNA biology, RNA secondary structure and formation of other RNA species. In vivo, the editing-dependent protein recoding of GRIA2 is the essential function of ADAR2, while ADAR1 editing prevents innate immune sensing of endogenous RNAs by MDA5 in both human and mouse. However, a significant proportion of A-to-I editing sites can be edited by both ADAR1 and ADAR2, particularly within the brain where both are highly expressed. The physiological function(s) of these shared sites, including those evolutionarily conserved, is largely unknown.

resultsTo generate completely A-to-I editing-deficient mammals, we crossed the viable rescued ADAR1-editing-deficient animals (Adar1

conclusionsWe conclude that ADAR1 and ADAR2 are non-redundant and do not compensate for each other's essential functions in vivo. Physiologically essential A-to-I editing comprises a small subset of the editome, and the majority of editing is dispensable for mammalian homeostasis. Moreover, in vivo biologically essential protein recoding mediated by A-to-I editing is an exception in mammals.

Indexed as

RNA EditingAdenosine DeaminaseAnimalsBrainFemaleHomeostasisMaleMiceRNA-Binding ProteinsTranscriptomeADAR1 protein, mouseADAR2 protein, mouseAdenosine DeaminaseRNA-Binding ProteinsADAR1ADAR2A-to-I editingEpitranscriptomeRNA editingRNA modification

Identifiers

PMID31815657
PMCPMC6900863
OpenAlexW2995709710

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.