Evidence map›Paper›PMID 36975179›Full record

ArticleEMBO reports2023

The phenotype of the most common human ADAR1p150 Zα mutation P193A in mice is partially penetrant.

Zhen Liang, Alistair M Chalk, Scott Taylor, Ankita Goradia, Jacki E Heraud-Farlow, Carl R Walkley

Open access · greenAbstract read
In one paragraph

Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Mouse models of type I interferonopathies.Human molecular genetics · 2025
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. ADAR1: from basic mechanisms to inhibitors.Trends in cell biology · 2025
    Review
  14. Article
  15. Review
  16. RNA editing and immune control: from mechanism to therapy.Current opinion in genetics & development · 2024
    Review
  17. Article
  18. Review
  19. Review
  20. Review
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

6 authors at 2 institutions in 1 country.

Zhen LiangSt Vincent's Institute of Medical Research, Fitzroy, Vic., Australia.ORCID 0000-0003-1487-1555
Alistair M ChalkSt Vincent's Institute of Medical Research, Fitzroy, Vic., Australia.ORCID 0000-0002-9630-6236
Scott TaylorSt Vincent's Institute of Medical Research, Fitzroy, Vic., Australia.ORCID 0000-0003-3394-1811
Ankita GoradiaSt Vincent's Institute of Medical Research, Fitzroy, Vic., Australia.
Jacki E Heraud-Farlow *St Vincent's Institute of Medical Research, Fitzroy, Vic., Australia.ORCID 0000-0002-3786-8474
Carl R Walkley *St Vincent's Institute of Medical Research, Fitzroy, Vic., Australia.ORCID 0000-0002-4784-9031
The University of Melbourne · AUSt Vincents Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ADAR1 -mediated A-to-I RNA editing is a self-/non-self-discrimination mechanism for cellular double-stranded RNAs. ADAR mutations are one cause of Aicardi-Goutières Syndrome, an inherited paediatric encephalopathy, classed as a "Type I interferonopathy." The most common ADAR1 mutation is a proline 193 alanine (p.P193A) mutation, mapping to the ADAR1p150 isoform-specific Zα domain. Here, we report the development of an independent murine P195A knock-in mouse, homologous to human P193A. The Adar1

Indexed as

RNA, Double-StrandedRNA EditingAdenosine DeaminaseAnimalsChildHumansMiceMutationPhenotypeADAR1 protein, mouseAdenosine DeaminaseRNA, Double-StrandedADAR1A-to-I RNA editingMDA5P193A mutationZα domain

Identifiers

PMID36975179
PMCPMC10157378
OpenAlexW4361190660

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.