Evidence map›Paper›PMID 27893733›Full record

ArticleNature genetics2017

ADARB1 catalyzes circadian A-to-I editing and regulates RNA rhythm.

Hideki Terajima, Hikari Yoshitane, Haruka Ozaki, Yutaka Suzuki, Shigeki Shimba, Shinya Kuroda, Wataru Iwasaki, Yoshitaka Fukada

Abstract read
PubMed Publisher
In one paragraph

Article in Nature genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 86 citations in OpenAlex.

  1. Two codes of RNA editing by deamination in human diseases.Experimental & molecular medicine · 2026
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  13. GluA1 Degradation by Autophagy Contributes to Circadian Rhythm Effects on Cerebral Ischemia Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
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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

8 authors at 2 institutions in 1 country.

Hideki TerajimaDepartment of Biological Sciences, School of Science, The University of Tokyo, Tokyo, Japan.
Hikari YoshitaneDepartment of Biological Sciences, School of Science, The University of Tokyo, Tokyo, Japan.
Haruka OzakiDepartment of Computational Biology, Graduate School of Frontier Sciences, The University of Tokyo, Chiba, Japan.ORCID 0000-0002-1606-2762
Yutaka SuzukiDepartment of Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Chiba, Japan.
Shigeki ShimbaDepartment of Health Science, School of Pharmacy, Nihon University, Chiba, Japan.
Shinya KurodaDepartment of Biological Sciences, School of Science, The University of Tokyo, Tokyo, Japan.
Wataru IwasakiDepartment of Biological Sciences, School of Science, The University of Tokyo, Tokyo, Japan.
Yoshitaka FukadaDepartment of Biological Sciences, School of Science, The University of Tokyo, Tokyo, Japan.
The University of Tokyo · JPNihon University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been proposed that the CLOCK-ARNTL (BMAL1) complex drives circadian transcription of thousands of genes, including Per and Cry family genes that encode suppressors of CLOCK-ARNTL-dependent transcription. However, recent studies demonstrated that 70-80% of circadian-oscillating mRNAs have no obvious rhythms in their de novo transcription, indicating the potential importance of post-transcriptional regulation. Our CLOCK-ChIP-seq analysis identified rhythmic expression of adenosine deaminase, RNA-specific, B1 (Adarb1, also known as Adar2), an adenosine-to-inosine (A-to-I) RNA-editing enzyme. RNA-seq showed circadian rhythms of ADARB1-mediated A-to-I editing in a variety of transcripts. In Adarb1-knockout mice, rhythms of large populations of mRNA were attenuated, indicating a profound impact of ADARB1-mediated A-to-I editing on RNA rhythms. Furthermore, Adarb1-knockout mice exhibited short-period rhythms in locomotor activity and gene expression. These phenotypes were associated with abnormal accumulation of CRY2. The present study identifies A-to-I RNA editing as a key mechanism of post-transcriptional regulation in the circadian clockwork.

Indexed as

AdenosineAdenosine DeaminaseAnimalsAryl Hydrocarbon Receptor Nuclear TranslocatorCircadian RhythmCryptochromesGene Expression RegulationHumansInosineLiverMaleMiceMice, Inbred C57BLMice, KnockoutRNARNA-Binding ProteinsADARB1 protein, humanAdenosineAdenosine DeaminaseArnt protein, mouseAryl Hydrocarbon Receptor Nuclear TranslocatorCry2 protein, mouseCryptochromesInosineRNARNA-Binding Proteins

Identifiers

PMID27893733
OpenAlexW2558378508

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.