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Article

ADAR1 interaction with Z-RNA promotes editing of endogenous double-stranded RNA and prevents MDA5-dependent immune activation.

Cell reports - 10 Aug 2021

de Reuver Richard, Dierick Evelien, Wiernicki Bartosz, Staes Katrien, Seys Leen, De Meester Ellen, Muyldermans Tuur, Botzki Alexander, Lambrecht Bart N, Van Nieuwerburgh Filip, Vandenabeele Peter, Maelfait Jonathan

Abstract excerpt

Loss of function of adenosine deaminase acting on double-stranded RNA (dsRNA)-1 (ADAR1) causes the severe autoinflammatory disease Aicardi-Goutières syndrome (AGS). ADAR1 converts adenosines into inosines within dsRNA. This process called A-to-I editing masks self-dsRNA from detection by the antiviral dsRNA sensor MDA5. ADAR1 binds to dsRNA in both the canonical A-form and the poorly defined Z conformation...

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Share to Adenosine Deaminase
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Immunity

Share to Interferon-Induced Helicase, IFIH1

Share to Interferon Type I

Share to RNA, Double-Stranded

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Source

Identifiers

PMID: 34380029
DOI: 10.1016/j.celrep.2021.109500

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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ADAR1 interaction with Z-RNA promotes editing of endogenous double-stranded RNA and prevents MDA5-dependent immune activation.PMID 34380029Read ↗

ADAR1 interaction with Z-RNA promotes editing of endogenous double-stranded RNA and prevents MDA5-dependent immune activationSemantic proximity Read ↗

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