ADAR1 entraps sinister cellular dsRNAs, thresholding antiviral responses
Language English Country Great Britain, England Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
34642093
DOI
10.1016/j.it.2021.09.013
PII: S1471-4906(21)00204-0
Knihovny.cz E-resources
- MeSH
- Adenosine Deaminase * genetics metabolism MeSH
- Antiviral Agents MeSH
- Autoimmune Diseases of the Nervous System * genetics MeSH
- RNA, Double-Stranded MeSH
- RNA Editing MeSH
- Humans MeSH
- Mice MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- ADAR1 protein, mouse MeSH Browser
- Adenosine Deaminase * MeSH
- Antiviral Agents MeSH
- RNA, Double-Stranded MeSH
ADAR1 edits adenosines to inosines in cellular double-stranded (ds)RNA, thereby preventing aberrant activation of antiviral dsRNA sensors, as well as interferon (IFN) induction in Aicardi-Goutières syndrome (AGS) encephalopathy. Recently, Nakahama et al., Tang et al., Maurano et al., and de Reuver et al. demonstrated that Adar1 Zα domain-mutant mice show aberrant MDA5 and PKR activation, developing encephalopathies; short Z-RNA patches within cellular dsRNA are unexpectedly crucial in causing aberrant antiviral responses.
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