ADAR1 entraps sinister cellular dsRNAs, thresholding antiviral responses

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 e...

Full description

Saved in:
Bibliographic Details
Published in:Trends in immunology 2021-11, Vol.42 (11), p.953-955
Main Authors: Keegan, Liam P., Vukić, Dragana, O’Connell, Mary A.
Format: Article
Language:English
Subjects:
Adenosine
Adenosine Deaminase - genetics
Adenosine Deaminase - metabolism
Animals
Antiviral Agents
Antiviral drugs
Autoimmune Diseases of the Nervous System - genetics
CRISPR
Double-stranded RNA
Dystonia
Encephalopathy
Humans
Interferon
Kinases
Lung cancer
Mice
Mutation
Proteins
RNA Editing
RNA, Double-Stranded
Sensors
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:1471-4906
1471-4981
DOI:10.1016/j.it.2021.09.013