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- W4387343457 abstract "Effective immunity requires the innate immune system to distinguish foreign nucleic acids from cellular ones. Cellular double-stranded RNAs (dsRNAs) are edited by the RNA-editing enzyme ADAR1 to evade being recognized as viral dsRNA by cytoplasmic dsRNA sensors, including MDA5 and PKR. The loss of ADAR1-mediated RNA editing of cellular dsRNA activates MDA5. Additional RNA-editing-independent functions of ADAR1 have been proposed, but a specific mechanism has not been delineated. We now demonstrate that the loss of ADAR1-mediated RNA editing specifically activates MDA5, whereas loss of the cytoplasmic ADAR1p150 isoform or its dsRNA-binding activity enabled PKR activation. Deleting both MDA5 and PKR resulted in complete rescue of the embryonic lethality of Adar1p150−/− mice to adulthood, contrasting with the limited or no rescue by removing MDA5 or PKR alone. Our findings demonstrate that MDA5 and PKR are the primary in vivo effectors of fatal autoinflammation following the loss of ADAR1p150." @default.
- W4387343457 created "2023-10-05" @default.
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- W4387343457 date "2023-10-01" @default.
- W4387343457 modified "2023-10-07" @default.
- W4387343457 title "ADAR1p150 prevents MDA5 and PKR activation via distinct mechanisms to avert fatal autoinflammation" @default.
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- W4387343457 doi "https://doi.org/10.1016/j.molcel.2023.09.018" @default.
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