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Deficiency of m6A RNA methylation promotes ZBP1-mediated cell death

Shuang, L.; Deng, X.; Deepak, P.; Basavaraj, R.; Sun, L.; Cheng, Y.; Li, J.-R.; Burke, M.; Britz, G.; Cheng, C.; Gao, Y.; Weng, Y.-L.

2024-06-30 molecular biology
10.1101/2024.06.29.601251 bioRxiv
Show abstract

m6A RNA methylation suppresses the immunostimulatory potential of endogenous RNA. Deficiency of m6A provokes inflammatory responses and cell death, but the underlying mechanisms remain elusive. Here we showed that the noncoding RNA 7SK gains immunostimulatory potential upon m6A depletion and subsequently activates the RIG-I/MAVS axis to spark interferon (IFN) signaling cascades. Concomitant excess of IFN and m6A deficiency synergistically facilitate the formation of RNA G-quadruplexes (rG4) to promote ZBP1-mediated necroptotic cell death. Collectively, our findings delineate a hitherto uncharacterized mechanism that links m6A dysregulation with ZBP1 activity in triggering inflammatory cell death.

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"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.