Our research focuses on understanding how cells respond to dangerous RNA species, including endogenous damaged RNA and exogenous virus RNA, under different stress and pathological conditions. Revealing the principles and molecular mechanisms underlying “toxic” RNA response will help gain insights into RNA-related disease mechanisms and identify potential therapeutic targets.
Biomolecules incur damage during stress conditions, and damage partitioning represents a vital survival strategy for cells. We identified a distinct stress granule (SG), marked by dsRNA helicase DHX9, which compartmentalizes ultraviolet (UV)-induced RNA, but not DNA, damage.
Viral RNA triggers innate immune responses. We found that the kinase CSNK1E enhances type I interferon production, whereas the phospholipase PLCB2 suppresses inflammatory responses. Both enzymes are critical for host defense and survival during RNA virus infection.