Fig. 6: Schematic model for NAT10-dependent ac4C modification in KSHV reactivation and inflammasome induction. | Nature Communications

Fig. 6: Schematic model for NAT10-dependent ac4C modification in KSHV reactivation and inflammasome induction.

From: NAT10-dependent N4‐acetylcytidine modification mediates PAN RNA stability, KSHV reactivation, and IFI16-related inflammasome activation

Fig. 6

The acetyltransferase NAT10 catalyzes ac4C deposition on KSHV PAN RNA, with acetyl-CoA serving as the acetyl donor. Genetic depletion of NAT10 results in ac4C loss and instability of PAN, preventing the latency-lytic transition of KSHV and virion production. Acetylated PAN may assist NAT10 to better recognize IFI16 mRNA with an unknown sensing mechanism, resulting in increased IFI16 translation efficiency and innate inflammasome induction.

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