GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE306nnn/GSE306149/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE306149GEOGSEfalseNAT10 Suppresses RNA Sensing Induced IFN-β Transactivation to Promote Viral Infection via Interfering with IRF3 ActivitiesCells can sense invading viruses and trigger type I interferons (IFN-α/β) to evoke antiviral innate immune response. Induction of IFNs needs to be fine-tuned to achieve the antiviral consequence while avoiding severe disruption of host cell homeostasis. Here, we reported that NAT10, the acetyltransferase of histone and N4-acetylcytidine (ac4C) RNA modification, promotes infection of RNA viruses via regulation of type I IFN signaling. Depletion of NAT10 increased the expression of IFN-β and interferon-stimulated genes (ISGs) upon stimulation of type I IFN antiviral signaling, while it impaired viral replication. NAT10 dynamically associated with the IFN-β promotor and negatively regulated IRF3 through modulation of long non-coding RNAs (lncRNAs) that inhibit IRFs. Consistently, the small molecule inhibitor of NAT10, Remodelin, increased IFN-β expression while inhibiting viral infections. Overall, our findings indicated that NAT10 is a negative regulator of type I IFN signaling, suggesting its potential as a target of antiviral treatment.2026/08/19GSE306149GSM9194094GSM9194104GSM9194103GSM9194105GSM9194100GSM9194099GSM9194102GSM9194101GSM9194096GSM9194095GSM9194098GSM919409724676306149Homo sapiens