{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yan Q"],"funding":["Foundation for the National Institutes of Health","National Natural Science Foundation of China","China Postdoctoral Science Foundation","NCI NIH HHS","Natural Science Foundation of Jiangsu Province"],"pagination":["6327"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10564894"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(1)"],"pubmed_abstract":["N-acetyltransferase 10 (NAT10) is an N<sup>4</sup>-acetylcytidine (ac<sup>4</sup>C) writer that catalyzes RNA acetylation at cytidine N<sup>4</sup> position on tRNAs, rRNAs and mRNAs. Recently, NAT10 and the associated ac<sup>4</sup>C have been reported to increase the stability of HIV-1 transcripts. Here, we show that NAT10 catalyzes ac<sup>4</sup>C addition to the polyadenylated nuclear RNA (PAN), a long non-coding RNA encoded by the oncogenic DNA virus Kaposi's sarcoma-associated herpesvirus (KSHV), triggering viral lytic reactivation from latency. Mutagenesis of ac<sup>4</sup>C sites in PAN RNA in the context of KSHV infection abolishes PAN ac<sup>4</sup>C modifications, downregulates the expression of viral lytic genes and reduces virion production. NAT10 knockdown or mutagenesis eras"],"journal":["Nature communications"],"pubmed_title":["NAT10-dependent N<sup>4</sup>-acetylcytidine modification mediates PAN RNA stability, KSHV reactivation, and IFI16-related inflammasome activation."],"pmcid":["PMC10564894"],"funding_grant_id":["BK20180084","82372243","R01 CA213275","82241067","81730062","81761128003","BK20180681","81902639","82172262","2019TQ0158","31800148","32170151","R01CA213275","2019M661889","81871642","82072275"],"pubmed_authors":["Li W","Ding X","Gao SJ","Yan Q","Ma X","Lu C","Jia X","Wang Z","Zhou J"],"additional_accession":[]},"is_claimable":false,"name":"NAT10-dependent N<sup>4</sup>-acetylcytidine modification mediates PAN RNA stability, KSHV reactivation, and IFI16-related inflammasome activation.","description":"N-acetyltransferase 10 (NAT10) is an N<sup>4</sup>-acetylcytidine (ac<sup>4</sup>C) writer that catalyzes RNA acetylation at cytidine N<sup>4</sup> position on tRNAs, rRNAs and mRNAs. Recently, NAT10 and the associated ac<sup>4</sup>C have been reported to increase the stability of HIV-1 transcripts. Here, we show that NAT10 catalyzes ac<sup>4</sup>C addition to the polyadenylated nuclear RNA (PAN), a long non-coding RNA encoded by the oncogenic DNA virus Kaposi's sarcoma-associated herpesvirus (KSHV), triggering viral lytic reactivation from latency. Mutagenesis of ac<sup>4</sup>C sites in PAN RNA in the context of KSHV infection abolishes PAN ac<sup>4</sup>C modifications, downregulates the expression of viral lytic genes and reduces virion production. NAT10 knockdown or mutagenesis eras","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Oct","modification":"2026-05-29T00:39:46.336Z","creation":"2025-02-18T23:52:45.855Z"},"accession":"S-EPMC10564894","cross_references":{"pubmed":["37816771"],"doi":["10.1038/s41467-023-42135-3"]}}