<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Su K</submitter><funding>Beijing Municipal Natural Science Foundation</funding><funding>National Natural Science Foundation of China</funding><pagination>490</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11468200</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>22(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Aberrant accumulation of R-loops leads to DNA damage, genome instability and even cell death. Therefore, the timely removal of harmful R-loops is essential for the maintenance of genome integrity. Nucleolar R-loops occupy up to 50% of cellular R-loops due to the frequent activation of Pol I transcription. However, the mechanisms involved in the nucleolar R-loop resolution remain elusive. The nucleolar acetyltransferase NAT10 harbors a putative RecD helicase domain (RHD), however, if NAT10 acts in the R-loop resolution is still unknown.&lt;h4>Methods&lt;/h4>NAT10 knockdown cell lines were constructed using CRISPR/Cas9 technology and short hairpin RNA targeting NAT10 mRNA, respectively. The level of R-loops was detected by immunofluorescent staining combined with RNase H treatme</pubmed_abstract><journal>Cell communication and signaling : CCS</journal><pubmed_title>NAT10 resolves harmful nucleolar R-loops depending on its helicase domain and acetylation of DDX21.</pubmed_title><pmcid>PMC11468200</pmcid><funding_grant_id>No. 7212061</funding_grant_id><funding_grant_id>No. 82173024</funding_grant_id><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Jiang Y</pubmed_authors><pubmed_authors>Sun S</pubmed_authors><pubmed_authors>Du X</pubmed_authors><pubmed_authors>Su K</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Zhang C</pubmed_authors><pubmed_authors>Zhao Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>NAT10 resolves harmful nucleolar R-loops depending on its helicase domain and acetylation of DDX21.</name><description>&lt;h4>Background&lt;/h4>Aberrant accumulation of R-loops leads to DNA damage, genome instability and even cell death. Therefore, the timely removal of harmful R-loops is essential for the maintenance of genome integrity. Nucleolar R-loops occupy up to 50% of cellular R-loops due to the frequent activation of Pol I transcription. However, the mechanisms involved in the nucleolar R-loop resolution remain elusive. The nucleolar acetyltransferase NAT10 harbors a putative RecD helicase domain (RHD), however, if NAT10 acts in the R-loop resolution is still unknown.&lt;h4>Methods&lt;/h4>NAT10 knockdown cell lines were constructed using CRISPR/Cas9 technology and short hairpin RNA targeting NAT10 mRNA, respectively. The level of R-loops was detected by immunofluorescent staining combined with RNase H treatme</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2026-07-15T13:11:35.893Z</modification><creation>2025-04-06T12:31:33.735Z</creation></dates><accession>S-EPMC11468200</accession><cross_references><pubmed>39394182</pubmed><doi>10.1186/s12964-024-01869-3</doi></cross_references></HashMap>