Similar Datasets
Project description:ac4C transcriptomes of Zebrafish and Worm
| PRJNA1130538 | ENA
Project description:NAT10-catalyzed N4-acetylcytidine (ac4C) has emerged as a vital post-transcriptional modulator on the coding transcriptome by promoting mRNA stability. To explore the transcriptome-wide profile of ac4C modification, we mapped the locations of ac4C modification on wild-type (WT) hESCs and NAT10 KD hESCs by NaCNBH3-based chemical ac4C sequencing (ac4C-seq).
2023-08-25 | GSE226747 | GEO
Project description:NAT10-catalyzed N4-acetylcytidine (ac4C) has emerged as a vital post-transcriptional modulator on the coding transcriptome by promoting mRNA stability. To explore the transcriptome-wide profile of ac4C modification, we mapped the locations of ac4C modification on wild-type (WT) hESCs and NAT10 KD hESCs by high-throughput ac4C RNA immunoprecipitation sequencing (ac4C-RIP-seq).
2023-08-25 | GSE226748 | GEO
Project description:RNA modification play vital roles in renal fibrosis. However, whether ac4C modification functions in renal fibrogenesis remains unknown. Here, we found that NAT10-ac4C axis plays pro—fibrotic role in kidney. ac4C RIP sequencing demonstrated NAT10-ac4C axis functions via regulating multiple master genes of exosome secretion in tubular epithelial cells. In summary, targeting NAT10-ac4C axis is a promising strategy for renal fibrosis.
2024-11-30 | GSE248203 | GEO
Project description:As a newly identified mRNA modification, the regulation of ac4C remains largely unexplored. RNA-binding proteins (RBPs) that specifically binds to ac4C modification and mediate downstream cellular activities (readers) have not been reported yet. We synthesized acetylated and non-acetylated RNA probes by in vitro transcription. The sequences of the probes were segments of FUS and 18s rRNA, which contain ac4C sites as reported. A biotin-RNA pulldown assay and mass spectrometry were performed with HEK 293T cell lysates.
2021-07-20 | PXD027014 | Pride
Project description:Pancreatic cancer is a lethal diease with high tendency of metastasis. Howerver, the mechanisms of pancreatic cancer are sitill unclear. To explore the roles of N4-acetylation (ac4C) RNA modification and its involved N-Acetyltransferase 10 (NAT10) in pancreatic ductal adenocarcinoma (PDAC), we performed profiling by high throughput sequencing. In this study, we investigate the effects of NAT10 knockdown on N4-acetylcytidine (ac4C) modification in mRNA within PANC-1 cells using ac4C-seq. By employing RNA interference to specifically knock down NAT10 expression in PANC-1 cells, we aim to elucidate its impact on ac4C RNA modifications, which have been implicated in various cellular processes and cancer progression. Total RNA was extracted and mRNA was captured and treated with sodium borohydride (NaBH4) for detection of ac4C sites.Following library preparation, sequencing was performed on an Illumina Novaseq 6000 platform. Bioinformatics analyses identified significant changes in ac4C modification patterns due to NAT10 depletion. This dataset provides a valuable resource for further exploration of ac4C modifications in mRNA and their role in PDAC.
2025-03-26 | GSE275963 | GEO
Project description:Hepatocellular carcinoma (HCC) is characterized by high morbidity and mortality, withlimited effective treatment options. NAT10 is the only known acetyltransferase formRNA ac4C modification and is recognized as a biomarker for HCC, promoting itsprogression. However, the critical role of NAT10 in hepatocarcinogenesis remains tobe fully elucidated, and the identification of suitable small-molecule inhibitors targetingNAT10 is of great interest. Here, we report that NAT10 promotes HCC progression bystabilizing SMAD3 mRNA through ac4C modification. Clinically, NAT10 is highlyexpressed in HCC tissues and is significantly associated with poor prognosis.Functionally, NAT10 downregulation inhibits HCC cell proliferation, invasion, andepithelial-mesenchymal transition (EMT), while promoting anoikis in vitro.Additionally, NAT10 depletion significantly impairs tumor growth, metastasis, andhepatocarcinogenesis in vivo. Mechanistically, NAT10 enhances oncogene SMAD3mRNA stability via ac4C modification, thereby activating TGF-β signaling pathway.We also identify a novel small-molecule inhibitor, NAT10-2023, which effectivelyblocks NAT10 activity. Notably, NAT10-2023 treatment significantly reducesintracellular RNA ac4C modification levels and disrupts NAT10-RNA interactions,leading to suppressed tumor progression. Overall, NAT10 drives HCC progression viaSMAD3 mRNA stability regulation and NAT10-2023 could be a promising therapeuticcandidate for targeting NAT10 in cancer treatment.
2026-05-18 | GSE297856 | GEO
Project description:Hepatocellular carcinoma (HCC) is characterized by high morbidity and mortality, withlimited effective treatment options. NAT10 is the only known acetyltransferase formRNA ac4C modification and is recognized as a biomarker for HCC, promoting itsprogression. However, the critical role of NAT10 in hepatocarcinogenesis remains tobe fully elucidated, and the identification of suitable small-molecule inhibitors targetingNAT10 is of great interest. Here, we report that NAT10 promotes HCC progression bystabilizing SMAD3 mRNA through ac4C modification. Clinically, NAT10 is highlyexpressed in HCC tissues and is significantly associated with poor prognosis.Functionally, NAT10 downregulation inhibits HCC cell proliferation, invasion, andepithelial-mesenchymal transition (EMT), while promoting anoikis in vitro.Additionally, NAT10 depletion significantly impairs tumor growth, metastasis, andhepatocarcinogenesis in vivo. Mechanistically, NAT10 enhances oncogene SMAD3mRNA stability via ac4C modification, thereby activating TGF-β signaling pathway.We also identify a novel small-molecule inhibitor, NAT10-2023, which effectivelyblocks NAT10 activity. Notably, NAT10-2023 treatment significantly reducesintracellular RNA ac4C modification levels and disrupts NAT10-RNA interactions,leading to suppressed tumor progression. Overall, NAT10 drives HCC progression viaSMAD3 mRNA stability regulation and NAT10-2023 could be a promising therapeuticcandidate for targeting NAT10 in cancer treatment.
2026-05-18 | GSE297009 | GEO
Project description:RNA modification represents an important post-transcriptional regulatory mechanism in acute myeloid leukemia (AML), however the function and mechanism of RNA acetylation ac4C in AML remains elusive. Here, we report that NAT10, as the ac4C writing enzyme, plays a critical oncogenic function in AML and represents a promising therapeutic target for AML. To understand the mechanisms underlying the function of NAT10 as an RNA ac4C writer in AML, we profiled ac4C modification in the transcriptome of MOLM13 cells using a refined ac4C RNA immunoprecipitation and high throughput sequencing (RacRIP-seq) protocol, and performed systematic calibration with a modification-free control library generated from the in vitro- transcribed MOLM13 transcriptome (referred to as IVT control) to eliminate most of the false- positive signals. We also applied the RacRIP-seq in NAT10 knockdown and control MOLM13 cells to characterize NAT10 targets.
2024-08-26 | GSE246505 | GEO
Project description:chemical ac4C sequencing (ac4C-seq) to identify mRNA ac4C sites
| PRJNA941322 | ENA