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Transcriptomic ac4C profiling in NAT10 knockdown acute myeloid leukemia cells

ABSTRACT: Transcriptomic ac4C profiling in NAT10 knockdown acute myeloid leukemia cells

PROVIDER: PRJNA1033531 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26561600_1.fastq.gz	Fastqsanger.gz
	SRR26561600_2.fastq.gz	Fastqsanger.gz
	SRR26561601_1.fastq.gz	Fastqsanger.gz
	SRR26561601_2.fastq.gz	Fastqsanger.gz
	SRR26561602_1.fastq.gz	Fastqsanger.gz

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Transcriptomic ac4C profiling in NAT10 knockdown acute myeloid leukemia cells

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

Quantitative proteomics analysis of acute myeloid leukemia cells after NAT10 knockdown

Project description:RNA modification represents an important post-transcriptional regulatory mechanism in acute myeloid leukemia (AML). Given that the critical function of ac4C in control RNA translation, we sought to investigate the global impact of ac4C on protein expression. To this end, we conducted tandem mass tag (TMT) labeling and quantitative proteomics in MOLM13 AML cells with or without the ac4c writer NAT10 silencing.

2024-08-26 | PXD055119 | Pride

Transcriptomic profiling in NAT10 knockdown acute myeloid leukemia cells

2024-08-26 | GSE246503 | GEO

ac4C-seq in NAT10-knockdown PANC-1 cells

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

NAT10-ac4C axis promote renal fibrosis

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

NAT10 modulates fatty acid metabolism of palmitate driven MCF7 in ac4C dependent manner

Project description:We show that non-toxic exogenous palmitate uptake in MCF7 cells promotes NAT10 expression and NAT10-dependent ac4C RNA modification. It was previously reported that NAT10 modulates the addition of ac4C on RNA transcripts in normal and cancer conditions. However, no study report the impact of NAT10 in palmitate driven cells. Here we performed RNA immunoprecipitation sequencing (RIP-seq) in palmitate loaded MCF7 knockdown with NAT10 siRNA. Based on the pathways and enrichment landscape identified. We found that ac4C peaks of fatty acid metabolic genes including ELOVL6, ACSL1, ACSL3, ACSL4, ACADSB and ACAT1 were significantly decreased upon knockdown with NAT10 siRNA. Overall, our results revealed the impact of NAT10 as a regulator of fatty acid metabolism in ac4C-dependent manner

2022-08-03 | GSE210017 | GEO

acRIP-seq to identify NAT10 mediates mRNA ac4C modification in colorectal cancer

Project description:We performedacRIP-seq between control CRC cells and CRC cells with NAT10 knockdown to identify NAT10 mediates mRNA ac4C modification

2022-08-19 | GSE202826 | GEO

ac4C-seq in NAT10-knockdown PANC-1 cells

Project description:ac4C-seq in NAT10-knockdown PANC-1 cells

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Transcriptomic profiling in NAT10 knockdown acute myeloid leukemia cells

Project description:Transcriptomic profiling in NAT10 knockdown acute myeloid leukemia cells

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ac4C RIP-seq analysis of AGS cells upon NAT10 knockout.

Project description:N4-acetylcytidine (ac4C), a conserved chemical modification in eukaryotic prokaryotes that is catalyzed by the N-acetyltransferase 10 (NAT10) enzyme, plays a crucial role in promoting mRNA stability and translation. However, the biological function and mechanisms of NAT10-mediated ac4C in human cancer were poorly defined. In order to investigate the regulatory mechanism of NAT10 in gastric cancer, we performed ac4C RIP-seq(acRIP-seq) analysis in AGS cells with NAT10 knockout compared with control in two repeats.

2024-07-07 | GSE180494 | GEO

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