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RNA-seq and acRIP-seq in NAT10-knockdown PDAC cells

ABSTRACT: RNA-seq and acRIP-seq in NAT10-knockdown PDAC cells

PROVIDER: PRJNA771546 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16352381_1.fastq.gz	Fastqsanger.gz
	SRR16352381_2.fastq.gz	Fastqsanger.gz
	SRR16352382_1.fastq.gz	Fastqsanger.gz
	SRR16352382_2.fastq.gz	Fastqsanger.gz
	SRR16352383_1.fastq.gz	Fastqsanger.gz

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RNA-seq and acRIP-seq in NAT10-knockdown PDAC cells

2025-03-26 | GSE185960 | 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

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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.

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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

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

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

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NAT10 promotes the progression of clear cell renal cell carcinoma by regulating ac4C acetylation of NFE2L3 and activating AKT/GSK3β signaling pathway

Project description:To determine the role of NAT10 in promoting the progression of ccRCC, we performed RNA sequencing (RNA-Seq) and ac4C-modified RNA immunoprecipitation sequencing (acRIP-seq) on four pairs of ccRCC tissues and their adjacent tissues. A comprehensive analysis of acRIP-seq and RNA-seq showed that the expression and acetylation levels of 199 transcripts were increased . We selected 11 candidate genes of interest and analyzed their acetylation levels. Since ac4C modification can improve mRNA stability, the 11 candidate genes were verified, and the results showed that only NFE2L3 mRNA levels decreased in 786-O cells and A498 cells after NAT10 stable knockdown , so we decided to study the mechanism of action of NFE2L3 in ccRCC.

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Identification of NAT10 targets in CRC by RNA immunoprecipitation and acethyl-RNA immunoprecipitation

Project description:To identify potential mRNAs that are acetylated by NAT10, RIP with a NAT10 antibody and acRIP with a ac4C antibody were conducted in DLD-1 and SW480 cells

2022-12-27 | GSE210385 | GEO

N-acetyltransferase NAT10 Controls Cell Fates via RNA Cytidine Acetylation

Project description:We show that NAT10-ac4C axis significantly regulates cell fates. To identify the molecular mechanisms of NAT10-ac4C-ANP32B axis in cell-fate transitions, we construct shNAT10 and shANP32B hESCs. acRIP-seq of shCTR and shNAT10 hESCs. We profiled ATAC-seq in shCTR, shNAT10, and shANP32B hESCs. We profiled H3K4me3 and H3K27me3 modifications and the binding of ANP32B by CUT&Tag in shCTR and shNAT10 hESCs.

2023-11-11 | GSE210504 | GEO

ac4C-seq in NAT10-knockdown PANC-1 cells

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

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The underlying mechanism by which NAT10 exerted carcinogenesis and its potential targets in MM

Project description:An acRIP experiment was performed in KMS28-PE WT and KMS28-PE NAT10-OE cells. We compared the peak summit of KMS28-PE WT and KMS28-PE NAT10 OE cells to find the differences between KMS28-PE WT and KMS28-PE NAT10 OE cells.

2024-06-01 | GSE199524 | GEO

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