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ABSTRACT: ac4C RIP

PROVIDER: PRJNA1082548 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR28178068_1.fastq.gz	Fastqsanger.gz
	SRR28178068_2.fastq.gz	Fastqsanger.gz
	SRR28178069_1.fastq.gz	Fastqsanger.gz
	SRR28178069_2.fastq.gz	Fastqsanger.gz
	SRR28178070_1.fastq.gz	Fastqsanger.gz

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Project description:ac4C RIP-seq

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ac4C-RIP-seq to identify mRNA ac4C peaks

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

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

ac4C-RIP-seq to identify mRNA ac4C peaks

Project description:ac4C-RIP-seq to identify mRNA ac4C peaks

| PRJNA941324 | ENA

Ac4c modifications down-regulation in macrophages promotes suppressive tumor microenvironment in HCC (RIP-Seq)

Project description:Ac4C-binding RNAs were analyzed by imprinting RNA-sequencing of anti-Ac4C antibody-retrieved complexes from macrophages lysate. We then performed gene expression profiling analysis using data obtained from RIP-seq of peritoneal macrophages incubated with IFN-G

2024-01-31 | GSE227526 | GEO

Dysregulated ac4C modification of mRNA in a mouse model of early stage Alzheimer's disease [acRIP-seq]

Project description:In this study, ac4C modifications in mRNA were investigated using three-month-old 5×FAD transgenic mice, a widely recognized model of Alzheimer's disease, along with age- and sex-matched wild-type (WT) controls. To elucidate the role of ac4C-modified mRNA in AD, we employed three analytical techniques: acetylated RNA immunoprecipitation sequencing (ac4C-RIP-seq), RNA sequencing (RNA-seq), and proteomic analysis. The first two were used to identify mRNAs carrying ac4C modifications and to quantify mRNA abundance, respectively.

2024-11-12 | GSE281676 | GEO

Dysregulated ac4C modification of mRNA in a mouse model of early stage Alzheimer's disease [mRNA-seq]

2024-11-12 | GSE281343 | GEO

Dysregulated ac4C modification of mRNA in a mouse model of early stage Alzheimer's disease.

Project description:In this study, ac4C modifications in mRNA were investigated using six-month-old 5×FAD transgenic mice, a widely recognized model of Alzheimer's disease, along with age- and sex-matched wild-type (WT) controls. To elucidate the role of ac4C-modified mRNA in AD, we employed three analytical techniques: acetylated RNA immunoprecipitation sequencing (ac4C-RIP-seq), RNA sequencing (RNA-seq), and proteomic analysis. The first two were used to identify mRNAs carrying ac4C modifications and to quantify mRNA abundance, respectively.

2025-01-02 | GSE285655 | GEO

Dysregulated ac4C modification of mRNA in a mouse model of early stage Alzheimer's disease [RNA-seq]

2025-01-11 | GSE286035 | GEO

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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