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Chemical ac4C sequencing (ac4C-seq) to identify mRNA ac4C sites

ABSTRACT: chemical ac4C sequencing (ac4C-seq) to identify mRNA ac4C sites

PROVIDER: PRJNA941322 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23716160_1.fastq.gz	Fastqsanger.gz
	SRR23716160_2.fastq.gz	Fastqsanger.gz
	SRR23716161_1.fastq.gz	Fastqsanger.gz
	SRR23716161_2.fastq.gz	Fastqsanger.gz
	SRR23716162_1.fastq.gz	Fastqsanger.gz

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chemical ac4C sequencing (ac4C-seq) to identify mRNA ac4C sites

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

ac4C-RIP-seq to identify mRNA ac4C peaks

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

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ac4C-RIP-seq to identify mRNA ac4C peaks

2023-08-25 | GSE226748 | 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

Dysregulated ac4C modification of mRNA in a mouse model of early stage Alzheimer's disease [mRNA-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 | GSE281343 | GEO

Identification of proteins specifically binding to ac4C RNA probes

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

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

| PRJNA837441 | ENA

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

2024-11-12 | GSE281676 | 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.

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NAT10 mediated ac4C tRNA modification promotes EGFR mRNA translation and gefitinib resistance in cancers

Project description:The diverse RNA modifications play essential functions in gene expression regulation. Aberrant RNA modifications are frequently associated with cancers, while the underlying mechanisms and clinical significance remain poorly understood. Here we revealed that the ac4C RNA acetyltransferase NAT10 is significantly upregulated in esophageal cancers (ESCA) and associated with poor ESCA prognosis. In addition, using cancer cell lines, xenograft tumor models, Nat10 conditional knockin and conditional knockout mice, in vivo ESCA tumorigenesis model and chemical inhibition approaches, we uncovered the critical physiological functions of NAT10 in promoting esophageal cancer tumorigenesis and progression in vitro and in vivo. Mechanistically, NAT10 depletion reduced the abundance of ac4C-modified tRNAs and significantly decreased the translation efficiencies of mRNAs enriched for ac4C-modified-tRNA decoded codons. We further identified EGFR as a key downstream target that facilitates NAT10’s oncogenic functions in promoting esophageal cancer progression. In terms of clinical significance, we demonstrated that NAT10 promotes esophageal cancer resistance to EGFR inhibitor gefitinib, and combination of NAT10 depletion and gefitinib treatment synergistically inhibits esophageal cancer progression in vitro and in vivo. Our data uncovered novel molecular mechanisms underlying esophageal cancer progression at the layer of mRNA translation control and provided molecular insights for development of effective cancer therapeutic strategies.

2023-02-16 | GSE225131 | GEO

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