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RNA-seq and acRIP-seq in NAT10 overexpression HaCaT cells [RIP-seq]

ABSTRACT: To elucidate the function of the RNA acetyltransferase NAT10 in keratinocytes and its regulatory impact on atopic dermatitis pathogenesis, we conducted RNA-seq and acRIP-seq of HaCaT cells overexpressing NAT10 versus empty-vector controls.

ORGANISM(S): Homo sapiens

PROVIDER: GSE304279 | GEO | 2026/06/09

REPOSITORIES: GEO

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RNA-seq and acRIP-seq in NAT10 overexpression HaCaT cells [RNA-seq]

Project description:To elucidate the function of the RNA acetyltransferase NAT10 in keratinocytes and its regulatory impact on atopic dermatitis pathogenesis, we conducted RNA-seq and acRIP-seq of HaCaT cells overexpressing NAT10 versus empty-vector controls.

2026-06-09 | GSE304278 | 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

NAT10-mediated ac4C-modification exacerbates ferroptosis by stabilizing HMOX1 in Deep vein thrombosis [acRIP-Seq]

Project description:In our study, we aimed to identify the mechanisms closely related to ac4C. Through acRIP-seq analysis, we found that NAT10 enhances the stability of HMOX1 via ac4C modification, which leads to iron overload and lipid peroxides. This forms a positive feedback loop that exacerbates DVT.

2026-01-28 | GSE307103 | GEO

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

Project description:RNA-seq and acRIP-seq in NAT10-knockdown PDAC cells

| PRJNA771546 | ENA

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

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

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

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

NAT10-mediated ac4C RNA acetylation stabilizes CXCL5/DEK mRNA to drive proliferation and metastasis in lung adenocarcinoma [RIP-Seq]

Project description:Investigating the epigenetic mechanisms underlying lung adenocarcinoma (LUAD) through the lens of N4-acetylcytosine (ac4C) modification could innovative cancer treatment strategies and targets. We used biological information methods to analyze shared data, with a focus on studying N-acetyltransferase 10 (NAT10), which is the only known ac4C "writer" protein. Our analysis revealed a significant upregulation of NAT10 expression in LUAD, a finding that was corroborated by investigations in both LUAD cancer tissue samples and cell lines. Subsequently, we employed CRISPR/Cas9 technology to knock out the NAT10 gene and analyzed the resulting knockout cells using acRIP-seq and RNA-seq techniques. Our findings demonstrated differential expression of the genes CXCL5 and DEK, and functional enrichment analysis indicated a strong association with the adhesion signaling pathway. Laboratory experiments revealed that NAT10 acts as an ac4C "writer," promoting the acetylation of CXCL5 and DEK and thus preventing the degradation of their mRNAs. Moreover, NAT10 was found to significantly affect the number of metastases and tumor growth following the injection of cancer cells into the tail vein of mice. Our research data suggests that targeting NAT10 has the potential to serve as a diagnostic biomarker or prognostic target for developing anti metastatic therapies aimed at disrupting the adhesion process.

2026-04-08 | GSE315123 | 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

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