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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE307103 | GEO | 2026/01/28

REPOSITORIES: GEO

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NAT10-mediated ac4C-modification exacerbates ferroptosis by stabilizing HMOX1 in Deep vein thrombosis

Project description:In our study, we aimed to identify the pathways and genes closely related to DVT. Through proteomic analysis, we found that the ferroptosis signaling pathway showed differential expression, and we also discovered that NAT10 (a key acetyltransferase modified by ac4C) was significantly overexpressed in DVT mice. Based on this discovery, we further investigated the downstream genes regulated by NAT10. We found that NAT10 enhances the stability of HMOX1 through ac4C modification, which results in iron overload and lipid peroxides, thereby forming a positive feedback loop that exacerbates DVT.

2026-01-26 | PXD067933 | Pride

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

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

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NAT10-mediated ac4C-modification exacerbates ferroptosis by stabilizing HMOX1 in Deep vein thrombosis

Project description:NAT10-mediated ac4C-modification exacerbates ferroptosis by stabilizing HMOX1 in Deep vein thrombosis

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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.

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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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Project description:Epigenetic regulation exerts a crucial role in maintaining the balance between self-renewal and differentiation of hematopoietic stem cells (HSCs), thereby sustaining normal hematopoiesis. Although emerging evidence has demonstrated the contribution of RNA N4-acetylcytidine (ac4C) modification and its catalytic enzyme Nat10 to numerous biological processes, particularly tumorigenesis, the landscape and function of ac4C in normal hematopoiesis remain unexplored. In this study, we characterize the landscape of ac4C across the hierarchy of hematopoietic stem and progenitor cells (HSPCs) using the ultra-low input acRIP-seq (ULAC-seq) and reveal a key role of Nat10 in the maintenance of HSCs.

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