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The effects of RNA binding activity and acetyltransferase enzyme activity of NAT10 on heart development

ABSTRACT: The effects of RNA binding activity and acetyltransferase enzyme activity of NAT10 on heart development

PROVIDER: PRJNA1144452 | ENA |

REPOSITORIES: ENA

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The effects of RNA binding activity and acetyltransferase enzyme activity of NAT10 on heart development

Project description:The goal of this study is to investigate whether RNA binding activity and acetyltransferase enzyme activity of NAT10 regulates heart development

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RNA Cytidine Acetyltransferase NAT10 Maintains T Cell Pathogenicity in Inflammatory Bowel Disease

Project description:The enzyme N-acetyltransferase 10 (NAT10), known as the exclusive catalyst for N4-acetylcytidine (ac4C) modification, has been associated with various cellular processes, including tRNA acetylation, 18S rRNA biogenesis, mRNA stability, and translational efficiency. Despite extensive investigation into its molecular mechanisms in vitro, the physiological function of NAT10 under normal conditions has remained largely undefined. In this study, we found that the deficiency of NAT10 led to a disruption of T cell development at steady state, and identified a pivotal role for NAT10 in preserving the pathogenicity of naïve CD4+ T cells to induce adoptive transfer colitis. Mechanistically, the lack of NAT10 triggers the diminished stability of the anti-apoptotic gene Bag3, initiating a cascade of events that includes the upregulation of apoptosis-related genes and an accelerated rate of apoptosis in T cells. Our findings reveal a previously unrecognized role of the NAT10-ac4C-Bag3 axis in maintaining T cell homeostasis in vivo.

2025-03-12 | GSE284711 | GEO

RNA Cytidine Acetyltransferase NAT10 Maintains T Cell Pathogenicity in Inflammatory Bowel Disease [ATAC-Seq]

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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

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Project description:The goal of this study is to investigate how NAT10 regulates heart development

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Project description:The goal of this study is to investigate how NAT10 regulates heart development in mice. mRNA profiles in hearts of Nat10flox/flox and cardiomyocyte-specific Nat10 knockout (Nat10-CKO) mice at 10 days old were generated by deep sequencing using Illumina novaseq x plus (n=3 for each group).

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Sequencing to Explore the Mechanism Network of N-acetyltransferase 10 (NAT10) Promoting Colorectal cancer in human colorectal cancer cell SW620

Project description:N-acetyltransferase 10 (NAT10), the only known mRNA ac4C “writer,” plays a significant role in several human diseases, including CRC and gastric cancer. As NAT10 can activate or repress important signaling pathways, such as the EMT pathway, DNA damage repair, or apoptosis, by catalyzing the ac4C modification of oncogene mRNA, targeting NAT10 shows great potential for inhibiting cancer cell malignant progression in vitro and in vivo. This complex network of colorectal cancer progression mediated by NAT10 remains to be identified, which can expand cancer therapy options. To identify potential NAT10-regulated ac4C targets, we checked mRNA sequencing in human colorectal cancer cell SW620.

2025-02-12 | GSE264582 | GEO

Sequencing to Explore the Mechanism Network of N-acetyltransferase 10 (NAT10) Promoting Colorectal cancer in human colorectal cancer cell SW620 [ac4CRIP]

Project description:N-acetyltransferase 10 (NAT10), the only known mRNA ac4C “writer,” plays a significant role in several human diseases, including CRC and gastric cancer. As NAT10 can activate or repress important signaling pathways, such as the EMT pathway, DNA damage repair, or apoptosis, by catalyzing the ac4C modification of oncogene mRNA, targeting NAT10 shows great potential for inhibiting cancer cell malignant progression in vitro and in vivo. This complex network of colorectal cancer progression mediated by NAT10 remains to be identified, which can expand cancer therapy options. To identify potential NAT10-regulated ac4C targets, we checked ac4CRIP Sequencing in human colorectal cancer cell SW620.

2025-02-12 | GSE265993 | GEO

Sequencing to Explore the Mechanism Network of N-acetyltransferase 10 (NAT10) Promoting Colorectal cancer in human colorectal cancer cell SW620 [RIP-seq]

Project description:N-acetyltransferase 10 (NAT10), the only known mRNA ac4C “writer,” plays a significant role in several human diseases, including CRC and gastric cancer. As NAT10 can activate or repress important signaling pathways, such as the EMT pathway, DNA damage repair, or apoptosis, by catalyzing the ac4C modification of oncogene mRNA, targeting NAT10 shows great potential for inhibiting cancer cell malignant progression in vitro and in vivo. This complex network of colorectal cancer progression mediated by NAT10 remains to be identified, which can expand cancer therapy options. To identify potential NAT10-regulated ac4C targets, we checked RIP-Transcriptome Sequencing in human colorectal cancer cell SW620.

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N-acetyltransferase NAT10 Controls Cell Fates

Project description:Here, we show that NAT10 is an essential regulator of cellular plasticity, and its catalyzed mRNA cytidine acetylation represents a new layer of epitranscriptomic modulation.

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