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Identification of mRNAs associated with NAT10 in mouse hearts

ABSTRACT: The goal of this study is to identify mRNAs associated with NAT10 in mouse hearts.

ORGANISM(S): Mus musculus

PROVIDER: GSE274009 | GEO | 2025/08/04

REPOSITORIES: GEO

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Identification of mRNAs associated with NAT10 in mouse hearts

Project description:Identification of mRNAs associated with NAT10 in mouse hearts

| PRJNA1144455 | ENA

Identification of ribosome-protected mRNA fragments (RPFs) associated with NAT10 in mouse hearts

Project description:The goal of this study is to identify ribosome-protected mRNA fragments (RPFs) to investigate gene expression dynamics at both transcriptional and translational levels associated with NAT10 in mouse hearts

2025-08-04 | GSE295333 | GEO

Identification of ribosome-protected mRNA fragments (RPFs) associated with NAT10 in mouse hearts

Project description:Identification of ribosome-protected mRNA fragments (RPFs) associated with NAT10 in mouse hearts

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The effects of NAT10 on heart development in mice

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).

2025-08-04 | GSE295332 | GEO

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

mouse embryonic stem cells heterochromatin-associated protein and Nat10 IP-MS

Project description:The sonication-resistant heterochromatin (srHC) fragments of mESCs were isolated by sucrose gradient ultracentrifugation, and the heterochromatin-associated proteins were enriched by Co-IP combined with mass spectrometry (Co-IP/MS) using anti-H3K9me3, IgG was used as a negative control. The Nat10 interacted proteins in mESCs were isolated by 3×Flag-Nat10 fusion protein overexpression and performed IP-MS using anti-Flag, IgG antibody was used as a negative control.

2025-06-23 | PXD056153 | Pride

Targeting NAT10 enhances healthspan and lifespan in a mouse model of human accelerated aging syndrome.

Project description:Targeting NAT10 enhances healthspan and lifespan in a mouse model of human accelerated aging syndrome.

2018-03-22 | E-MTAB-6578 | biostudies-arrayexpress

NAT10-mediated N4-acetylcytidine of RNA Contributes to Post-transcriptional Regulation of Mouse Oocyte Maturation In Vitro

Project description:N4-acetylcytidine (ac4C), a newly identified epigenetic modification within mRNAs, has been characterized as a crucial regulator of mRNA stability and translation efficiency. And NAT10 is the only known RNA acetyltransferase. In our study, we documented the down-regulated expression of both ac4C and NAT10 during meiotic maturation of mouse oocytes. NAT10 knockdown resulted in ac4C reduction and impaired mouse oocyte maturation in vitro. These results indicated that NAT10-mediated ac4C modification plays a critical regulatory role in oocyte meiotic maturation. We further performed high-throughput sequencing with NAT10-overexpressed HEK293T cells and NAT10-binding transcripts to investigate the genes modulated by NAT10-mediated ac4C modification.

2021-07-11 | GSE179429 | GEO

NAT10-mediated mRNA N4-acetylcytidine Modifications in Mouse Oocytes Constitute a Checkpoint of Ovarian Follicle Development [NAT10-smart-seq2]

Project description:During mammalian follicular development, the correct establishment of the epitranscriptome in oocytes is essential for precise gene repression and the acquisition of developmental competence. N4-acetylcytidine (ac4C) is a conserved posttranscriptional RNA modification catalyzed by the only known “writer”, N-acetyltransferase 10 (NAT10). NAT10-targeted transcripts in oocytes and their functions in supporting folliculogenesis are poorly understood. In this study, we showed that oocyte-specific knockout of Nat10 resulted in retardation of oocyte growth with defective follicular development, premature ovarian failure, and female sterility. We profiled the ac4C landscape in the ovarian transcriptome and identified many folliculogenesis-related oocyte genes with ac4C modifications. Loss of Nat10 in oocytes eliminated ac4C signals, resulting in the downregulation of numerous oocyte-derived transcripts with reduced stability. Moreover, Nat10-deletion in oocytes or mutations in these ac4C sites led to decreased levels of protein translation, whereas the introduction of ac4C into these mRNAs increased their translational efficiencies. In addition, our data showed that the distinct gene expression patterns in granulosa cells within arrested secondary follicles were disrupted, and the identity of granulosa cells was altered by Nat10 deletion in oocytes. Taken together, these findings provide evidence that NAT10-mediated ac4C modification is a crucial regulatory factor in the maintenance of oocyte competence and that it constitutes a checkpoint for ovarian folliculogenesis beyond the secondary follicle stage.

2026-05-04 | GSE266989 | GEO

NAT10 inhibition improves cellular phenotypes of Hutchinson-Gilford progeria syndrome by restoring the Transportin-1 pathway

Project description:In this experiment, we aim to examine the role of NAT10 inhibition in Hutchinson-Gilford progeria syndrome (HGPS), a rare but devastating premature ageing syndrome caused by a mutation in the LMNA gene. NAT10 inhibition improves HGPS cellular phenotypes by releasing Transportin-1 (TNPO1) from the cytoplasm, restoring the TNPO1 pathway and allowing hnRNPA1 and NUP153 nuclear import, TPR anchorage at the nuclear pore complexes and RanGTP gradient re-balancing. We have promoted NAT10 inhibition by two ways in normal or patient derived primary skin fibroblasts; the NAT10 inhibitor Remodelin, and an siRNA directly targeting NAT10 (siNAT10). In addition, we have also used an siRNA against TNPO1 and a combined siTNPO1 and siNAT10 treatment. This is a 2-factor design, with treatment (Remodelin vs untreated, or siNAT10 vs siCT) and condition (HGPS vs normal fibroblasts) as the two conditions. Transcriptional profiling was performed using HumanHT-12 v4 Expression BeadChip microarrays, and all conditions were run in triplicate.

2018-06-25 | E-MTAB-6651 | biostudies-arrayexpress

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