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Identification of mRNAs associated with NAT10 in mouse hearts

ABSTRACT: Identification of mRNAs associated with NAT10 in mouse hearts

PROVIDER: PRJNA1144455 | ENA |

REPOSITORIES: ENA

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Identification of mRNAs associated with NAT10 in mouse hearts

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

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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

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

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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

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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).

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Targeting NAT10 inhibits hepatocarcinogenesis via ac4C-mediated

Project description:Hepatocellular carcinoma (HCC) is characterized by high morbidity and mortality, withlimited effective treatment options. NAT10 is the only known acetyltransferase formRNA ac4C modification and is recognized as a biomarker for HCC, promoting itsprogression. However, the critical role of NAT10 in hepatocarcinogenesis remains tobe fully elucidated, and the identification of suitable small-molecule inhibitors targetingNAT10 is of great interest. Here, we report that NAT10 promotes HCC progression bystabilizing SMAD3 mRNA through ac4C modification. Clinically, NAT10 is highlyexpressed in HCC tissues and is significantly associated with poor prognosis.Functionally, NAT10 downregulation inhibits HCC cell proliferation, invasion, andepithelial-mesenchymal transition (EMT), while promoting anoikis in vitro.Additionally, NAT10 depletion significantly impairs tumor growth, metastasis, andhepatocarcinogenesis in vivo. Mechanistically, NAT10 enhances oncogene SMAD3mRNA stability via ac4C modification, thereby activating TGF-β signaling pathway.We also identify a novel small-molecule inhibitor, NAT10-2023, which effectivelyblocks NAT10 activity. Notably, NAT10-2023 treatment significantly reducesintracellular RNA ac4C modification levels and disrupts NAT10-RNA interactions,leading to suppressed tumor progression. Overall, NAT10 drives HCC progression viaSMAD3 mRNA stability regulation and NAT10-2023 could be a promising therapeuticcandidate for targeting NAT10 in cancer treatment.

2026-05-18 | GSE297009 | GEO

Targeting NAT10 inhibits hepatocarcinogenesis via ac4C-mediated.

2026-05-18 | GSE297856 | 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

Identification of Khib substrates of histone regulated by NAT10

Project description:Having established NAT10’s regulatory role in lysine 2-hydroxyisobutyrylation, we aimed to identify the histone Khib sites targetedby NAT10. To this end, we extracted and digested core histones from cells with or without NAT10 depletion, followed by chemical derivatization of amine groups. The resulting peptides were analyzed by data-independent acquisition (DIA) mass spectrometry to detect the NAT10-modulated Khib sites.

2026-01-27 | PXD066039 | Pride

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