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The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [m6A-RIP-seq]

ABSTRACT: m6A-RIP sequencing of primary hepatic stellate cells (HSCs) isolated from Control and HSC-specific Mettl3-knockout (Mettl3 cKO) mouse liver tissues.

ORGANISM(S): Mus musculus

PROVIDER: GSE207908 | GEO | 2022/07/13

REPOSITORIES: GEO

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The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [RNA-seq]

Project description:RNA sequencing of LX2 cell line (a human hepatic stellate cell line). METTL3 overexpression or downreguation were achieved by lenti-virus transduction.

2022-07-13 | GSE207909 | GEO

The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [m6A-RIP-seq]

Project description:The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [m6A-RIP-seq]

| PRJNA857667 | ENA

The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis

Project description:The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis

| PRJNA857659 | ENA

The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [RNA-seq]

Project description:The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [RNA-seq]

| PRJNA857666 | ENA

Exploring the Impact of m6A Methyltransferase Mettl3 on MASLD through Multi-Omics Analysis

Project description:Background: N6-methyladenosine (m6A) RNA modification plays a crucial role in various biological events and is implicated in various metabolic-related diseases. However, its role in MASLD remains unclear. This study aims to investigate the impact of Mettl3 on MASLD through multi-omics analysis, with a focus on exploring its potential mechanisms of action. Methods: MASLD mouse models were established by feeding a high-fat diet for 12 weeks, and Mettl3 stable overexpression AML12 cell models were constructed via lentiviral transfection. Subsequent transcriptomic and proteomic analyses, as well as integrated analysis between different omics datasets, were conducted. Results: Mettl3 expression significantly increased in MASLD mouse models. In the transcriptomic and proteomic analyses, we identified 848 genes with significant inconsistencies between transcriptomic and proteomic datasets. GO/KEGG enrichment terms may involve post-transcriptional modifications, particularly Mettl3-mediated m6A modification. Subsequently, through integrated proteomic analysis of Mettl3-overexpressed AML12 cell models and MASLD mouse models, we selected the top 20 co-upregulated and co-downregulated GO/KEGG terms as the main biological processes influenced by Mettl3 in MASLD. By intersecting with pathways obtained from previous integrated analyses, we identified GO/KEGG terms affected by Mettl3-induced m6A modification. Protein-protein interaction analysis of proteins involved in these pathways highlighted GAPDH, ENO1, and TPI1 as three key hub genes. Conclusion: In MASLD, Mettl3 regulates the glycolytic pathway through m6A modification, influencing the occurrence and development of the disease via the key hub genes GAPDH, ENO1, and TPI1. These findings expand our understanding of MASLD and provide strong evidence for potential therapeutic targets and drug development.

2024-09-20 | PXD050565 | Pride

METTL3-dependent m6A modification programs human neural progenitor cell proliferation [RIP-seq]

Project description:To investigate whether the role of METTL3 in hNPCs is dependent on its m6A activity,samples form neural progenitor cell (NPC) differentiation in the small molecule-assisted shut-off (SMASh) tagged hESC groups were collected. Gene expression levels were quantitated by RNA-seq analysis, and the potential target genes were identified by MeRIP-seq analysis and RIP-seq.

2023-11-22 | GSE242520 | GEO

m6A methyltransferase Mettl3 is essential for neuronal homeostasis and sleep via modulating Npy in mice

Project description:To unravel the underlying mechanisms how neuronal Mettl3 loss induces the activation of microglia, we performed RNA-sequencing (RNA-seq) with the thalamic tissues of 2- and 4-month-old Ctrl and cKO mice, respectively.

2025-02-12 | GSE262033 | GEO

m6A-RIP-seq of mRNA in yw, Mettl3, Mettl14 and Hakai flies

Project description:In order to obtain a stringent m6A methylome in Drosophila adults, we performed m6A-RIP-seq in yw control (male and female), Mettl3 (male), Mettl14 (male) and Hakai (male) mutant flies. We find that the effective m6A modification, which depends on the writer complex, is mostly distributed in 5’ UTR and near start codon in Drosophila, in contrast to the mammalian system. We define a set of high-confident m6A methylation sites shared by Mettl3, Mettl14 and Hakai, indicating that Hakai is a core component of the m6A writer complex. We also find differential methylation pattern in certain loci between male and female flies.

2021-03-01 | GSE155662 | GEO

Mettl3-RIP-sequencing of NK cells

Project description:Mettl3-RIP-sequencing of NK cells

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m6A/m-Seq of mouse adult cortex of Mettl3 cKO or Fto cKO mice

Project description:N6-Methyladenosine (m6A) and N6,2′-O-dimethyladenosine (m6Am) are abundant mRNA modifications that regulate transcript processing and translation. The role of both, here termed m6A/m, in the stress response in the adult brain in vivo are currently unknown. Here, we investigated the effect of gene deletion of Mettl3, a m6A methyltransferase, and Fto, a m6A and m6Am demethlyase, induced in adulthood in excitatory neurons of the neocortex and hippocampus (Camk2a-Cre Mettl3 or Fto cKO) on the cortical epitranscriptome. PolyA-RNA-fragments from 3-5 replicates per group were processed both as m6A/m-sample (RNA immunoprecipiation RIP with an m6A and m6Am antibody) and RNA-input sample.

2018-07-10 | GSE113793 | GEO

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