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M6A-seq analysis of Wild Type and Mettl3-/- BMDMs (bone-marrow-derived macrophages) Transcriptomes

ABSTRACT: m6A-seq analysis of Wild Type and Mettl3-/- BMDMs (bone-marrow-derived macrophages) Transcriptomes

PROVIDER: PRJNA609443 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11211681_1.fastq.gz	Fastqsanger.gz
	SRR11211681_2.fastq.gz	Fastqsanger.gz
	SRR11211682_1.fastq.gz	Fastqsanger.gz
	SRR11211682_2.fastq.gz	Fastqsanger.gz
	SRR11211683_1.fastq.gz	Fastqsanger.gz

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m6A-seq analysis of Wild Type and Mettl3-/- BMDMs (bone-marrow-derived macrophages) Transcriptomes

Project description:To investigate the role of METTL3-mediated m6A modification in macrophage, we performed m6A-sequencing to map the m6A modification in bone-marrow-derived macrophages (BMDMs) in wild type (WT) and Mettl3-/- mice.

2021-01-19 | GSE146140 | GEO

m6A-seq analysis of Mettl3fl/fl (WT) and Mettl3fl/fl,LyzM-cre (cKO) bone-marrow-derived macrophages(BMDMs) transcriptomes

Project description:To investigate the role of RNA methyltransferase METTL3-mediated m6A modification in macrophage, we performed m6A-sequencing to map the m6A modification in bone-marrow-derived macrophages (BMDMs) from Mettl3fl/fl (WT) and Mettl3fl/fl,LyzM-cre (cKO) mice

2021-10-01 | GSE184971 | GEO

m6A-seq analysis of Mettl3fl/fl (WT) and Mettl3fl/fl,LyzM-cre (cKO) bone-marrow-derived macrophages (BMDMs) transcriptomes after co-culturing with MC38 cells

Project description:To investigate the role of RNA methyltransferase METTL3-mediated m6A modification in macrophage after co-culturing with MC38 cells, we performed m6A-sequencing to map the m6A modification in bone-marrow-derived macrophages (BMDMs) from Mettl3fl/fl (WT) and Mettl3fl/fl,LyzM-cre (cKO) mice

2022-01-01 | GSE189994 | GEO

m6A modification maps of mRNA in bone marrow-derived macrophages (BMDMs) from mouse

Project description:We report the application of sequencing technology for high-throughput profiling of mRNA m6A methylation in mice BMDMs with or without PBS treatment. By obtaining over thirty billion bases of sequence from m6A antibody immunoprecipitated mRNA, we generated m6A methylation maps of mouse BMDMs in the presence or absence of LPS. We find that SOCS1 mRNA methylation is robustly enhanced by LPS treatment in WT BMDMs, leading to the increase of SOCS1 expression. However, LPS challenge fails to increase SOCS1 expression in the M14-/- BMDMs, indicating m6A modification plays a cirital role in the SOCS1 expression. This study provides a framework for the application of comprehensive mRNA m6A profiling towards characterization of BMDMs.

2020-12-09 | GSE153511 | GEO

RNA-seq analysis of Mettl3fl/fl and LysM-cre, Mettl3fl/fl BMDMs (bone-marrow-derived macrophages) Transcriptomes

Project description:To comprehensively learn about the mechanisms of METTL3-mediated pro-tumoral functions, we performed RNA-sequencing to identify differentially expressed genes in bone-marrow-derived macrophages (BMDMs) in Mettl3fl/fl (WT) and LysM-cre, Mettl3fl/fl (KO) mice after co-cultured with MC38 cell line.

2022-01-01 | GSE182865 | GEO

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-m6A-YTHDF1 axis promotion of mitochondrial dysfunction in metabolic dysfunction–associated steatotic liver disease (MASLD)

Project description:The N6-methyladenosine (m6A) mRNA modification and the mitochondrial respiratory chain (MRC) hold paramount importance in the advancement of MASLD. This study thoroughly investigates the relationship and impact of m6A mRNA modification and mitochondrial function in the progression of MASLD. Here we report that the mRNA and protein levels of mitochondrial respiratory chain (MRC) subunits showed inconsistent trends in vivo experiments. Abnormal m6A modification and mitochondrial dysfunction in MASLD were attributed to the upregulation of methyltransferase like 3 (Mettl3) and the downregulation of YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) induced by high-fat foods. Mettl3 promoted the MRC's function. However, knockout of the reader protein YTHDF1, which plays a crucial role in the m6A modification process, counteracted the effect of Mettl3 and suppressed MRC. In MASLD, damage to the MRC may be regulated by the Mettl3-m6A-YTHDF1 complex axis, especially by the role of YTHDF1. Our research has offered a novel perspective on the involvement of m6A mRNA methylation in the pathogenesis of MASLD.

2024-09-20 | PXD047819 | Pride

Bone marrow and BMDMs (unstimulated) RNA-seq

Project description:Examination of differentially expressed genes during macrophage differentiations (bone marrow vs. BMDMs)

2021-02-01 | GSE150573 | GEO

M6A-seq analysis of wild type and Mettl3-cKO liver tissues' transcriptomes

Project description:To investigate the role of METTL3-mediated m6A modification in liver, we performed m6A-sequencing to map the m6A modification in liver tissues of wild type (WT) and liver-sepcific Mettl3-KO mice.

2023-10-01 | GSE185142 | GEO

m6A modification maps of mRNA in bone marrow-derived macrophages (BMDMs) from mouse

Project description:m6A modification maps of mRNA in bone marrow-derived macrophages (BMDMs) from mouse

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