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Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network

ABSTRACT: Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network

PROVIDER: PRJNA815660 | ENA |

REPOSITORIES: ENA

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Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network [Liver RNA-seq]

Project description:Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network [Liver RNA-seq]

| PRJNA815662 | ENA

Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network [m6A-RIP-RNA-seq]

Project description:Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network [m6A-RIP-RNA-seq]

| PRJNA815663 | ENA

Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network [Primary hepatocyte RNA-seq]

Project description:Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network [Primary hepatocyte RNA-seq]

| PRJNA815661 | ENA

Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network [Liver RNA-seq]

Project description:RNA sequencing of livers tissues from control and hepatocyte-specific Mettl3 knockout with ALB-Cre (Mettl3 cKO) mice at different time points after birth.

2022-05-26 | GSE198512 | GEO

Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network [Primary hepatocyte RNA-seq]

Project description:RNA sequencing of primary hepatocytes from Control and and hepatocyte-specific Mettl3 knockout with ALB-Cre (Mettl3 cKO) mice after Actinomycin D treatment.

2022-05-26 | GSE198513 | GEO

Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-05-25 | GSE197564 | GEO

Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network [m6A-RIP-RNA-seq]

Project description:m6A-RIP sequencing of mouse liver tissues at different time points after birth.

2022-05-26 | GSE198511 | GEO

Mettl3-dependent m6A modification in postnatal liver

Project description:Liver-specific deficiency of Mettl3 causes liver injury. By performing RNA sequencing (RNA-seq) analysis on the Mettl3-deficient versus control livers, we identified the potential target genes that were closely associated with the liver phenotype in liver-specific Mettl3 knockout mice. RNA-seq analysis revealed extensive metabolic reprogramming in Mettl3-deficient livers. These results demonstrated that Mettl3 coordinates metabolic homeostasis and functional maturation during postnatal liver development.

2022-03-09 | GSE197799 | GEO

Mettl3-dependent m6A modification in postnatal liver

Project description:Mettl3-dependent m6A modification in postnatal liver

| PRJNA812059 | ENA

Primarily Dissecting the Autonomous and Cooperative Functions of METTL3 and METTL14 in mRNA Modification and Tumor Progression

Project description:METTL3 and METTL14 are considered to faithfully form the m6A writing complex in a 1:1 ratio, regulating the fate of mRNA by adding m6A modifications. However, recent studies have shown inconsistent expression and prognostic value of METTL3 and METTL14 in some tumors, suggesting that they may not be faithful in tumors. Pan-cancer analysis based on TCGA data reveals significant differences in expression, function, tumor burden correlation, and immune correlation between METTL3 and METTL14, especially in esophageal squamous cell carcinoma (ESCC). Knockdown of METTL3 significantly inhibits the cell proliferation in vitro and in vivo in ESCC EC109 cells, while the impact of METTL14 knockdown on proliferation is limited, and it cannot abolish the expression of METTL3 protein. mRNA-seq results indicate that METTL3 independently regulates the expression of 1615 genes, while only 776 genes are co-regulated by METTL3 and METTL14. Furthermore, through immunofluorescence co-localization, it is observed that METTL3 and METTL14 have certain inconsistencies in cellular localization. HPLC-MS results show that METTL3 independently binds to the Nop56p-associated pre-rRNA complex and mRNA splicing complex, separate from METTL14. Through bioinformatics and various omics studies, we have preliminarily discovered that METTL3 independently regulating tumor cell proliferation, and the participation in mRNA splicing may be a critical molecular mechanism. Our study provides an experimental basis and theoretical foundation for further understanding of the m6A writing complex and tumor therapy targeting METTL3.

2024-02-01 | PXD048886 | Pride

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