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Dynamic analysis of m6A methylation spectroscopy during progression and reversal of hepatic fibrosis

ABSTRACT: Dynamic analysis of m6A methylation spectroscopy during progression and reversal of hepatic fibrosis

PROVIDER: PRJNA558972 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9911010_1.fastq.gz	Fastqsanger.gz
	SRR9911010_2.fastq.gz	Fastqsanger.gz
	SRR9911020_1.fastq.gz	Fastqsanger.gz
	SRR9911020_2.fastq.gz	Fastqsanger.gz
	SRR9911011_1.fastq.gz	Fastqsanger.gz

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Dynamic analysis of m6A methylation spectroscopy during progression and reversal of hepatic fibrosis

Project description:We constructed a model of progression and reversal of hepatic fibrosis by intraperitoneal injection of carbon tetrachloride (CCl4). Dynamic m6A methylation was evaluated using MeRIP-Seq technique in the progression and reversal of hepatic fibrosis, and of the normal age-matched control groups. Genes with differentially m6A methylated sites and expression were analyzed to reveal the over-represented gene ontologies and pathways at different stages

2022-07-01 | GSE135462 | GEO

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

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

2022-07-13 | GSE207908 | 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

Identifying interaction proteins of METTL16 using co immunoprecipitation and mass spectroscopy

Project description:METTL16 has recently been identified as an RNA methyltransferase that installs m6A marks on a few transcripts. But its function in cytosol remains unclear. Puromycin-labelling and renilla luciferase assay revealed that METTL16 can promote translation efficiency in an m6A-independent manner. To explore the mechanism, we performed co-immunoprecipitation using METTL16 antibody and mass spectroscopy to identify its interaction proteins. Moreover, we find that METTL16 is essential for tumorigenesis of non-small cell lung cancer.

2024-08-03 | PXD032068 | Pride

Comprehensive Analysis of Transcriptome‐wide M6A Methylation for Hepatic Ischemia Reperfusion Injury in Mice

Project description:Background: Hepatic ischemia reperfusion injury (IRI) is a complex clinical complication during surgery and often leads to cell damage and dysfunction. N6-Methyladenosine (m6A) is an emerging epigenetic modification that plays key roles in the regulation of biological functions and cellular mechanisms in IR injury in different organs. However, the understanding of m6A-modified mRNAs in hepatic IRI is limited. Methods: Methylated RNA immunoprecipitation with high-throughput sequencing (MeRIP-seq) and RNA sequencing (RNA-seq) were used to profile the transcriptome-wide distribution of m6A methylation for hepatic IRI in mice. Results: In this study, there were 2061 nonoverlapping m6A peaks within 22471 coding gene transcripts (mRNAs) in the sham group and 2669 nonoverlapping m6A peaks within 22766 coding gene transcripts in the hepatic IR group. The distribution of m6A peaks was especially enriched in the coding sequence (CDS) and 3'UTR. Moreover, functional enrichment analysis demonstrated that the significantly enriched terms of genes with upmethylated m6A sites were the mRNA surveillance pathway, purine metabolism and metabolic pathways, and the significantly enriched terms of genes with downmethylated m6A sites were the Rap1 signaling pathway, sphingolipid signaling pathway, platelet activation, Wnt signaling pathway, chemokine signaling pathway and focal adhesion. Furthermore, we identified a relationship between differentially methylated genes and differentially expressed genes to obtain the three overlapping predicted target genes (Fnip2, Phldb2, and Pcf11). Conclusions: Our study first identified a transcriptome-wide map of m6A mRNAs in hepatic IRI. An in-depth analysis according to methylation modifications will provide effective treatment strategies and a theoretical basis for future research in terms of molecular mechanisms.

2023-05-12 | GSE190216 | GEO

Transcriptional dynamics of hepatic stellate cells in experimental acute liver injury, liver fibrosis and liver fibrosis reversal.

Project description:Transcriptional dynamics of hepatic stellate cells in experimental acute liver injury, liver fibrosis and liver fibrosis reversal.

| PRJNA734630 | ENA

HIV-1 m6A methylome investigation by m6A-SAC-seq

Project description:Despite effective antiretroviral therapy at reducing HIV-1 viral loads to undetectable levels, the presence of latently infected CD4+ T cells poses a major barrier to HIV-1 cure. N6-methyladenosine (m6A) modification of viral and cellular RNA has a functional role in regulating HIV-1 infection. m6A modification of HIV-1 RNA can affect its stability, translation, and splicing in cells and suppresses type-I interferon induction in macrophages. However, the function of m6A modification in regulating HIV-1 latency reactivation remains unknown. We used the Jurkat T cell line-derived HIV-1 latency model (J-Lat cells) to investigate changes in m6A levels of cellular RNA in response to latency reversal. We observed a significant increase in m6A levels of total cellular RNA upon reactivation of latent HIV-1 in J-Lat cells. This increase in m6A levels was transient and returned to steady-state levels despite continued high levels of viral gene expression in reactivated cells compared to control cells. Upregulation of m6A levels occurred without significant changes in the protein expression of m6A writers or erasers that add or remove m6A, respectively. Knockdown of m6A writers in J-Lat cells significantly reduced HIV-1 reactivation. Treatment of a m6A writer inhibitor reduced cellular RNA m6A levels along with reduction in HIV-1 reactivation. Furthermore, using m6A-specific sequencing, we identified cellular RNAs that are differentially m6A-modified during HIV-1 reactivation in J-Lat cells. Knockdown of identified m6A-modified RNA validate these results with established primary CD4+ T-cell models of HIV-1 latency. These results showed the importance of m6A RNA modification in HIV-1 latency reversal.

2024-10-01 | GSE273614 | GEO

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

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m6A level and isoform characterization sequencing (m6A-LAIC-seq) reveal the census and complexity of the m6A epitranscriptome

Project description:N6-methyladenosine (m6A) is a widespread reversible chemical modification of RNAs, implicated in many aspects of RNA metabolism. Little quantitative information exists as to either how many transcript copies of particular genes are m6A modified (âm6A levelsâ), or the relationship of m6A modification(s) to alternative RNA isoforms. To deconvolute the m6A epitranscriptome, we developed m6A level and isoform-characterization sequencing (m6A-LAIC-seq). We found that cells exhibit a broad range of non-stoichiometric m6A levels with cell type specificity. At the level of isoform characterization, we discovered widespread differences in use of tandem alternative polyadenylation (APA) sites by methylated and nonmethylated transcript isoforms of individual genes. Strikingly, there is a strong bias for methylated transcripts to be coupled with proximal APA sites, resulting in shortened 3â untranslated regions (3â-UTRs), while nonmethylated transcript isoforms tend to use distal APA sites. m6A-LAIC-seq yields a new perspective on transcriptome complexity and links APA usage to m6A modifications. m6A-LAIC-seq of H1-ESC and GM12878 cell lines, each cell line has two replicates

2016-06-24 | E-GEOD-66086 | biostudies-arrayexpress

Circadian Clock Regulation of Hepatic Lipid Metabolism by Modulation of m6A mRNA Methylation [siMettl3]

Project description:Circadian transcriptional rhythms are necessary for lipid metabolic homeostasis. Disruptions can lead to metabolic diseases. Whether epigenetic N6-methyladenosine (m6A) mRNA methylation impacts circadian regulation of lipid metabolism is unclear. Here, we show m6A mRNA methylation oscillations in murine liver depend upon a functional circadian clock. Hepatic deletion of Bmal1 increased m6A mRNA methylation, particularly of PPaRα. Inhibition of m6A methylation via knockdown of m6A methyltransferase METTL3 decreased PPaRα m6A abundance and increased PPaRα mRNA lifetime and expression, reducing lipid accumulation in cells in vitro. Our data suggest YTH domain family 2 (YTHDF2, a m6A binding protein) binds to PPaRα, prolonging its lifetime and mRNA expression. Reactive oxygen species accumulation increased PPaRα transcript m6A levels, revealing a possible mechanism for circadian clock disruption on m6A mRNA methylation. These data suggest m6A RNA methylation is important for circadian clock regulation of downstream genes and lipid metabolism that impacts metabolic outcome.

2018-06-21 | GSE102620 | GEO

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