Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The m6A reader YTHDF1 attenuates fulminant hepatitis via MFG-E8 translation in an m6A dependent manner [RNA-seq]

ABSTRACT: We report the application of RNA-Seq, m6A-Seq and RIP-Seq to find out YTHDF1 regulate the target genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE228274 | GEO | 2023/08/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The m6A reader YTHDF1 attenuates fulminant hepatitis via MFG-E8 translation in an m6A dependent manner [m6a-seq]

Project description:We report the application of RNA-Seq, m6A-Seq and RIP-Seq to find out YTHDF1 regulate the target genes.

2023-08-21 | GSE228277 | GEO

The m6A reader YTHDF1 attenuates fulminant hepatitis via MFG-E8 translation in an m6A dependent manner [RIP-seq]

Project description:We report the application of RNA-Seq, m6A-Seq and RIP-Seq to find out YTHDF1 regulate the target genes.

2023-08-21 | GSE228280 | GEO

The m6A reader YTHDF1 attenuates fulminant hepatitis via MFG-E8 translation in an m6A dependent manner

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

2023-08-21 | GSE228282 | GEO

The m6A reader YTHDF1 attenuates fulminant hepatitis via MFG-E8 translation in an m6A dependent manner

Project description:The m6A reader YTHDF1 attenuates fulminant hepatitis via MFG-E8 translation in an m6A dependent manner

| PRJNA949190 | ENA

The m6A reader YTHDF1 attenuates fulminant hepatitis via MFG-E8 translation in an m6A dependent manner [m6a-seq]

Project description:The m6A reader YTHDF1 attenuates fulminant hepatitis via MFG-E8 translation in an m6A dependent manner [m6a-seq]

| PRJNA949188 | ENA

The m6A reader YTHDF1 attenuates fulminant hepatitis via MFG-E8 translation in an m6A dependent manner [RIP-seq]

Project description:The m6A reader YTHDF1 attenuates fulminant hepatitis via MFG-E8 translation in an m6A dependent manner [RIP-seq]

| PRJNA949195 | ENA

The m6A reader YTHDF1 attenuates fulminant hepatitis via MFG-E8 translation in an m6A dependent manner [RNA-seq]

Project description:The m6A reader YTHDF1 attenuates fulminant hepatitis via MFG-E8 translation in an m6A dependent manner [RNA-seq]

| PRJNA949185 | ENA

The m<sup>6</sup>A reader YTHDF1 attenuates fulminant hepatitis via MFG-E8 translation in an m<sup>6</sup>A dependent manner.

Project description:Background and Aims: N6-methyladenosine (m6A) is the most common post-transcriptional modification of RNA in eukaryotes, which has been demonstrated to play important roles in various biological processes. However, its roles in fulminant hepatitis remain largely unknown. In the current study, YTHDF1 expression was found to be significantly downregulated in the livers among patients, as well as murine models with fulminant hepatitis versus normal controls. Thus, we hypothesized that YTHDF1 protects against fulminant hepatitis and investigated the underlying molecular mechanisms. Methods: Fulminant hepatitis was induced by D-GalN/LPS in conventional YTHDF1 knockout (YTHDF1-/-) mice, hepatocyte-specific YTHDF1 overexpression (AAV8- YTHDF1) mice, and corresponding control mice. Primary hepatocytes were cultured and subjected to LPS insult in vitro. Hepatic histology, cell death, oxidative stress and mitochondrial function were examined to assess liver damage. The molecular mechanisms of YTHDF1 function were explored using multi-omics analysis. Results: Ablation of YTHDF1 exacerbated hepatic apoptosis and reactive oxygen species (ROS) production and increased the number of aberrant mitochondria, while YTHDF1 overexpression resulted in the opposite effects. Multiomics analysis identified MFG-E8 as the direct target of YTHDF1. YTHDF1 augmented the translation of MFG-E8 in an m6A-dependent manner without effect on its mRNA expression, thereby restoring mitochondrial function. Additionally, administration of MFG-E8 almost completely reversed the YTHDF1 deficiency-mediated exacerbation of liver injury. Conclusions: The current study suggested that the m6A reader YTHDF1 alleviates cell death, enhances antioxidant capacity and restores mitochondrial function in fulminant hepatitis by promoting MFG-E8 protein translation in an m6A-dependent manner.

| S-EPMC10411475 | biostudies-literature

Explore the effect of m6A reader YTHDF1 on RNAs half-life

Project description:In order to evaluate mRNA dynamic, we performed 4SU-TT-seq to estimate RNA synthesis and degradation rates in HEK293 cell line. After 1h exposure to the nucleoside analog 4-thiouridine (4SU), 4sU is incorporated into newly transcribed RNA, and the resulting 4sU-labeled RNAs are isolated and sequenced. The sequencing results revealed that parts of mRNAs in YTHDF1 deficient cells tends to be more stable than mRNAs from wild type

2022-11-13 | GSE143994 | GEO

Effect of YTHDF1 on concanavalin A-induced hepatitis

Project description:To investigate the effect of YTHDF1 on concanavalin A (ConA)-induced hepatitis , we performed RNA-seq with the total RNA extracted from the moue liver. Ythdf1-/- or wild type mice were intravenously injected with ConA (8 mg/kg) or saline for 8 hours. Then, the livers were collected, homogenized, and subjected to total RNA extraction.

2023-08-08 | GSE238229 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data