Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effects of m6A modification and YTHDF2 knockdown on global mRNA turnover

ABSTRACT: We developed a method to deconvolute decays of m6A mRNAs and their unmethylated isoforms from total RNAs across the transcriptome and combined this method with the knockdown of m6A reader protein to study the effect on global mRNA turnover.

ORGANISM(S): Homo sapiens

PROVIDER: GSE218263 | GEO | 2025/02/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Differential effects of m6A modification and YTHDF2 knockdown on global mRNA turnover

Project description:We developed a method to deconvolute decays of m6A mRNAs and their unmethylated isoforms from total RNAs across the transcriptome and combined it with the knockdown of m6A reader protein to study it's effect on global mRNA turnover.

2025-02-01 | GSE181814 | GEO

Effects of m6A modification on turnover of newly synthesized mRNAs at the transcriptome level.

Project description:We developed a method to deconvolute decays of m6A mRNAs and their unmethylated isoforms from newly synthesized total RNAs across the transcriptome to study the effects of m6A modification on decays of not only the m6A-modified RNA pool but also the unmehnylated isoform pool.

2025-02-01 | GSE218267 | GEO

Effects of m6A modification and YTHDF2 knockdown on global mRNA turnover

Project description:Effects of m6A modification and YTHDF2 knockdown on global mRNA turnover

| PRJNA902825 | ENA

Differential effects of m6A modification and YTHDF2 knockdown on global mRNA turnover

Project description:Differential effects of m6A modification and YTHDF2 knockdown on global mRNA turnover

| PRJNA753517 | ENA

MOV10 facilitates messenger RNA decay in an N6-methyladenosine (m6A)-dependent manner to maintain the mouse embryonic stem cells state

Project description:N6-methyladenosine (m6A) is the most predominant internal mRNA modification in eukaryotes, recognised by its reader proteins (so-called m6A-readers) for regulating subsequent mRNA fates – splicing, export, localization, decay, stability and translation – to control several biological processes. Although a few m6A-readers have been identified, yet the list is incomplete. Here, we identify a new m6A-reader protein, MOV10, in mouse embryonic stem cells (mESCs). MOV10 recognises m6A-containing mRNAs with a conserved GGm6ACU motif. Mechanistic studies uncover that MOV10 bound m6A-containing mRNAs facilitate mRNA decay within the cytoplasmic processing bodies (P-bodies) in an m6A-dependent manner. Moreover, MOV10 decays the Gsk-3ß mRNA through m6A that stabilises the ß-CATENIN expression of a Wnt/ß-catenin signalling pathway to regulate downstream target expression of NANOG for maintaining the mESC state. Thus, our findings reveal how a newly identified m6A-reader, MOV10 mediates mRNA decay via m6A that impact ESC biology.

2024-01-15 | GSE181821 | GEO

Cell cycle-dependent YTHDF2 promotes mitotic entry by repressing WEE1

Project description:The m6A modification regulates mRNA stability and translation. Here we show that transcriptomic m6A modification is dynamic and the m6A reader protein YTHDF2 promotes mRNA decay during the cell cycle. Depletion of YTHDF2 leads to the delay of mitotic entry due to overaccumulation of WEE1, a negative regulator of CDK1. We demonstrate that WEE1 transcripts contain m6A modification, which promotes their decay through the m6A reader YTHDF2. Moreover, we found that YTHDF2 protein stability is dependent on CDK1 activity. Thus, CDK1, YTHDF2, and WEE1 form a feedforward regulatory loop to promote mitotic entry. We further identified CUL1, CUL4A, DDB1, and SKP2 as components of E3 ubiquitin ligase complexes that mediate YTHDF2 proteolysis. Our study provides insights into how cell cycle mediators modulate transcriptomic m6A modification, which in turn regulates the cell cycle.

2020-01-01 | GSE134700 | GEO

SLAM-Seq analysis of Ythdf2-deficient pre-leukemic cells

Project description:The mRNA m6A reader YTHDF2 is overexpressed in a broad spectrum of human acute myeloid leukemias (AML). To study the role of YTHDF2 on mRNA decay rates in leukemia, c-Kit+ cells from foetal livers of Ythdf2fl/fl; Vav-iCre (Ythdf2CKO) and Ythdf2fl/fl (Ythdf2CTL) 14.5 dpc embryos were transduced with Meis1 and Hoxa9 oncogenes and serially re-plated to generate pre-leukemic cells. Medium with 4SU was used for pre-leukemic cells labelling for 12 hours and was later replaced with 4SU-free medium (time 0). Cells were collected immediately after medium change and at 1, 3 and 9 hours for library generation. RNA from Ythdf2CKO (n=3 biological replicates) and Ythdf2CTL (n=3 biological replicates) pre-leukemic cells were used for SLAM-seq library generation.

2019-04-05 | E-MTAB-7784 | biostudies-arrayexpress

YTHDF2 mediates the mRNA degradation in prostate cancer in m6A-dependent way

Project description:As the crucial m6A reader, YTHDF2 usually degrades the target mRNAs by recognizing the m6A modified sites, consequently altering m6A levels of each mRNA. In this study, we used m6A MeRIP sequencing to detect the m6A modification alterations in prostate cancer (PCa) cell line after knocking down YTHDF2 and identify how YTHDF2 promote the PCa progression by mediating the mRNA degradation in m6A-dependent way.

2020-11-09 | GSE129408 | GEO

YTHDF2 iCLIP in glioblastoma stem cells

Project description:Glioblastoma is a universally lethal cancer driven by glioblastoma stem cells (GSCs). Here, we interrogated N6-methyladenosine (m6A) mRNA modifications in GSCs by methyl RNA-immunoprecipitation followed by sequencing (meRIP-seq) and transcriptome analysis, finding transcripts marked by m6A often upregulated. Interrogating m6A regulators, GSCs displayed preferential expression as well as in vitro and in vivo dependency of the m6A reader, YTHDF2, in contrast to normal neural stem cells (NSCs). While YTHDF2 has been reported to destabilize mRNAs, YTHDF2 stabilized the oncogene transcripts, MYC and VEGFA, in GSCs in an m6A-dependent manner. We identified IGFBP3 as a downstream effector of the YTHDF2-MYC axis in GSCs and IGF1/IGF1R inhibitor, Linsitinib, as preferentially targeting YTHDF2-expressing cells, inhibiting the viability of GSCs without affecting NSCs and impairing in vivo glioblastoma growth. Thus, YTHDF2 links RNA epitranscriptomic modifications and GSC growth, laying the foundation for the YTHDF2-MYC-IGFBP3 axis as a specific and novel therapeutic target in glioblastoma.

2020-09-29 | GSE158020 | GEO

Transcriptomic Analysis of the m6A Reader YTHDF2 in the Maintenance and Differentiation of Human Embryonic Stem Cells

Project description:As the most abundant internal modification on mRNAs, N6-methyladenosine (m6A) has been discovered to be involved in different biological processes. Mostly determined by m6A methyl-transferases (m6A writers) and demethylases (m6A erasers), different cell types possess differential m6A profiles of transcriptomes. However, the interpretation of the m6A-encoded epitranscriptomic information needs m6A readers to bind and recruit different machinery for regulating the target mRNAs, which in turn, may regulate cell fates. The functions of the m6A readers in the regulation of the maintenance and differentiation of human embryonic stem cells (hESCs) remain largely unknown. In this study, we deleted the whole genomic region of the m6A reader YTHDF2, and discovered that YTHDF2 is dispensible for the maintenance, but probably important for the differention of hESCs, especially for the differentiation towares ectoderm. Furthermore, we identified ROBO1 as a potential target gene by DF2 in regulating hESC to neuroectoderm differentiation. This study reveals the potential roles of the m6A reader DF2 in regulating the specification of neuroectodermal cell fate.

2025-03-11 | GSE268806 | 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