Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mapping translation in wild-type and METTL5 knockout (KO) HepG2 cells

ABSTRACT: Mapping translation in wild-type and METTL5 knockout (KO) HepG2 cells

PROVIDER: PRJNA729866 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14525700.fastq.gz	Fastqsanger.gz
	SRR14525701.fastq.gz	Fastqsanger.gz
	SRR14525702.fastq.gz	Fastqsanger.gz
	SRR14525703.fastq.gz	Fastqsanger.gz
	SRR14525704.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Mapping translation in wild-type and METTL5 knockout (KO) HepG2 cells

Project description:We performed ribosome profiling on wild-type and METTL5 KO HepG2 cells to investigate translation changes due to loss of METTL5.

2021-05-19 | GSE174419 | GEO

Mapping translation in wild-type and METTL5 knockout (KO) mice

Project description:We performed ribosome profiling on wild-type and METTL5 KO mice to investigate translation changes due to loss of METTL5.

2021-11-19 | GSE188798 | GEO

Mapping translation in wild-type and METTL5 knockout (KO) mice

Project description:Mapping translation in wild-type and METTL5 knockout (KO) mice

| PRJNA780403 | ENA

Mapping N6-methyladenosine (m6A) peaks in wild-type and METTL5 knockout (KO) HeLa cells

Project description:We report the application of MeRIP-seq to map m6A peaks in wild type and METTL5 KO HeLa cells to investigate targets of the m6A methyltransferase METTL5.

2021-05-19 | GSE174420 | GEO

Transcriptomic analysis of wild-type (WT) and METTL5 knockout (KO) mice

Project description:We report the application of next-generation sequencing to analyze the transcriptomes of brains and livers of WT and METTL5 KO mice to understand the role(s) of METTL5 in these organs.

2021-05-19 | GSE174418 | GEO

Gene expression profiles of METTL5-Wild type(WT) knockout(KO) in HCC cells

Project description:HCC cell line, Huh-7 cells and HCC-LM3 cells, was transfected with METTL5 sgRNA to knockout METTL5 expression., and check the downstream mRNA changes.

2023-01-06 | GSE203329 | GEO

RNA-seq and Ribo-seq of WT and METTL5 KO mECS.

Project description:Covalent chemical modifications of cellular RNAs directly impact all biological processes. However, our mechanistic understanding of the enzymes catalysing these modifications, their substrates and biological functions remains vague. Here, we undertook a systematic screen to uncover new RNA methyltransferases. We demonstrate that the methyltransferase-like 5 (METTL5) protein catalyses m6A in 18S rRNA at position A1832. We report that absence of Mettl5 in mouse embryonic stem cells (mESCs) results in a changes gene expression, decrease in translation rate, spontaneous loss of pluripotency and compromised differentiation potential. Mice lacking METTL5 recapitulate symptoms of patients with METTL5 mutations, thereby providing a new mouse disease model. Overall, our work highlights the importance of m6A in rRNA in stemness, differentiation, development and diseases.

2020-04-15 | GSE144313 | GEO

Mapping N6-methyladenosine (m6A) peaks in wild-type and METTL5 knockout (KO) HeLa cells

Project description:Mapping N6-methyladenosine (m6A) peaks in wild-type and METTL5 knockout (KO) HeLa cells

| PRJNA729867 | ENA

Transcriptomic analysis of wild-type (WT) and METTL5 knockout (KO) mice

Project description:Transcriptomic analysis of wild-type (WT) and METTL5 knockout (KO) mice

| PRJNA729865 | ENA

Loss of m6A methyltransferase METTL5 promotes cardiac hypertrophy through translational control of SUZ12

Project description:The methyltransferase-like5 (METTL5), which catalyzes m6A in 18S rRNA at position A1832, has been shown to regulate the efficient of mRNA translation in the differentiation of ES cell and the growth of cancer cells. It remains unknown that whether and how METTL5 regulates cardiac hypertrophy. In this study, we generated a mouse model (METTL5-cKO) with cardiac-specific abolishment of METTL5 in vivo. Loss function of METTL5 promotes pressure overload-induced cardiomyocyte hypertrophy and adverse remodeling. The regulatory function of METTL5 in hypertrophic growth of cardiomyocyte were further confirmed with both gain- and loss-of-function approaches in primary isolated cardiomyocytes. Mechanically, METTL5 was identified to modulate the mRNA translation of SUZ12, a core component of PRC2 complex, and further regulate the transcriptome shift during cardiac hypertrophy. Therefore, our study uncover an important translational regulator of cardiac hypertrophy.

2022-02-13 | GSE186615 | 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