Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MRNA-sequencing of METTL3-deficient NK cells

ABSTRACT: mRNA-sequencing of METTL3-deficient NK cells

PROVIDER: PRJNA746336 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15128326_1.fastq.gz	Fastqsanger.gz
	SRR15128326_2.fastq.gz	Fastqsanger.gz
	SRR15128327_1.fastq.gz	Fastqsanger.gz
	SRR15128327_2.fastq.gz	Fastqsanger.gz
	SRR15128328_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Protemics of Mettl3-deficient NK cells

Project description:With mass spectrometry， we aim to find the differentially expressed proteins in Mettl3-deficient NK cells

2021-07-20 | PXD025823 |

mRNA-sequencing of METTL3-deficient NK cells

Project description:Purpose: For comparing the transcript changes, we conducted mRNA-sequencing of splenic NK cells from Ncr1Cre-Mettl3fl/fl (cKO) and Mettl3fl/fl (WT) mice. Method: Firstly, The splenic NK cells (CD45.2+CD3-NK1.1+NKp46+) are purified via Fluorescence activated Cell Sorting (FACS), then frozen in -80 °C ultra-low temperature refrigerator, followed by High-throughput sequencing, in three replicates, using Illumina Hiseq 1500 platform. Result: Using standard data process workflow, we found the differentailly expressed genes in NK cells from Ncr1Cre-Mettl3fl/fl (cKO) mice, compared with those from Mettl3fl/fl (WT) mice.

2021-07-20 | GSE180053 | GEO

Mettl3-RIP-sequencing of NK cells

Project description:m6A modification plays vital roles in regulating mRNA lifecycle, thus controlling the biological process of multiple cell types. Here we intended to discover the binding sites of Mettl3 protein on mRNA of NK cells. Total RNAs were isolated from WT splenic NK cells, and subjected to standard RIP protocol. The library products corresponding to 200-500 bps were enriched, quantified and finally sequenced on Illumina Novaseq 6000 sequencer with PE150 model. Mettl3 binding sites were located primarily in the 3’ untranslated regions (UTRs), coding sequences (CDSs) region and near stop codons.

2021-07-20 | GSE173325 | GEO

Mettl3-RIP-sequencing of NK cells

Project description:Mettl3-RIP-sequencing of NK cells

| PRJNA725188 | ENA

Mettl3-RIP-sequencing and m6A-MeRIP-sequencing of NK cells

Project description:Mettl3-RIP-sequencing and m6A-MeRIP-sequencing of NK cells

| PRJNA725178 | ENA

METTL3 promotes translation in human cancer cells

Project description:we find METTL3 associates with polyribosomes and promotes translation. METTL3 depletion inhibits translation, and both wild-type and catalytically inactive METTL3 promote translation when tethered to the 3' untranslated region (UTR) of a reporter mRNA. Mechanistically, METTL3 enhances mRNA translation through an interaction with the translation initiation machinery. m6A seq in A549 and H1299 cells, RNA seq in METTL3 knockdown cells

2016-07-03 | E-GEOD-76367 | biostudies-arrayexpress

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

Differentially expressed genes in Mettl3-deficient livers compared to control livers

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 | GSE197800 | GEO

Expression data of Rag2-deficient Ets1++ and Rag2-deficient Ets1-- mature NK cells and WT bone marrow progenitors

Project description:Expression profiling of Rag2-deficient Ets1++ and Rag2-deficient Ets1-- mature NK cells and WT bone marrow progenitors, WT T cells, and WT Pro B cells WT Hematopoietic progenitors, CD4 T cells, Pro B cells, and WT and Ets1-deficient NK cells were FACs sorted. RNA was subsequently extracted, labelled, and hybridized to Affymetrix microarrays. The goal if this experiment was to identify Ets1 dependent genes in NK cells

2012-08-09 | E-GEOD-37301 | biostudies-arrayexpress

mRNA circularization by METTL3-eIF3h enhances translation

Project description:N6-methyladenosine (m6A) modification of mRNA catalyzed by METTL3 is enriched at a subset of stop codons. METTL3 can promote translation but the mechanism and widespread relevance remain unknown. Here we show that METTL3 enhances translation only when tethered to reporter mRNA at sites close to the stop codon supporting a mRNA looping mechanism for ribosome recycling and translational control. Electron microscopy revealed the topology of individual polyribosomes with single METTL3 foci found in close proximity to 5’ cap-binding proteins. We identify a direct physical and functional interaction between METTL3 and the eukaryotic translation initiation factor 3 subunit h (eIF3h). METTL3 promotes translation of a large subset of oncogenic mRNAs, including BRD4 that are also m6A-modified in human primary lung tumors. The METTL3-eIF3h interaction is required for enhanced translation, formation of densely packed polyribosomes, and oncogenic transformation. METTL3 depletion inhibits tumorigenicity and sensitizes lung cancer cells to BRD4 inhibition. These findings uncover a mRNA looping mechanism of translation control and identify METTL3-eIF3h as a potential cancer therapeutic target.

2018-09-21 | GSE117299 | 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