Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Differenatiation of mRNA expression in METTL3-depleted macrophages

ABSTRACT: Differenatiation of mRNA expression in METTL3-depleted macrophages

PROVIDER: PRJNA791903 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17319874_1.fastq.gz	Fastqsanger.gz
	SRR17319874_2.fastq.gz	Fastqsanger.gz
	SRR17319875_1.fastq.gz	Fastqsanger.gz
	SRR17319875_2.fastq.gz	Fastqsanger.gz
	SRR17319876_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Differenatiation of mRNA expression in PTX3-depleted macrophages

Project description:Differenatiation of mRNA expression in PTX3-depleted macrophages

| PRJNA792950 | ENA

Differenatiation of mRNA expression in METTL3-depleted macrophages

Project description:N6-methyladenosine (m6A), the most prevalent internal messenger RNA modification, plays critical roles in diverse biological processes. To characterize the potential involvement of METTL3 in macrophage function, transcriptome sequencing (RNA-seq) was performed in human THP1-derived macrophages with METTL3 depletion. We identified 266 genes that were differentially expressed in METTL3-depleted macrophages (≥ 1.5-fold change, P < 0.05), among which 44% (118 genes) were downregulated and 56% (148 genes) were upregulated. Notably, M2 macrophages activation-associated genes were robustly enhanced in METTL3-depleted macrophages. This study highlights the critical roles of m6A on regulation macrophages homeostasis.

2023-10-06 | GSE192533 | GEO

mRNA-seq of neuronal compartments in shRNA-mediated + small-molecule knockdown of Mettl3 in mouse primary cortical neurons (mPCN)

Project description:To study the effect of m6A modifications on subcellular mRNA localization we depleted m6A writer Mettl3 with shRNA and small molecule from mouse primary cortical neurons (mPCN) and sequenced neuritic and somatic compartments in parallel with scrambled shRNA control.

2023-07-12 | E-MTAB-11570 | 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

METTL3-mediated Klf9 mRNA stabilization contributes to white adipose tissue beiging

Project description:The induction of beige adipocytes in white adipose tissue (WAT), also known as WAT beiging, improves glucose and lipid metabolism. However, the regulation of WAT beiging at the posttranscriptional level remains elusive. Here, we report that METTL3, the methyltransferase of N6-methyladenosine (m6A) mRNA modification, is induced during WAT beiging in mice. Adipose-specific depletion of Mettl3 gene undermines WAT beiging. Transcriptomic analysis of m6A modifications and mRNA expression level reveals global reduction of m6A-modified mRNAs in Mettl3-depleted beige adipose tissue. In particular, METTL3-catalyzed m6A installation on Krüppel-like factor 9 (Klf9) mRNA prevents its degradation. We further demonstrate that the m6A reader protein IGF2BP3 mediates the stabilization of m6A-modified Klf9 mRNA. Overexpressioin of KLF9 protein reverses the impaired WAT beiging elicited by Mettl3 deletion. These findings uncover a novel epitranscriptional mechanism in WAT beiging and identify METTL3-KLF9 axis as a potential therapeutic target for obesity-associated disorders.

2023-02-03 | GSE178884 | GEO

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

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

mRNA circularization by METTL3-eIF3h enhances translation

Project description:mRNA circularization by METTL3-eIF3h enhances translation

| PRJNA481680 | ENA

mRNA-sequencing of METTL3-deficient NK cells

Project description:mRNA-sequencing of METTL3-deficient NK cells

| PRJNA746336 | ENA

m6A-seq analysis of Wild Type and Mettl3-/- BMDMs (bone-marrow-derived macrophages) Transcriptomes

Project description:To investigate the role of METTL3-mediated m6A modification in macrophage, we performed m6A-sequencing to map the m6A modification in bone-marrow-derived macrophages (BMDMs) in wild type (WT) and Mettl3-/- mice.

2021-01-19 | GSE146140 | 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