Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Mock or VSV treated WT and Mettl3 crispr iBMDM]

ABSTRACT: TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Mock or VSV treated WT and Mettl3 crispr iBMDM]

PROVIDER: PRJNA669757 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12833268_1.fastq.gz	Fastqsanger.gz
	SRR12833268_2.fastq.gz	Fastqsanger.gz
	SRR12833269_1.fastq.gz	Fastqsanger.gz
	SRR12833269_2.fastq.gz	Fastqsanger.gz
	SRR12833270_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Mock or VSV treated WT and Mettl3 crispr iBMDM]

Project description:mRNA m6A modification is involved in regulation of immune system. However, its function in antiviral immunity is controversial, and how immune responses regulate m6A modification is unknown. We here found TBK1, a key kinase of antiviral pathways, phosphorylated the core m6A methyltransferase METTL3 at Serine 67. The phosphorylated METTL3 interacted with translational complex and enhanced proteins translation, including IRF3, and facilitated antiviral responses. TBK1 also promoted METTL3 activation and m6A modification, which is required for stabilizing IRF3 mRNA. Type I IFN induction was severely impaired in METTL3 deficient cells. Mettl3flfl-lyz2-Cre mice were significantly more susceptible to IAV-induced lethality than control mice. Consistently, Ythdf1—/— mice cannot control viral infection and showed higher mortality than control mice due to decreased IRF3 expression. Together, we demonstrated that innate signals activated METTL3 via TBK1, and METTL3 and m6A modification secured antiviral immunity by promoting mRNA stability and protein translation.

2020-10-19 | GSE159567 | GEO

TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Mock or VSV treated WT and Ythdf1-KO BMDM]

2020-10-31 | GSE160481 | GEO

TBK1-METTL3 axis facilitates antiviral immunity [MeRIP-seq]

2020-11-04 | GSE160790 | GEO

TBK1-METTL3 axis facilitates antiviral immunity

Project description:TBK1-METTL3 axis facilitates antiviral immunity

| PRJNA669704 | ENA

TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Brain from WT and Mettl3 heterozygous kd]

Project description:mRNA m6A modification is involved in regulation of immune system. However, its function in antiviral immunity is controversial, and how immune responses regulate m6A modification is unknown. We here found TBK1, a key kinase of antiviral pathways, phosphorylated the core m6A methyltransferase METTL3 at Serine 67. The phosphorylated METTL3 interacted with translational complex and enhanced proteins translation, including IRF3, and facilitated antiviral responses. TBK1 also promoted METTL3 activation and m6A modification, which is required for stabilizing IRF3 mRNA. Type I IFN induction was severely impaired in METTL3 deficient cells. Mettl3flfl-lyz2-Cre mice were significantly more susceptible to IAV-induced lethality than control mice. Consistently, Ythdf1-/- mice cannot control viral infection and showed higher mortality than control mice due to decreased IRF3 expression. Together, we demonstrated that innate signals activated METTL3 via TBK1, and METTL3 and m6A modification secured antiviral immunity by promoting mRNA stability and protein translation.

2020-10-14 | GSE159421 | GEO

TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Mock or VSV treated WT and Ythdf1-KO BMDM]

Project description:TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Mock or VSV treated WT and Ythdf1-KO BMDM]

| PRJNA673356 | ENA

TBK1-METTL3 axis facilitates antiviral immunity [MeRIP-seq]

Project description:TBK1-METTL3 axis facilitates antiviral immunity [MeRIP-seq]

| PRJNA674508 | ENA

Whole genome RNA-seq analysis of wild type or HIPK2-/- immortalized bone marrow-derived macrophages (iBMDM), with or without vesicular stomatitis virus (VSV) infection

Project description:Wild type or HIPK2-/- immortalized bone marrow-derived macrophages (iBMDM) were infected with VSV for 6h, followed by whole genome RNA-seq analysis. Conclusions: HIPK2 deficiency aggravates viral infection and inhibited the production of IFNβ.

2017-12-15 | GSE108080 | GEO

TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Brain from WT and Mettl3 heterozygous kd]

Project description:TBK1-METTL3 axis facilitates antiviral immunity [RNA-seq: Brain from WT and Mettl3 heterozygous kd]

| PRJNA668900 | ENA

Genome-wide maps of chromatin state in iBMDM (immortalized bone-marrow-derived macrophages) cells without or with virus infection

Project description:iBMDM cells were infected with VSV (Vesicular Stomatitis Virus) or HSV-1 (Herpes Simplex Virus 1) for 8 hours, followed by CHIP-seq analysis with H3K27AC antibody. We find that chromatin state changed with virus infection, some enhacer and superenhancer were induced to promote anti-viral gene expression. Conclusions: virus infection induce enhancer and superenhancer activation.

2018-07-07 | GSE116750 | 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