Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial Infections II

ABSTRACT: Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial Infections II

PROVIDER: PRJNA804131 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17914000_1.fastq.gz	Fastqsanger.gz
	SRR17914000_2.fastq.gz	Fastqsanger.gz
	SRR17914001_1.fastq.gz	Fastqsanger.gz
	SRR17914001_2.fastq.gz	Fastqsanger.gz
	SRR17914002_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 56

Similar Datasets

Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial and Viral Infections I

Project description:N6-methyladenosine (m6A) is a dynamic post-transcriptional RNA modification influencing all aspects of mRNA biology. Here, we examined cellular m6A epitranscriptomes during infections of herpes simplex virus type 1 (HSV-1) and lipopolysaccharide (LPS) stimulation to identify m6A-regulated innate immune response genes. We showed that a significant portion of cellular genes including many innate immune response genes underwent m6A modifications in 5’UTR and 3’UTR, from which we identified common and distinct m6A-modified genes under different stimulating conditions.

2022-03-21 | GSE196269 | GEO

Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial Infections II

Project description:N6-methyladenosine (m6A) is a dynamic post-transcriptional RNA modification influencing all aspects of mRNA biology. Here, we examined cellular m6A epitranscriptomes during P.aeruginosa infection to identify m6A-regulated innate immune response genes with or without ALKBH5 knockdown. We showed that a significant portion of cellular genes including many innate immune response genes underwent m6A modifications in 5’UTR and 3’UTR, from which we identified common and distinct m6A-modified genes under different stimulating conditions.

2022-03-21 | GSE196270 | GEO

Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial and Viral Infections

Project description:Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial and Viral Infections

| PRJNA804128 | ENA

Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial and Viral Infections I

Project description:Distinct N6-methyladenosine (m6A) Regulation of Innate Immune Responses During Bacterial and Viral Infections I

| PRJNA804132 | ENA

N6-methyladenosine Modulates Messenger RNA Translation Efficiency

Project description:N6-methyladenosine (m6A) is the most abundant internal messenger (mRNA) modification in mammalian mRNA. This modification is reversible and non-stoichiometric, which potentially adds an additional layer of variety and dynamic control of mRNA metabolism. The m6A-modified mRNA can be selectively recognized by the YTH family “reader” proteins. The preferential binding of m6A-containing mRNA by YTHDF2 is known to reduce the stability of the target transcripts; however, the exact effects of m6A on translation has yet to be elucidated. Here we show that another m6A reader protein, YTHDF1, promotes ribosome loading of its target transcripts. YTHDF1 forms a complex with translation initiation factors to elevate the translation efficiency of its bound mRNA. In a unified mechanism of translation control through m6A, the YTHDF2-mediated decay controls the lifetime of target transcripts; whereas, the YTHDF1-based translation promotion increases the translation efficiency to ensure effective protein production from relatively short-lived transcripts that are marked by m6A. PAR-CLIP and RIP was used to identify YTHDF1 binding sites followed by ribosome profling and RNA seq to assess the consequences of YTHDF1 siRNA knock-down

2015-06-09 | E-GEOD-63591 | biostudies-arrayexpress

YTHDF3 improves translation initiation of mRNAs with N6-methyladenosine methylation at 5’ untranslated region by facilitating eIF2AK2 recruitment in oxaliplatin-resistant colorectal cancer - RIP-seq dataset

Project description:Oxaliplatin as a first-line drug frequently causes the chemo-resistance on colorectal cancer (CRC). N6-methyladenosine (m6A) methylation has been largely acknowledged in multiple biological functions. However, the molecular mechanisms underlying the m6A methylation in modulating anticancer drug resistance in CRC are still obscure. In present study, RIP-seq was conducted to investigate the occupancy of N6-methyladenosine RNA binding protein 3 (YTHDF3) served as “readers” that can recognize m6A modification site in HCT116 cells with oxaliplatin resistance (HCT116R). Then, YTHDF3 was knockdown by siRNA in HCT116 cells with oxaliplatin resistance, and RIP-seq was further conducted to investigate m6A methylation of HCT116, HCT116R and HCT116R cells with YTHDF3 knockdown.

2022-02-04 | E-MTAB-11321 | biostudies-arrayexpress

Widespread N6-methyladenosine-dependent RNA Structural Switches Regulate RNA-Protein Interactions

Project description:We show that N6-methyladenosine (m6A), the most abundant internal modification in mRNA/lncRNA with still poorly characterized function, alters RNA structure to facilitate the access of RBM for heterogeneous nuclear ribonucleoprotein C (hnRNP C). We term this mechanism m6A-switch. Through combining PAR-CLIP with Me-RIP, we identify 39,060 m6A-switches among hnRNP C binding sites transcriptome-wide. We show that m6A-methyltransferases METTL3 or METTL14 knockdown decreases hnRNP C binding at 16,582 m6A-switches. Taken together, 2,798 m6A-switches of high confidence are identified to mediate RNA-hnRNP C interactions and affect diverse biological processes including cell cycle regulation. These findings reveal the biological importance of m6A and provide insights into the sophisticated regulation of RNA-RBP interactions through m6A-induced RNA structural remodeling. Measure the m6A methylated hnRNP C binding sites transcriptome-wide by PARCLIP-MeRIP; measure the differential hnRNP C occupancies upon METTL3/METTL14 knockdown by PAR-CLIP; measure RNA abundance and splicing level changes upon HNRNPC, METTL3 and METTL14 knockdown

2015-02-27 | E-GEOD-56010 | biostudies-arrayexpress

N6-methyladenosine (m6A) modification in HEK (primary human epidermal keratinocytes)

Project description:We conducted an analysis of N6-methyladenosine (m6A) modifications in HEK (primary human epidermal keratinocytes). The primary aim of this investigation was to establish a molecular framework elucidating the role of m6A modifications in modulating the functional of keratinocytes.

2024-08-20 | GSE269500 | GEO

N6-methyladenosine (m6A) profiling of mouse liver

Project description:N6-methyladenosine (m6A) profiling of mouse liver

| PRJNA489387 | ENA

N6-methyladenosine (m6A) profiling in 60 YRI LCLs

Project description:N6-methyladenosine (m6A), the most abundant messenger RNA (mRNA) modification, has emerged as a critical post-transcriptional mechanism that regulates various aspect of mRNA metabolism including pre-mRNA processing, mRNA export, mRNA stability and translation efficiency. However the genetics basis of m6A is largely unexplored. In this work, we mapped m6A-QTLs in 60 LCLs and used the resulting tens of thousands of QTLs to provide insights to m6A biology and its contribution to human complex trait.

2020-05-04 | GSE125377 | 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