Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-Seq of control and EJC factor (EIF4A3, RBM8A, MAGOH) knockdowns in part with EIF4A3 rescue in HeLa Tet-Off cells

ABSTRACT: RNA-Seq of control and EJC factor (EIF4A3, RBM8A, MAGOH) knockdowns in part with EIF4A3 rescue in HeLa Tet-Off cells

PROVIDER: PRJEB46520 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR6349300_1.fastq.gz	Fastqsanger.gz
	ERR6349300_2.fastq.gz	Fastqsanger.gz
	ERR6349310_1.fastq.gz	Fastqsanger.gz
	ERR6349310_2.fastq.gz	Fastqsanger.gz
	ERR6349320_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 60

Similar Datasets

RNA-Seq of control and EJC factor (EIF4A3, RBM8A, MAGOH) knockdowns in part with EIF4A3 rescue in HeLa Tet-Off cells

Project description:The exon junction complex is involved in gene expression regulation on multiple co- and post-transcriptional levels. We aimed to investigate in HeLa Tet-Off cells which gene expression alterations can be observed upon knockdown of core EJC factors (EIF4A3, RBM8A and MAGOH) or upon EIF4A3 knockdown and rescue with EIF4A3 wild type construct by using RNA-Seq analyses. The rescue construct was stably integrated into the genome using the PiggyBac transposon system. As control Luciferase (Luc) siRNA was used.

2022-05-06 | E-MTAB-10771 | biostudies-arrayexpress

Transcriptome analyses of EJC haploinsufficient neocortices

Project description:RNA sequencing of E10.5 neocortices from control, Magoh, Rbm8a, and Eif4a3 haploinsufficient embryos (generated with Emx1-Cre)

2016-09-01 | GSE85576 | GEO

PYM1 controls non-canonical EJC occupancy and maintains homeostatic expression of membrance targeted transcripts

Project description:During pre-mRNA splicing in the nucleus, the spliceosome deposits the Exon Junction Complex (EJC) ~24 nucleotides upstream of exon-exon junctions. The EJC core thus deposited comprises of EIF4A3, RBM8A and MAGOH and remains stably bound to RNA to modulate mRNA fate at multiple post-transcriptional steps until its disassembly during translation. Such EJC disassembly is proposed to be mediated by PYM1, a factor that can bind both the ribosome and the RBM8A/MAGOH heterodimer of the EJC core. Here, we investigated the role of PYM1 in regulating EJC binding in human embryonic kidney 293 (HEK293) cells using a MAGOH mutant that assembles into EJC but is impaired in PYM1 interaction. We find that EJCs lacking PYM1 interaction show no defect in translation dependent disassembly. Surprisingly, PYM1 interaction deficient EJCs are enriched on sites away from the canonical EJC binding position including on transcripts without introns or fewer and longer exons. Additionally, acute reduction and elevation of PYM1 levels in HEK293 cells result in a modest NMD inhibition and stabilization of mRNAs that localize to endoplasmic reticulum associated TIS-granules and are characterized by fewer and longer exons. These gene expression changes are mirrored in flavivirus infected cells, suggesting a potential role for PYM1 in host-pathogen interactions, as flaviviruses are known to target this protein.

2025-07-31 | GSE289360 | GEO

Role of the Exon Junction Complex in Danio rerio

Project description:The exon junction complex (EJC) is composed of three core proteins Rbm8a, Magoh and Eif4a3 and is thought to play a role in several post-transcriptional processes. In this study we focus on understanding the role of EJC in zebrafish development. We identified transcriptome-wide binding sites of EJC in zebrafish via RNA:protein immunoprecipitation followed by deep sequencing (RIP-Seq). We find that, as in human cells, zebrafish EJC is deposited about 24 nts upstream of exon-exon junctions. We also identify transcripts regulated by Rbm8a and Magoh in zebrafish embryos using whole embryo RNA-seq from rbm8a mutant, magoh mutant and wild-type sibling embryos. This study shows that nonsense mediated mRNA decay is dysregulated in zebrafish EJC mutants.

2019-07-30 | GSE135019 | GEO

The Exon Junction Complex Core Represses Cancer-specific Mature mRNA Re-splicing: A Potential Key Role in Terminating Splicing

Project description:Using the TSG101 pre-mRNA, we previously discovered cancer-specific re-splicing of mature mRNA that generates aberrant transcripts/proteins. The fact that mRNA is aberrantly re-spliced in various cancer cells implies there must be an important mechanism to prevent deleterious re-splicing on the spliced mRNA in normal cells. We thus postulated that the mRNA re-splicing is controlled by specific repressors and we searched for repressor candidates by siRNA-based screening for mRNA re-splicing activity. We found that knock-down of EIF4A3, which is a core component of the exon junction complex (EJC), significantly promoted mRNA re-splicing. Remarkably, we could recapitulate cancer-specific mRNA re-splicing in normal cells by knock-down of any of the core EJC proteins, EIF4A3, MAGOH or RBM8A (Y14), implicating the EJC core as the repressor of mRNA re-splicing often observed in cancer cells. We propose that the EJC core is a critical mRNA quality control factor to prevent over-splicing of mature mRNA.

2021-06-15 | GSE178102 | GEO

eIF4A3 interactome by IP-MS in mouse ESCs

Project description:RNA helicases are involved in multiple steps of RNA metabolism to direct their roles in gene expression, yet their functions in pluripotency control remain largely unexplored. Starting from an RNAi screen of RNA helicases, we identified that eIF4A3, a DEAD-box (Ddx) helicase component of the exon junction complex (EJC), is essential for the maintenance of embryonic stem cells (ESCs). We mapped the eIF4A3 interactomes in mouse ESCs, revealing that eIF4A3 is widely involved in the post-transcriptional regulation of gene expression. Mechanistically, we show that eIF4A3 post-transcriptionally controls the pluripotency-related cell cycle regulators and that its depletion causes cellular differentiation via cell cycle dysregulation. Specifically, eIF4A3 is required for the efficient nuclear export of Ccnb1 mRNA, which encodes Cyclin B1, a key component of the pluripotency-promoting pathway during cell cycle progression of ESCs. Our results reveal a previously unappreciated role of eIF4A3 and its associated EJC in the post-transcriptional cell cycle control in maintaining stem cell pluripotency.

2023-03-11 | PXD031362 | Pride

Transcriptome-wide modulation of splicing by the exon junction complex

Project description:We report that knockdown of EJC core proteins, eIF4A3, Y14, Magoh, causes a transcript-wide changes in alternative splicing, as well as some transcriptional changes. These changes are specific to EJC core proteins, and KD of UPF1 protein caused different sets of alterantive splicing changes. These changes are linked to the rate of transcription.

2014-11-14 | GSE63091 | GEO

Transcriptome-wide modulation of splicing by the exon junction complex

2014-11-14 | E-GEOD-63091 | biostudies-arrayexpress

Mammalian UPF3A and UPF3B activate NMD independently of their EJC binding

Project description:Nonsense-mediated mRNA decay (NMD) can occur independently of some NMD factors such as UPF3B. We have performed total RNA-Seq in HCT116 cells under NMD factor knockout (with CRISPR-Cas9) and/or knockdown (with siRNA transfection) conditions to identify mRNA substrates regulated by different NMD factors. We have also performed RIPiT-Seq to identify the footprints of three compositionally distinct EJCs that contain the following pairs of proteins: MAGOH-EIF4A3, UPF3B-EIF4A3 or CASC3-EIF4A3 in WT HCT116 cells.

2022-04-23 | GSE179843 | GEO

mRNAseq of Drosophila S2 cells after knockdown of EJC components

Project description:This study used Drosophila melanogaster S2 cells treated with siRNA against the EJC components mago or eIF4A3, or a non-targeting control siRNA (three samples per condition). mRNA-seq libraries were prepared from the samples and the data was used to examine 'RS-exons' - exons which reconstitute a 5' splice site when they are spliced to the upstream exon. In contrast to mammalian cells, RS-exons are not recursively spliced out from Drosophila transcripts after perturbation of the EJC.

2018-10-15 | E-MTAB-7271 | biostudies-arrayexpress

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