Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bud13 Promotes a Type I Interferon Response by Countering Intron Retention in Irf7

ABSTRACT: Bud13 Promotes a Type I Interferon Response by Countering Intron Retention in Irf7

PROVIDER: PRJNA505512 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8187890.fastq.gz	Fastqsanger.gz
	SRR8187900.fastq.gz	Fastqsanger.gz
	SRR8187910.fastq.gz	Fastqsanger.gz
	SRR8187920.fastq.gz	Fastqsanger.gz
	SRR8187930.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 64

Similar Datasets

Bud13 Promotes a Type I Interferon Response by Countering Intron Retention in Irf7

Project description:Intron retention (IR) has emerged as an important mechanism of gene expression control. Despite this, the factors that control IR events remain poorly understood. We observed consistent IR in one intron of the Irf7 gene and identified Bud13 as an RNA-binding protein that acts at this intron to increase the amount of successful splicing. Deficiency in Bud13 led to increased IR, decreased mature Irf7 transcript and protein levels, and consequently to a dampened type I interferon response. This impairment of Irf7 production in Bud13 deficient cells compromised their ability to withstand VSV infection. Global analysis of Bud13 knockdown and BUD13 cross-linking to RNA revealed a subset of introns that share many characteristics with the one found in Irf7 and are spliced in a Bud13-dependent manner. Deficiency of Bud13 led to decreased mature transcript from genes containing such introns. Thus, by acting as an antagonist to IR, Bud13 facilitates the expression of genes at which IR occurs.

2018-11-15 | GSE122543 | GEO

Macrophage development and activation involve coordinated intron retention in key inflammatory regulators

Project description:Monocytes and macrophages are essential components of the innate immune system. Herein, we report that intron retention (IR) plays an important role in the development and function of these cells. Using mRNA sequencing, bioinformatics analyses and RT-qPCR validation, we identified differential IR and altered expression of key genes involved in macrophage development and function, both in vitro and in vivo. We demonstrate that decreased IR in nuclear-detained mRNA is coupled to increased expression of genes encoding regulators of macrophage transcription, phagocytosis and inflammatory signalling, including ID2, IRF7, ENG and LAT. We further show that this dynamic IR program persists during the polarisation of resting macrophages into activated macrophages. In the presence of proinflammatory stimuli, intron-retaining CXCL2 and NFKBIZ transcripts in macrophages are rapidly spliced, leading to timely expression of these key inflammatory regulators by macrophages. Our study provides novel insights into the molecular mechanisms controlling vital regulators of the innate immune response.

2020-05-27 | PXD017391 | Pride

Intron retention analysis using isogrowth profiling

Project description:Intron retention analysis using isogrowth profiling

| PRJNA648363 | ENA

Intron retention analysis using isogrowth profiling

Project description:We present an analysis of intron retention under stress from two different drugs and their combinations in yeast Saccharomyces cerevisiae. We previously established isogrowth profiling, a method to abstract the non-specific effects of growth rate inhibition from the specific effect of perturbation by a small molecule: two drugs are used at varied ratios, but at fixed overall growth inhibition. Here, cycloheximide and LiCl were used at seven different ratios along the 50% growth inhibition isobole and the total ribodepleted RNA was sequenced. This allowed us to gauge the changes in intron retention due to the used drugs, while ensuring that the effects are not caused by growth inhibition. We found a prominent increase in intron retention under LiCl treatment that preferentially affects introns contained in the transcripts of ribosomal proteins.

2022-02-15 | GSE155060 | GEO

Dynamic intron retention modulates gene expression in the monocytic differentiation pathway

Project description:We determined the role of intron retention in murine monocyte differentiation

2021-11-22 | GSE168231 | GEO

Towards resolution of the intron retention paradox in breast cancer

Project description:We explored intron retention patterns in normal breast epithelial cells (MCF10A) and estrogen receptor positive (ER+) breast cancer cells (MCF7).

2022-12-31 | GSE196557 | GEO

Stress-induced transcriptional readthrough into neighboring genes is linked to intron retention

Project description:Exposure to certain stresses leads to readthrough transcription downstream of gene ends. Here we found that this phenomenon impacts the expression of genes located downstream to readthrough genes, whereby readthrough transcription proceeds into downstream genes, termed read-in genes. Using polyA-selected RNA-seq data from mouse fibroblasts, we identified widespread read-in in heat shock, oxidative and osmotic stress conditions. Read-in genes share distinctive genomic characteristics; they are extremely short, mainly due to less, shorter, introns, and they are highly GC rich. Furthermore, using ribosome footprint profiling we found that the translation of genes with high degrees of read-in is significantly reduced. Strikingly, read-in genes show extremely high levels of intron retention during stress, mostly in their first intron. While read-in genes share features that are generally associated with increased likelihood of intron retention, such as short introns and high GC content, intron retention in read-in genes during stress exceeds greatly beyond what is expected given their genomic properties. Finally, we found that first introns in read-in genes have weaker 5’ and 3’ splice sites. Our data portray a relationship between read-in and intron retention, suggesting it may have co-evolved to facilitate reduced translation of read-in genes during stress.

2022-10-27 | GSE197536 | GEO

Interferon Regulatory Factor 7 (IRF7) in aging of adipose-derived mesenchymal stromal cells

Project description:We found that Interferon Regulatory Factor 7 (IRF7) is upregulated in adipose-derived stromal cells (MSC) of 12 months-old (middle-age) mice compared with 1 month-old mice. To go in depth into the role of IRF7 in aging of MSC we knocked-down it in 12 months MSC and assessed the transcriptional changes though whole-genome microarray analysis. We investigated the transcriptional changes induced by the Interferon Regulatory Factor 7 (IRF7) knock-down in mesenchymal stromal cells established from the inguinal fat pad of 12-months-old mice.

2021-03-10 | GSE168533 | GEO

Irf7 orchestrates the immunological reaction in cardiomyocytes upon Adar1 deletion

Project description:Adenosine deaminases acting on RNA (Adar1 and Adar2) catalyze I-to-A RNA editing, a post-transcriptional mechanism involved in multiple cellular functions. The role of Adar1-dependent RNA editing in cardiomyocytes (CMs) remains unclear. Here we show that conditional deletion of Adar1 in CMs results in myocarditis progressively evolving into dilated cardiomyopathy and heart failure at only 6 months of age. Adar1 depletion drives activation of interferon signaling genes (ISGs) in the absence of apoptosis and cytokine activation, and reduces the hypertrophic response of CMs upon pressure overload. Interestingly, ablation of the cytosolic sensor MDA5 prevents cardiac ISG activation and delays disease onset, but does not rescue the long-term lethal phenotype elicited by conditional deletion of Adar1. Retention of a single catalytically inactive Adar1 allele in CMs, in combination with MDA5 depletion, however, completely restores the cardiac function and prevents heart failure. Finally, ablation of interferon regulatory factor 7 (Irf7) attenuates the phenotype of Adar1-deficient CMs to a similar extent as MDA5 depletion, highlighting Irf7 as the main regulator of the immune response triggered by lack of Adar1 in CMs.

2022-08-24 | PXD024974 | Pride

Gene expression and intron retention analysis of ZCRB1-knockdown human cells

Project description:ZCRB1 is a RNA binding protein involved in the Minor Spliceosome. Here, we used shRNAs to knock down ZCRB1 in HCT116 cells to analysis the function of ZCRB1 in gene expression and intron retention.

2023-04-10 | GSE182830 | 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