Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The LncRNA Fendrr Regulates Lung Development via its Triplex Forming Site the Expression of Fibrosis Genes

ABSTRACT: Long non-coding RNAs are a very versatile class of molecules that have important roles in regulating a cells function, including regulating other genes on the transcriptional level. One of these mechanisms is that RNA can directly interact with DNA by recruiting additional components such as proteins to these sites via a RNA:dsDNA triplex formation. We genetically deleted the triplex forming sequence from the lncRNA Fendrr in mice and find that this FendrrBox is partially required for Fendrr function. we We find that the loss of the triplex forming site in developing lungs causes a dysregulation of gene programs, associated with lung fibrosis. Deregulated genes that contain a FendrrBox binding element in their promoter are regulated by Wnt signaling, together with Fendrr, implicating that Fendrr acts in concert with Wnt signaling to regulate lung fibrosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE186703 | GEO | 2023/04/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The LncRNA Fendrr Regulates Lung Development via its Triplex Forming Site the Expression of Fibrosis Genes

Project description:The LncRNA Fendrr Regulates Lung Development via its Triplex Forming Site the Expression of Fibrosis Genes

| PRJNA775610 | ENA

Human lung cancer Cells: Control vs. FENDRR stably over-expressed lung cancer cells

Project description:Transcriptional profiling of human lung cancer cell lines A549 comparing control cells transfected with an empty lentiviral expression vector pEZ-Lv201 and A549 cells transfected with a pEZ-Lv201-FENDRR. The latter forms a FENDRR stably over-expressed cell lines. Goal was to to assess the alteration of gene expression profiles caused by FENDRR upregulation.

2016-11-15 | GSE89828 | GEO

Mycobacterium triplex

Project description:Mycobacterium triplex genome

| PRJEB5744 | ENA

Mycobacterium triplex

Project description:Mycobacterium triplex overview

| PRJNA247427 | ENA

Trimethylamine N-oxide Aggravates Neuro-inflammation via lncRNA Fendrr/miR-145-5p/PXN axis in Vascular Dementia Rats

Project description:Vascular dementia (2VO) is the second-most cause of dementia, and our previous investigation showed that Trimethylamine-N-oxide (TMAO) exacerbates cognitive dysfunction and neuropathological changes in 2VO rats. Therefore, this study is aimed to evaluate the mechanism of TMAO in 2VO. Bilateral common carotid artery (2VO) model was established in rats and TMAO (120 mg/kg) was administered for 8 consecutive weeks, 4 weeks preoperatively and 4 weeks postoperatively. High-throughput sequencing was performed to find out the effects of TMAO treatment on lncRNA expression in rat hippocampus and bioinformatics analysis was conducted to identify potential downstream targets. Learning and spatial memory capacities were measured, as well as inflammatory factors. Nissl staining was used to observe neuronal injury in the CA1 area of the hippocampus. TMAO administration upregulated lncRNA Fendrr expression in the rat hippocampus, while the damaging effects of TMAO were counteracted after knockdown of Fendrr. Fendrr was highly expressed in 2VO rats and sponged miR-145-5p, which targets PXN. Silencing of Fendrr or PXN, or promotion of miR-145-5p improved neurological function injury, reduced neuronal damage, as well as repressed inflammation response. Inhibition of miR-145-5p abrogated up Fendrr knockdown mediated influence on 2VO rats. Taken together, our results showed that TMAO inhibits the miR-145-5p/PXN axis by increasing the Fendrr expression, thus exacerbating the development of 2VO.

2024-10-30 | GSE249873 | GEO

Isolation and genome-wide characterization of cellular DNA:RNA triplex structures IV

Project description:RNA can directly bind to purine-rich DNA via Hoogsteen base pairing, forming a DNA:RNA triple helical structure that anchors the RNA to specific sequences and allows guiding of transcription regulators to distinct genomic loci. To unravel the prevalence of DNA:RNA triplexes in living cells, we have established a fast and cost-effective method that allows genome-wide mapping of DNA:RNA triplex interactions. In contrast to previous approaches applied for the identification of chromatin-associated RNAs, this method uses protein-free nucleic acids isolated from chromatin. High-throughput sequencing and computational analysis of DNA-associated RNA revealed a large set of RNAs which originate from non-coding and coding loci, including repeat elements. Combined analysis of DNA-associated RNA and RNA-associated DNA identified genomic DNA:RNA triplex structures. The results suggest that triplex formation is a general mechanism of RNA-mediated target-site recognition, which has major impact on biological functions.

2018-12-20 | GSE120849 | GEO

Isolation and genome-wide characterization of cellular DNA:RNA triplex structures III

2018-12-20 | GSE120848 | GEO

Isolation and genome-wide characterization of cellular DNA:RNA triplex structures II

2018-12-20 | GSE120846 | GEO

Isolation and genome-wide characterization of cellular DNA:RNA triplex structures I

2018-12-20 | GSE120845 | GEO

ChIRP-MS dataset generated from Peptidylprolyl isomerase A guides SENP5/GAU1 DNA-lncRNA triplex generation for driving tumorigenesis

Project description:The three-stranded DNA-RNA triplex hybridization is involved in various biological processes, including gene expression regulation, DNA repair, and chromosomal stability. However, the DNA-RNA triplex mediating mechanisms underlying tumorigenesis remain to be fully elucidated. In gastric cancer, we performed ChIRP-MS in order to further capture the trimer-forming lncRNA binding protein.

2024-09-20 | PXD056041 | Pride

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