Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Long non-coding RNA lnc-TSSK2-8 activates canonical Wnt/β-catenin signaling through small shock proteins HSPA6 and CRYAB

ABSTRACT: Long non-coding RNA lnc-TSSK2-8 activates canonical Wnt/β-catenin signaling through small shock proteins HSPA6 and CRYAB

PROVIDER: PRJNA698585 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13602689.fastq.gz	Fastqsanger.gz
	SRR13602690.fastq.gz	Fastqsanger.gz
	SRR13602691.fastq.gz	Fastqsanger.gz
	SRR13602692.fastq.gz	Fastqsanger.gz
	SRR13602693.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Long non-coding RNA lnc-TSSK2-8 activates canonical Wnt/β-catenin signaling through small shock proteins HSPA6 and CRYAB

Project description:Congenital heart defect (CHD) is the most common birth defect worldwide. Copy number variations (CNVs) have been revealed as an important source of pathogenic factor of CHD. 22q11.2 deletion syndrome is the most common microdeletion disorder which has been frequently associated with conotruncal malformations. By now, the dosage sensitive geneTBX1 has been adopted as the major pathogenic gene responsible for 22q11.2 deletion-related heart defects. Here we report the lncRNA lnc-TSSK2-8, which is encompassed in the 22q11.2 region, could activate the canonical Wnt/ -catenin signaling by protecting -catenin from ubiquitination and degradation. Such effects were mediated by two short heat shock proteins HSPA6 and CRYAB, whose expression were regulated by lnc-TSSK2-8 through the ceRNA mechanism. In clinical practice, pathogenesis of CNV were always attributed to haploinsufficiency of protein coding genes. Here we report the 22q11.2 lncRNA lnc-TSSK2-8 significantly activate canonical Wnt/ -catenin signaling, which has major roles in cardiac out flow tract development and should act upstream of TBX1. Our results suggested that lncRNAs should contribute to the etiology of CNV related CHD.

2021-06-02 | GSE165927 | GEO

lnc-EAPV binding proteins in C57BL/6J BMDMs

Project description:Endogenous retroviruses (ERVs) are transposable elements that cause host genome instability and usually play deleterious roles such as tumorigenesis. Recent advances also suggest that this 'enemy within' may encode viral mimic to induce antiviral immune responses through viral sensors. Here, through whole genome RNA-seq we discovered a full-length ERV-derived long non-coding RNA (lncRNA), designated lnc-EPAV (ERV-derived lncRNA positively regulates antiviral responses), as a positive regulator of NF-κB signaling. Lnc-EPAV expression was rapidly up-regulated by viral RNA mimic or RNA viruses to facilitate the expression of RELA, an NF-κB subunit that plays a critical role in antiviral responses. In turn, RELA promoted the transcription of lnc-EPAV to form a positive feedback loop. Transcriptome analysis of lnc-EPAV-silenced macrophages, combined with gain- and loss-of-function experiments, showed that lnc-EPAV was critical for induction of type I interferon (IFN) and inflammatory cytokine expression by RNA viruses. Consistently, lnc-EPAV-deficient mice exhibited reduced expression of type I IFNs, and consequently increased viral loads and mortality following lethal RNA virus infection. Mechanistically, lnc-EPAV promoted expression of RELA by competitively binding to and displacing SFPQ, a transcriptional repressor of RELA. The binding between ERV-derived RNAs and SFPQ also existed in human cells. Altogether, our work demonstrates an alternative mechanism by which ERVs regulate antiviral immune responses.

2018-11-07 | PXD011577 | Pride

Epidermal growth factor activates β-catenin via integrin-linked kinase to control proliferation of mesenchymal stromal cells.

Project description:Mesenchymal stromal cells (MSCs) are located in bone marrow where they help to maintain bone homeostasis and repair through the ability to expand in response to mitotic stimuli and differentiate into skeletal linages. The signalling mechanisms that enable precise control of MSC function remain unclear. Here, we have identified a non-canonical epidermal growth factor (EGF) signalling pathway in MSCs, which acts via integrin-linked kinase (ILK) to activate β-catenin, a key component of Wnt signalling. EGF induces nuclear translocation of β-catenin in MSCs but does not drive T cell factor (TCF)-mediated transactivation of Wnt target genes, and we demonstrate by Design of Experiments statistical analysis that the EGF/β-catenin and Wnt/β-catenin pathways do not cross-talk following co-stimulation with multiple concentrations of both ligands. By examining EGF-regulated genes in MSCs by RNA-Sequencing, we identified gene sets that were exclusively regulated by the EGF/b-catenin pathway, which were distinct from canonical EGF-regulated genes. In contrast, the expression of subsets of canonical EGF signalling gene targets were significantly influenced by b-catenin activation. These newly-identified EGF signalling pathways cooperate to enable EGF-mediated proliferation of MSCs by alleviating the suppression of cell cycle pathways induced by canonical EGF signalling.

2018-10-24 | GSE121697 | GEO

Heat shock factor 1 specifically potentiates c-MYC-mediated transcription independently of the canonical heat-shock response

Project description:Heat shock factor 1 specifically potentiates c-MYC-mediated transcription independently of the canonical heat-shock response

| PRJNA820032 | ENA

Heat shock factor 1 specifically potentiates c-MYC-mediated transcription independently of the canonical heat-shock response

Project description:Despite its pivotal roles in biology, how the transcriptional activity of c-MYC is attuned quantitatively remain poorly defined. Here, we show that heat shock factor 1 (HSF1), the master transcriptional regulator of the heat-shock response, acts as a key modifier of the c-MYC-mediated transcription. HSF1 deficiency diminishes c-MYC DNA binding and dampens its transcriptional activity genome-widely. Mechanistically, c-MYC, MAX, and HSF1 assemble into a transcription factor complex on DNAs and, surprisingly, the DNA binding of HSF1 is dispensable. Instead, HSF1 physically recruits the histone acetyltransferase GCN5, thereby promoting histone acetylation and augmenting c-MYC transcriptional activity. Thus, our studies reveal that HSF1 specifically potentiates the c-MYC-mediated transcription, distinct from its role in the canonical heat-shock response. Importantly, this mechanism of action engenders two distinct c-MYC activation states, primary and advanced, which may be important to accommodate diverse physiological and pathological conditions.

2023-05-22 | GSE199462 | GEO

Inhibition of canonical Wnt/β-catenin signaling is involved in leflunomide (LEF)-mediated cytotoxic effects on renal carcinoma cells

Project description:Inhibition of canonical Wnt/β-catenin signaling is involved in leflunomide (LEF)-mediated cytotoxic effects on renal carcinoma cells

2016-03-31 | GSE77433 | GEO

Transcriptome analysis of Wnt knockdown embryos reveals candidate canonical Wnt/β-catenin target genes during Xenopus laevis gastrulation

Project description:The canonical Wnt/β-catenin signaling pathway plays multiple roles during Xenopus gastrulation, including posteriorization of the neural plate, patterning of the mesoderm, and induction of the neural crest. Wnt signaling stabilizes β-catenin, which then activates target genes. However, few targets of this signaling pathway that mediate early developmental processes are known. Here we sought to identify transcriptional targets of the Wnt/β-catenin signaling pathway using a genome-wide approach.

2016-04-25 | GSE77364 | GEO

biotin RNA pulldown assay of lnc-GD2H and mass spectrometry

Project description:Vectors carrying lnc-GD2H and antisense lnc-GD2H were linearized with the corresponding restriction enzymes to prepare template DNAs for in vitro transcription. Biotinylated RNAs were mixed with proteins extracted from C2C12 cells, followed by targeting of the RNAs with streptavidin beads. After SDS-PAGE following RNA pulldown, the differentially expressed proteins were enzymolyzed and used for MS analysis.

2021-05-18 | PXD025292 | Pride

The differential expression of lncRNAs in wnt/β-catenin pathway activation or inactivation of triple-negative breast cancer.

Project description:To screen the associated lncRNAs with wnt/β-catenin pathway activation of TNBC,through lncRNA microarray profiling between activated and inactivated wnt/β-catenin pathway of TNBC tissues, lnc-WAL (wnt/β-catenin associated lncRNA; WAL) was selected as the top upregulated lncRNA in wnt/β-catenin pathway activation compared with the inactivation group.

2024-07-05 | GSE270306 | GEO

Inhibition of canonical Wnt/Î²-catenin signaling is involved in leflunomide (LEF)-mediated cytotoxic effects on renal carcinoma cells

Project description:Inhibition of canonical Wnt/Î²-catenin signaling is involved in leflunomide (LEF)-mediated cytotoxic effects on renal carcinoma cells In the study presented here, 4 samples [2 control groups (Caki-2 treated with 0.1%DMSO for 48h) and 2 experimental groups (Caki-2 treated with 200Î¼M leflunomide for 48h)], were used to acquire expression profiles ofÂ 115 up-regulated and 176 down-regulated mRNA

2016-03-31 | E-GEOD-77433 | 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