Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation (ChIP-seq)

ABSTRACT: YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation (ChIP-seq)

PROVIDER: PRJNA702452 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13731713.fastq.gz	Fastqsanger.gz
	SRR13731714.fastq.gz	Fastqsanger.gz
	SRR13731715.fastq.gz	Fastqsanger.gz
	SRR13731716.fastq.gz	Fastqsanger.gz
	SRR13731717.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 34

Similar Datasets

YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation (ChIP-seq)

Project description:The YAP and TAZ paralogues, the ultimate effectors of the Hippo signaling pathway, are deregulated in many cancer types. They are transcriptional co-activators that are recruited to their target sites, primarily by TEAD proteins. Here, we show that YAP and TAZ are also recruited by JUNB and STAT3, key factors that mediate an epigenetic switch linking inflammation to breast cellular transformation. YAP and TAZ directly interact with JUNB and STAT3 via a WW domain that is important for transformation, co-occupy many target sites in vivo via the sequence motifs of AP-1 and (to a lesser extent) STAT3, and stimulate transcriptional activation by AP-1 proteins. A small minority of target sites are YAP- or TAZ-specific, and they are associated with different sequence motifs and gene classes. YAP/TAZ, JUNB, and STAT3 directly regulate a common set of target genes that overlap, but are distinct from, those regulated by YAP/TAZ and TEADs. The set of target genes regulated by YAP/TAZ, STAT3, and JUNB is associated with poor survival in breast cancer patients with the triple-negative form of the disease.

2021-02-18 | GSE166941 | GEO

YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation (RNA-seq)

2021-02-18 | GSE166942 | GEO

YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation

Project description:YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation

| PRJNA702446 | ENA

YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation (RNA-seq)

Project description:YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation (RNA-seq)

| PRJNA702453 | ENA

YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation.

Project description:The YAP and TAZ paralogs are transcriptional co-activators recruited to target sites by TEAD proteins. Here, we show that YAP and TAZ are also recruited by JUNB (a member of the AP-1 family) and STAT3, key transcription factors that mediate an epigenetic switch linking inflammation to cellular transformation. YAP and TAZ directly interact with JUNB and STAT3 via a WW domain important for transformation, and they stimulate transcriptional activation by AP-1 proteins. JUNB, STAT3, and TEAD co-localize at virtually all YAP/TAZ target sites, yet many target sites only contain individual AP-1, TEAD, or STAT3 motifs. This observation and differences in relative crosslinking efficiencies of JUNB, TEAD, and STAT3 at YAP/TAZ target sites suggest that YAP/TAZ is recruited by different forms of an AP-1/STAT3/TEAD complex depending on the recruiting motif. The different classes of YAP/TAZ target sites are associated with largely non-overlapping genes with distinct functions. A small minority of target sites are YAP- or TAZ-specific, and they are associated with different sequence motifs and gene classes from shared YAP/TAZ target sites. Genes containing either the AP-1 or TEAD class of YAP/TAZ sites are associated with poor survival of breast cancer patients with the triple-negative form of the disease.

| S-EPMC8463077 | biostudies-literature

YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-18 | GSE166943 | GEO

Widespread association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth [ChIP-Seq]

Project description:The goal of this study was to identify YAP/TAZ direct transcriptional targets and transcriptional partners, through ChIP-sequencing and gene expression profiling. ChIP-seq analysis of YAP, TAZ, TEAD4 and JUN in MDA-MB-231 cells. Two independent replicates were analysed for each TF, as well as for negative controls.

2015-08-03 | E-GEOD-66081 | biostudies-arrayexpress

Aortic samples of inducible vascular smooth muscle specific KO of YAP/TAZ

Project description:YAP and TAZ are transcriptional co-activators and downstream effectors of the Hippo pathway, which play crucial roles in organ size control and cancer pathogenesis. Genetic deletion of YAP/TAZ has revealed their critical importance for embryonic development of the heart, vasculature and gastrointestinal mesenchyme. The aim of this study was to determine the long term role of YAP/TAZ in adult vascular smooth muscle in vivo. We used the novel Itga8-CreERT2 mouse for deletion of YAP/TAZ (i8-Y/T-KO).

2023-08-13 | GSE240233 | GEO

Transcriptional effects of YAP/TAZ depletion during oncogene-mediated transformation in mouse astrocyte

Project description:To understand the role of YAP/TAZ during gliomagenesis, we compared the transcriptomes of control and YAP/TAZ knockout astrocytes derived from newborn mice, transformed with oncogenic HER2.

2020-10-02 | GSE133463 | GEO

Yap and Taz regulate retinal pigment epithelial cell fate

Project description:The optic vesicle comprises a pool of bi-potential progenitor cells from which the retinal pigment epithelium (RPE) and neural retina fates segregate during ocular morphogenesis. Several transcription factors and signaling pathways have been shown to be important for RPE maintenance and differentiation, but an understanding of the initial fate specification and determination of this ocular cell type is lacking. We show that Yap/Taz-Tead activity is necessary and sufficient for optic vesicle progenitors to adopt RPE identity in zebrafish. A Teadresponsive transgene is expressed within the domain of the optic cup from which RPE arises, and Yap immunoreactivity localizes to the nuclei of prospective RPE cells. yap (yap1) mutants lack a subset of RPE cells and/or exhibit coloboma. Loss of RPE in yap mutants is exacerbated in combination with taz (wwtr1) mutant alleles such that, when Yap and Taz are both absent, optic vesicle progenitor cells completely lose their ability to form RPE. The mechanism of Yap dependent RPE cell type determination is reliant on both nuclear localization of Yap and interaction with a Tead co-factor. In contrast to loss of Yap and Taz, overexpression of either protein within optic vesicle progenitors leads to ectopic pigmentation in a dosagedependent manner. Overall, this study identifies Yap and Taz as key early regulators of RPE genesis and provides a mechanistic framework for understanding the congenital ocular defects of Sveinsson’s chorioretinal atrophy and congenital retinal coloboma. 60 pooled eyes from 36 hpf wild type or vsx2:Gal4/dsRed:14xUAS:YapS87A embryos were pooled for one sample. Three wild type and three vsx2:Gal4/dsRed:14xUAS:YapS87A pools were analyzed for RNA.

2015-08-06 | E-GEOD-71681 | 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