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Links from GEO DataSets

Items: 20

1.

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

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing; Third-party reanalysis
Platforms:
GPL16791 GPL17811
25 Samples
Download data: CEL
Series
Accession:
GSE66083
ID:
200066083
2.

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

(Submitter supplied) The goal of this study was to identify YAP/TAZ direct transcriptional targets and transcriptional partners, through ChIP-sequencing and gene expression profiling. Keywords: Expression profiling by array
Organism:
Homo sapiens
Type:
Expression profiling by array; Third-party reanalysis
Platform:
GPL17811
12 Samples
Download data: CEL
Series
Accession:
GSE66082
ID:
200066082
3.

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

(Submitter supplied) The goal of this study was to identify YAP/TAZ direct transcriptional targets and transcriptional partners, through ChIP-sequencing and gene expression profiling.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
13 Samples
Download data: NARROWPEAK
Series
Accession:
GSE66081
ID:
200066081
4.

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

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL11154
70 Samples
Download data: TXT
Series
Accession:
GSE166943
ID:
200166943
5.

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

(Submitter supplied) 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. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
36 Samples
Download data: TXT
6.

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

(Submitter supplied) 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. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
34 Samples
Download data: BED
Series
Accession:
GSE166941
ID:
200166941
7.

Regulatory network controlling tumor-promoting inflammation in human cancers

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL9115 GPL11154
19 Samples
Download data: TXT
Series
Accession:
GSE115599
ID:
200115599
8.

Regulatory network controlling tumor-promoting inflammation in human cancers [RNA-seq]

(Submitter supplied) Using an inducible, inflammatory model of breast cellular transformation, we describe the transcriptional regulatory network mediated by STAT3, NF-kB, and AP-1 factors on a genomic scale. These regulators form transcriptional complexes that directly regulate the expression of hundreds of genes in oncogenic pathways, such as cell proliferation, metastasis, angiogenesis, apoptosis and metabolism, via a positive feedback loop. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
9 Samples
Download data: TXT
9.

Regulatory network controlling tumor-promoting inflammation in human cancers [ChIP-seq]

(Submitter supplied) Using an inducible, inflammatory model of breast cellular transformation, we describe the transcriptional regulatory network mediated by STAT3, NF-kB, and AP-1 factors on a genomic scale. These regulators form transcriptional complexes that directly regulate the expression of hundreds of genes in oncogenic pathways, such as cell proliferation, metastasis, angiogenesis, apoptosis and metabolism, via a positive feedback loop. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9115
10 Samples
Download data: TXT
Series
Accession:
GSE115597
ID:
200115597
10.

Genome-scale identification of transcription factors that mediate an inflammatory network during breast cellular transformation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
43 Samples
Download data: BW, TXT
Series
Accession:
GSE100259
ID:
200100259
11.

RNA-seq during MCF10A-ER-Src cell transformation and upon factor knockdowns

(Submitter supplied) We performed RNA-seq to examine RNA expression profiles during MCF10A-ER-Src cell transformation and upon knockdowns of transcription factors
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
10 Samples
Download data: BW
12.

ChIP-seq for histone modifications during MCF10A-ER-Src cell transformation

(Submitter supplied) We performed ChIP-seq for histone modifications to map chromatin status and dynamics during MCF10A-ER-Src cell transformation.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
29 Samples
Download data: TXT
Series
Accession:
GSE100257
ID:
200100257
13.

DNase-seq during MCF10A-ER-Src cell transformation

(Submitter supplied) We performed DNase-seq to study the dynamic genome-wide chromatin accessibility during MCF10A-ER-Src cell transformation.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: BW
Series
Accession:
GSE100255
ID:
200100255
14.

Role of BET proteins in YAP/TAZ-dependent transcription

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL16791
57 Samples
Download data: BEDGRAPH
Series
Accession:
GSE102409
ID:
200102409
15.

Role of BET proteins in YAP/TAZ-dependent transcription [RNA-seq 2]

(Submitter supplied) We compared the impact of small molecules on the transcriptional profile of triple negative breast cancer cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
7 Samples
Download data: BEDGRAPH
16.

Role of BET proteins in YAP/TAZ-dependent transcription [RNA-seq 1]

(Submitter supplied) We performed RNA-seq experiments to identify YAP/TAZ target genes in triple negative breast cancer cells, and evaluate the relevance of BET proteins for their expression.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
14 Samples
Download data: TXT
17.

Role of BET proteins in YAP/TAZ-dependent transcription [ChIP-seq]

(Submitter supplied) We performed ChIP-seq experiments to investigate the role of BET proteins in YAP/TAZ transcriptional activity.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
36 Samples
Download data: BW
Series
Accession:
GSE102406
ID:
200102406
18.

A non-canonical role of YAP/TEAD is required for activation of estrogen-regulated enhancers in breast cancer

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL21290
47 Samples
Download data: BW
Series
Accession:
GSE125609
ID:
200125609
19.

A non-canonical role of YAP/TEAD is required for activation of estrogen-regulated enhancers in breast cancer [GRO-seq]

(Submitter supplied) Estrogen and estrogen receptor alpha (ERα) signaling plays an essential role in ERα-positive breast cancer. ERα mainly occupies on distal enhancers within genome and requires the cooperation of additional co-factors to tune the enhancer activity. Through in vivo proximity-dependent labeling technique BioID, we identified YAP1 and TEAD4 protein as novel co-regulators of ERα. YAP and TEAD are nuclear effectors of the Hippo pathway regulating cell proliferation, organ size and tumorigenesis. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21290
6 Samples
Download data: BW
20.

A non-canonical role of YAP/TEAD is required for activation of estrogen-regulated enhancers in breast cancer [RNA-seq]

(Submitter supplied) Estrogen and estrogen receptor alpha (ERα) signaling plays an essential role in ERα-positive breast cancer. ERα mainly occupies on distal enhancers within genome and requires the cooperation of additional co-factors to tune the enhancer activity. Through in vivo proximity-dependent labeling technique BioID, we identified YAP1 and TEAD4 protein as novel co-regulators of ERα. YAP and TEAD are nuclear effectors of the Hippo pathway regulating cell proliferation, organ size and tumorigenesis. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21290
12 Samples
Download data: TXT
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Supplemental Content

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