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accession-icon GSE66368
EphB2 promotes progression of cutaneous squamous cell carcinoma
  • organism-icon Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219), Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

EphB2 Promotes Progression of Cutaneous Squamous Cell Carcinoma.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE66359
Analysis of the gene expression profile in normal human epidermal keratinocytes and cutaneous squamous cell carcinoma cell lines
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The incidence of keratinocyte-derived skin cancer, cutaneous squamous cell carcinoma (cSCC) is increasing worldwide making it the second most common metastatic skin cancer.

Publication Title

EphB2 Promotes Progression of Cutaneous Squamous Cell Carcinoma.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE66361
Analysis of the gene expression profile in cutaneous squamous cell carcinoma cells after EphB2 knockdown
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219), Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The role of Eph/ephrin signaling in numerous biological processes has been established. However, Eph/ephrin signaling has been shown to have complex role in tumor progression. The role of EphB2 receptor in the progression of cutaneous squamous cell carcinoma (cSCC) has not been studied before.

Publication Title

EphB2 Promotes Progression of Cutaneous Squamous Cell Carcinoma.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE92357
GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE92354
GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis (2 of 3)
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Microvascular endothelial cells (EC) are increasingly recognized as organ-specific gatekeepers of their microenvironment. Microvascular EC instruct neighboring cells in their organ-specific vascular niches by angiocrine factors that comprise secreted growth factors/angiokines, but also extracellular matrix molecules and transmembrane proteins. The molecular regulators, however, that drive organ-specific microvascular transcriptional programs and thereby regulate angiodiversity, are largely elusive. Opposite to continuous barrier-forming EC, liver sinusoids are a prime model of discontinuous, permeable micro-vessels. Here, we show that transcription factor GATA4 controls liver sinusoidal endothelial (LSEC) specification and function. LSEC-restricted deletion of GATA4 caused transformation of discontinuous liver sinusoids into continuous capillaries. Capillarization was characterized by ectopic basement membrane deposition and formation of an abundantly VE-Cadherin expressing continuous endothelium. Correspondingly, ectopic expression of GATA4 in cultured continuous EC mediated downregulation of continuous EC transcripts and upregulation of LSEC genes. Regarding angiocrine functions, the switch from discontinuous LSEC to continuous EC during embryogenesis caused liver hypoplasia, fibrosis, and impaired colonization by hematopoietic progenitor cells resulting in anemia and embryonic lethality. Thus, GATA4 acts as master regulator of hepatic microvascular specification and acquisition of organ-specific vascular competence indispensable for liver development. The data also establish an essential role of the hepatic microvasculature for embryonic hematopoiesis.

Publication Title

GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE92356
GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis (3 of 3)
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Microvascular endothelial cells (EC) are increasingly recognized as organ-specific gatekeepers of their microenvironment. Microvascular EC instruct neighboring cells in their organ-specific vascular niches by angiocrine factors that comprise secreted growth factors/angiokines, but also extracellular matrix molecules and transmembrane proteins. The molecular regulators, however, that drive organ-specific microvascular transcriptional programs and thereby regulate angiodiversity, are largely elusive. Opposite to continuous barrier-forming EC, liver sinusoids are a prime model of discontinuous, permeable micro-vessels. Here, we show that transcription factor GATA4 controls liver sinusoidal endothelial (LSEC) specification and function. LSEC-restricted deletion of GATA4 caused transformation of discontinuous liver sinusoids into continuous capillaries. Capillarization was characterized by ectopic basement membrane deposition and formation of an abundantly VE-Cadherin expressing continuous endothelium. Correspondingly, ectopic expression of GATA4 in cultured continuous EC mediated downregulation of continuous EC transcripts and upregulation of LSEC genes. Regarding angiocrine functions, the switch from discontinuous LSEC to continuous EC during embryogenesis caused liver hypoplasia, fibrosis, and impaired colonization by hematopoietic progenitor cells resulting in anemia and embryonic lethality. Thus, GATA4 acts as master regulator of hepatic microvascular specification and acquisition of organ-specific vascular competence indispensable for liver development. The data also establish an essential role of the hepatic microvasculature for embryonic hematopoiesis.

Publication Title

GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE92352
GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis (1 of 3)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Microvascular endothelial cells (EC) are increasingly recognized as organ-specific gatekeepers of their microenvironment. Microvascular EC instruct neighboring cells in their organ-specific vascular niches by angiocrine factors that comprise secreted growth factors/angiokines, but also extracellular matrix molecules and transmembrane proteins. The molecular regulators, however, that drive organ-specific microvascular transcriptional programs and thereby regulate angiodiversity, are largely elusive. Opposite to continuous barrier-forming EC, liver sinusoids are a prime model of discontinuous, permeable micro-vessels. Here, we show that transcription factor GATA4 controls liver sinusoidal endothelial (LSEC) specification and function. LSEC-restricted deletion of GATA4 caused transformation of discontinuous liver sinusoids into continuous capillaries. Capillarization was characterized by ectopic basement membrane deposition and formation of an abundantly VE-Cadherin expressing continuous endothelium. Correspondingly, ectopic expression of GATA4 in cultured continuous EC mediated downregulation of continuous EC transcripts and upregulation of LSEC genes. Regarding angiocrine functions, the switch from discontinuous LSEC to continuous EC during embryogenesis caused liver hypoplasia, fibrosis, and impaired colonization by hematopoietic progenitor cells resulting in anemia and embryonic lethality. Thus, GATA4 acts as master regulator of hepatic microvascular specification and acquisition of organ-specific vascular competence indispensable for liver development. The data also establish an essential role of the hepatic microvasculature for embryonic hematopoiesis.

Publication Title

GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE47194
Tissue-specific pioneer factors associate with androgen receptor cistromes and transcription programs
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Tissue-specific pioneer factors associate with androgen receptor cistromes and transcription programs.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE47181
Tissue-specific pioneer factors associate with androgen receptor cistromes and transcription programs. [microarray]
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

We report the in vivo androgen receptor (AR) binding sites in murine prostate, epididymis and kidney in response to physiological androgen testosterone using ChIP-sequencing and gene expression profiling by microarray. From AR cistrome analysis, we identified tissue-specific collaborating factors i.e. FoxA1 in prostate, Hnf4a in kidney and AP2a in epididymis and validated by ChIP-seq. The ChIP experiments have been performed using antibodies specific to AR, FoxA1, Hnf4a, AP-2a and IgG non-specific antibody as a negative control.

Publication Title

Tissue-specific pioneer factors associate with androgen receptor cistromes and transcription programs.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE31341
The Phytoestrogen Genistein Is a Tissue-Specific Androgen Receptor Modulator
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

We report that the phytoestrogen genistein acts as a tissue-specific androgen receptor modulator in mouse using a novel androgen reporter mouse line and gene expression profiling. Genistein is a partial androgen agonist/antagonist in prostate, brain, and testis but not in skeletal muscle or lung. Gene expression profiling has been done from prostates of intact and castrated male mice treated with genistein or vehicle. Gene expression profiling was also done from prostates of estradiol-treated intact male mice.

Publication Title

The phytoestrogen genistein is a tissue-specific androgen receptor modulator.

Sample Metadata Fields

Sex, Specimen part

View Samples

refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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