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accession-icon GSE53335
Regulation of inducible genes in epithelial to mesenchymal transition by chromatinized PKC-theta
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st), Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE53266
Gene expression changes in a breast cancer stem cell model.
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Epithelial to mesenchymal transition (EMT) is activated during cancer invasion and metastasis, enriches for cancer stem cells (CSCs), and contributes to therapeutic resistance and disease recurrence. The epithelial cell line MCF7, can be induced to undergo EMT with the induction of PKC by PMA. 5-10% of the resulting cells have a CSC phenotype. This study looks at the transcriptome of these cells and how it differs from cells with a non-CSC phenotype.

Publication Title

Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE11035
Effect of 5HTT knockout and heterozygosity in whole mouse lung
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Rationale: While modulation of the serotonin transporter (5HTT) has shown to be a risk factor for pulmonary arterial hypertension for almost 40 years, there is a lack of in vivo data about the broad molecular effects of pulmonary inhibition of 5HTT. Previous studies have suggested effects on inflammation, proliferation, and vasoconstriction. The goal of this study was to determine which of these were supported by alterations in gene expression in serotonin transporter knockout mice. Methods: Eight week old normoxic mice with a 5-HTT knock-out (5HTT-/-) and their heterozygote(5HTT+/-) or wild-type(5HTT+/+) littermates had right ventricular systolic pressure(RVSP) assessed, lungs collected for RNA, pooled, and used in duplicate in Affymetrix array analysis. Representative genes were confirmed by quantitative RT-PCR and western blot. Results: RVSP was normal in all groups. Only 124 genes were reliably changed between 5HTT-/- and 5HTT+/+ mice. More than half of these were either involved in inflammatory response or muscle function and organization; in addition, some matrix, heme oxygenase, developmental, and energy metabolism genes showed altered expression. Quantitative RT-PCR for examples from each major group confirmed changes seen by array, with an intermediate level in 5HTT+/- mice. Conclusions: These results for the first time show the in vivo effects of 5HTT knockout in lungs, and show that many of the downstream mechanisms suggested by cell culture and ex vivo experiments are also operational in vivo. This suggests that the effect of 5HTT on pulmonary vascular function arises from its impact on several systems, including vasoreactivity, proliferation, and immune function.

Publication Title

Gene expression in lungs of mice lacking the 5-hydroxytryptamine transporter gene.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE5255
Loss of BMPR2 Signaling in Smooth Muscle in Mouse Lung
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Mice expressing a doxycycline-inducible dominant negative BMPR2 transgene expressed only in smooth muscle are activated for one or eight weeks, and compared to transactivator-only mice also fed doxycycline. All mice are 12 weeks of old at sacrifice.

Publication Title

Molecular effects of loss of BMPR2 signaling in smooth muscle in a transgenic mouse model of PAH.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE11018
Effect of BMPR2-R899X mutation in lung with and without elevated RVSP
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Familial pulmonary arterial hypertension (fPAH) is associated with mutations in BMPR2. Many of these mutations occur in the BMPR2 tail domain, leaving the SMAD functions intact. In order to determine the in vivo consequences of BMPR2 tail domain mutation, we created a smooth-muscle specific doxycycline inducible BMPR2 mutation with an arginine to termination mutation at amino acid 899. When these SM22-rtTA x TetO7-BMPR2R899X mice had transgene induced for 9 weeks, starting at 4 weeks of age, they universally developed pulmonary vascular pruning as assessed by fluorescent microangiography. Approximately half the time the induced animals developed elevated right ventricular systolic pressures (RVSP), associated with extensive pruning, muscularization of small pulmonary vessels, and development of large structural pulmonary vascular changes. These lesions included large numbers of macrophages and T-cells in their adventitial compartment, as well as CD133 positive cells in the lumen. Small vessels filled with CD45 positive and sometimes CD3 positive cells were a common feature in all SM22-rtTA x TetO7-BMPR2R899X mice. Gene array experiments show changes in stress response, muscle organization and function, proliferation and apoptosis, and developmental pathways before RVSP increases. Our results show that the primary phenotypic result of BMPR2 tail domain mutation in smooth muscle is pulmonary vascular pruning leading to elevated RVSP, associated with early dysregulation in multiple pathways with clear relevance to PAH. This model should be useful to the research community in examining early molecular and physical events in the development of PAH, and as a platform to validate potential treatments.

Publication Title

Mice expressing BMPR2R899X transgene in smooth muscle develop pulmonary vascular lesions.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE101742
Estrogen regulated genes in BCK4 tumors
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Genes regulated in different tumor regions, cells isolated by LCM

Publication Title

Estrogen induces c-Kit and an aggressive phenotype in a model of invasive lobular breast cancer.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE53148
Gene expression profiles in vitiligo lesional skin
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

CXCL10 is critical for the progression and maintenance of depigmentation in a mouse model of vitiligo.

Sample Metadata Fields

Specimen part

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accession-icon GSE53147
Genome-wide analysis of gene expression within vitiligo mouse skin
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Skin samples from mice in a model of vitiligo were selected for gene expression profiling in order to identify active inflammatory pathways.

Publication Title

CXCL10 is critical for the progression and maintenance of depigmentation in a mouse model of vitiligo.

Sample Metadata Fields

Specimen part

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accession-icon GSE7823
Murine Pulmonary Response to Chronic Hypoxia is Strain Specific
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

6-8 week old BL6, FVB/N and SV129 mouse strains were kept in normoxia or hypobaric hypoxia for 4 weeks and then phenotyped by echocardiogram and right ventricular heart catheterization, followed by tissue collection. In addition, Affymetrix expression analysis was conducted in a paired fashion.

Publication Title

Murine pulmonary response to chronic hypoxia is strain specific.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE28043
Bmpr2 mutation in murine PMVEC
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Pulmonary arterial hypertension (PAH) is thought to be driven by dysfunction of pulmonary vascular microendothelial cells (PMVEC). Most hereditary PAH is associated with BMPR2 mutations.

Publication Title

Physiologic and molecular consequences of endothelial Bmpr2 mutation.

Sample Metadata Fields

Specimen part

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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)

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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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