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accession-icon GSE40927
Conversion of human fibroblasts into vascular cells
  • organism-icon Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Conversion of human fibroblasts to angioblast-like progenitor cells.

Sample Metadata Fields

Sex, Specimen part, Cell line

View Samples
accession-icon GSE40793
Conversion of human fibroblasts into vascular cells (gene expression)
  • organism-icon Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

We report a novel technique to reprogram human fibroblasts into endothelial and smooth muscle cells using partial iPSC reprogramming and chemically defined media. Using appropriate media conditions for differentiation of human pluripotent cells to CD34+ vascular progenitor cells, we show that temporary expression of pluripotent transcription factors and treatment with chemically-defined media, will induce differentiation of human fibroblasts to CD34+ vascular progenitor cells. Sorted CD34+ cells can then be directed to differentiate into vascular endothelial cells expressing a variety of smooth muscle markers.

Publication Title

Conversion of human fibroblasts to angioblast-like progenitor cells.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon SRP080121
Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and FXRalpha-/- testicular Transcriptomes
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The goals of this study are to define the putatitve impacts of FXRalpha deficiency in testicular physiology Overall design: Testis mRNA profiles of 10-day old wild type (WT) and FXralpha-/- mice were generated by deep sequencing, on 5 individual mice for each geneotype, sequence on flowcell HS168.

Publication Title

The Bile Acid Nuclear Receptor FXRα Is a Critical Regulator of Mouse Germ Cell Fate.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE77628
Pals1 haplo-insufficiency in nephrons results in proteinuria and cyst formation
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Mammalian nephrons are the physiological subunits of mammalian kidneys which consist of different highly apicobasally polarized epithelial cell types. In epithelial cells polarization is controlled by evolutionary conserved CRB, PAR, or SRIB complexes. Here, we focused on the role of Pals1/Mpp5 in the nephron. Pals1, a core component of the apical membrane determining CRB complex, is highly expressed in renal tubular epithelial and glomerular epithelial cells (podocytes). Surprisingly, haplo-deficient mice, lacking one Pals1/Mpp5 allele in the nephron developed a strong phenotype, accompanied by cyst formation and severe renal filtration barrier defects, which subsequently lead to death after 6-8 weeks. Supporting studies in Drosophila nephrocytes, and epithelial cell culture models elucidated the role of Pals1 as a dose dependent upstream regulator of the crosstalk between Hippo- and TGF-signaling during nephrogenesis.

Publication Title

Pals1 Haploinsufficiency Results in Proteinuria and Cyst Formation.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE13093
Feeding schedule and the circadian clock shape rhythms in hepatic gene expression
  • organism-icon Mus musculus
  • sample-icon 64 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Time of feeding and the intrinsic circadian clock drive rhythms in hepatic gene expression.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13060
The effects of temporally restricted feeding on hepatic gene expression
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Temporally restricted feeding is known to impact the circadian clock. This dataset shows the effects of temporally restricted feeding on the hepatic transcriptome.

Publication Title

Time of feeding and the intrinsic circadian clock drive rhythms in hepatic gene expression.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13062
The effects of temporally restricted feeding on hepatic gene expression of Cry1, Cry2 double KO mice
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Restricted feeding impacts the hepatic circadian clock of WT mice. Cry1, Cry2 double KO mice lack a circadian clock and are thus expected to show rhythmical gene expression in the liver. Imposing a temporally restricted feeding schedule on these mice shows how the hepatic circadian clock and rhythmic food intake regulate rhythmic transcription in parallel

Publication Title

Time of feeding and the intrinsic circadian clock drive rhythms in hepatic gene expression.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13063
Effects of extensive fasting and subsequent feeding on hepatic transcription
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Temporally restricted feeding has a profound effect on the circadian clock. Fasting and feeding paradigms are known to influence hepatic transcription. This dataset shows the dynamic effects of refeeding mice after a 24hour fasting period.

Publication Title

Time of feeding and the intrinsic circadian clock drive rhythms in hepatic gene expression.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE46990
Gene expression changes induced by expression of MN1 deletion mutants in murine bone marrow cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Extensive molecular profiling of leukemias and preleukemic diseases has revealed that distinct clinical entities, like acute myeloid (AML) and T-lymphoblastic leukemia, share the same pathogenetic mutations. It is not well understood how the cell of origin, accompanying mutations, extracellular signals or structural differences in a mutated gene determine the phenotypic identity of the malignant disease. We studied the relationship of different protein domains of the MN1 oncogene and their effect on the leukemic phenotype, building on the ability of MN1 to induce leukemia without accompanying mutations. We found that the most C-terminal domain of MN1 was required to block myeloid differentiation at an early stage, and deletion of an extended C-terminal domain resulted in loss of myeloid identity and cell differentiation along the T-cell lineage in vivo. Megakaryocytic/erythroid lineage differentiation was blocked by the most N-terminal domain. In addition, the N-terminus was required for proliferation and leukemogenesis in vitro and in vivo through upregulation of HoxA9, HoxA10 and Meis2. Our results provide evidence that a single oncogene can modulate cellular identity of leukemic cells based on its active domains. It is therefore likely that different mutations in the same oncogene may impact cell fate decisions and phenotypic appearance of malignant diseases.

Publication Title

Cell fate decisions in malignant hematopoiesis: leukemia phenotype is determined by distinct functional domains of the MN1 oncogene.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE99039
A blood-based gene signature characterizing Idiopathic Parkinson's disease
  • organism-icon Homo sapiens
  • sample-icon 558 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Establishing reliable biomarkers for assessing and validating clinical diagnosis at early prodromal stages of Parkinsons disease is crucial for developing therapies to slow or halt disease progression. Here, we present the largest study to date using whole blood gene expression profiling from over 500 individuals to identify an 87-gene blood-based signature. Our gene signature effectively differentiates between idiopathic PD patients and controls in both a validation cohort and an independent test cohort, and further highlights mitochondrial metabolism and ubiquitination/proteasomal degradation as potential pathways disrupted in Parkinsons disease.

Publication Title

Analysis of blood-based gene expression in idiopathic Parkinson disease.

Sample Metadata Fields

Sex, Specimen part, Subject

View Samples
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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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