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accession-icon GSE56009
E2f and Myc transcriptional programs and chromatin binding landscapes in the small intestines
  • organism-icon Mus musculus
  • sample-icon 48 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

Redeployment of Myc and E2f1-3 drives Rb-deficient cell cycles.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE56006
Expression data from control, E2f TKO, Myc KO and E2f/Myc QKO crypts
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Combined ablation of Myc and E2f1-3 results in disruption of crypt-villus integrity in the small intestine due to a S-G2 cell cycle blockade.

Publication Title

Redeployment of Myc and E2f1-3 drives Rb-deficient cell cycles.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE56007
Expression data from control, Rb KO and Rb/Myc DKO tissues (villi and crypts)
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Loss of Myc corrects abrrant transcription in Rb KO villi, while these genetic manipulation does not lead to major gene expression changes in crypts.

Publication Title

Redeployment of Myc and E2f1-3 drives Rb-deficient cell cycles.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE71383
Balanced E2F transcriptional output is essential for tumor suppression in the liver
  • organism-icon Mus musculus
  • sample-icon 92 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

E2f8 mediates tumor suppression in postnatal liver development.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE71380
E2f regulation of gene expression in the liver [1 mo]
  • organism-icon Mus musculus
  • sample-icon 59 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

E2Fs are regulators of the cell cycle and are involved in development. In this study we examine transcriptional changes occurring the liver in E2f1 (1KI) and E2f3b (3bKI) knock in mice. These mice have E2f1 or E2f3b knocked into the E2F3a locus resulting in loss of E2f3a and expression of E2f1 or E2f3b from the E2f3a locus as originally described In Tsai et. al., Nature 2008.

Publication Title

E2f8 mediates tumor suppression in postnatal liver development.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE71381
E2f regulation of gene expression in the liver [12 mo]
  • organism-icon Mus musculus
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

E2Fs are regulators of the cell cycle and are involved in development and hepatocellular carcinoma. In this study we examine transcriptional changes occurring the liver in E2f1 (1KI) and E2f3b (3bKI) knock in mice. These mice have E2f1 or E2f3b knocked into the E2F3a locus resulting in loss of E2f3a and expression of E2f1 or E2f3b from the E2f3a locus as originally described In Tsai et. al., Nature 2008.

Publication Title

E2f8 mediates tumor suppression in postnatal liver development.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE64302
Expression Data from PtenF341V and Null Mouse Embryonic Fibroblasts
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

PTEN imparts tumor suppression in mice by cell autonomous and non-autonomous mechanisms. Whether these two tumor suppressor mechanisms are mediated through similar or distinct signaling pathways is not known. Here we generated and analyzed knockin mice that express a series of human cancer-derived mutant alleles of PTEN that differentially alter the Akt axis in either stromal or tumor cell compartments of mammary glands. We find that cell non-autonomous tumor suppression by Pten in stromal fibroblasts strictly requires activation of P-Akt signaling, whereas cell autonomous tumor suppression in epithelial tumor cells is independent of overt canonical pathway activation. These findings expose distinct Akt-dependent and independent tumor suppressor functions of PTEN in stromal fibroblasts and tumor cells, respectively, that can be used to guide clinical care of breast cancer patients

Publication Title

Noncatalytic PTEN missense mutation predisposes to organ-selective cancer development in vivo.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE64303
Expression Data from Pten mutant epithelial cells
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

PTEN imparts tumor suppression in mice by cell autonomous and non-autonomous mechanisms. Whether these two tumor suppressor roles are mediated through similar or distinct signaling pathways is not known. Here we generated and analyzed knockin mice that express a series of human cancer-derived mutant alleles of PTEN in either stromal or tumor cell compartments of mammary glands. We find that cell non-autonomous tumor suppression by Pten in stromal fibroblasts strictly requires activation of P-Akt signaling, whereas cell autonomous tumor suppression in epithelial tumor cells is independent of overt canonical pathway activation

Publication Title

Noncatalytic PTEN missense mutation predisposes to organ-selective cancer development in vivo.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon SRP117905
Differentiation of functional endothelial cells from human iPS cells
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Endothelial cell (EC) therapy may promote vascular growth or reendothelization in a variety of disease conditions. However, the production of a cell therapy preparation containing differentiated, dividing cells presenting typical EC phenotype, functional properties and chemokine profile is challenging. We focused on comparative analysis of seven small molecule-mediated differentiation protocols of ECs from human induced pluripotent stem cells. Differentiated cells showed a typical surface antigen pattern of ECs as characterized with flow cytometry analysis, functional properties, such as tube formation and ability to uptake acetylated LDL. Gene expression analysis by RNA sequencing revealed an efficient silencing of pluripotency genes and upregulation of genes related to cellular adhesion during differentiation. In addition, distinct patterns of transcription factor expression were identified during cellular reprogramming providing targets for more effective differentiation protocols in the future. Altogether, our results suggest that the most optimal EC differentiation protocol includes early inhibition of Rho-associated coiled-coil kinase and activation of cyclic adenosine monophosphate signaling, and inhibition of transforming growth factor beta signaling after mesodermal stage. These findings provide the first systematic characterization of the most potent signalling factors and small molecules used to generate ECs from human induced pluripotent stem cells. Consequently, this work improves the existing EC differentiation protocols and opens up new avenues for controlling cell fate for regenerative EC therapy. Overall design: Comparison of the effects of signalling factors and small molecules on endothelial cell differentiation from induced pluripotent stem cells using RNA-Seq. Following small molecules and growth factors were used in different combinations and time courses: 10 uM TGFß-inhibitor SB431542, 10 uM ROCK-inhibitor Y-27632, 20 ng/ml recombinant human BMP-4 and 0,25 mM 8-Br-cAMP. In all groups without TGFß-inhibitor at day 1 in the differentiation, it was added at day 4. In those groups with BMP-4 at day 1, it was removed at day 4. Differentiating ECs were passaged every 4-6 days using Accutase.

Publication Title

Temporal Dynamics of Gene Expression During Endothelial Cell Differentiation From Human iPS Cells: A Comparison Study of Signalling Factors and Small Molecules.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE32056
The effect of trypsin-2 on human tongue squamous cell carcinoma cell line gene expression
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The level of trypsin-2 has been shown to correlate with the malignancy and metastatic potential of many cancer.

Publication Title

Trypsin-2 enhances carcinoma invasion by processing tight junctions and activating ProMT1-MMP.

Sample Metadata Fields

Specimen part, Cell line

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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