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accession-icon GSE104890
PAX5 transduction of Pax5-/- pro-B cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

After 5 days in culture with 2ng/ml of IL7, Pax5-/- transduced pro-B cells with PAX5A or PAX5B cDNA were sorted according to their EGFP positivity and total RNA was extracted.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE74600
Transcriptomic analysis and ChIP-seq in CCE-Rx cells to identify SOX2 transcription factor target genes
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Targeted resequencing identifies PTCH1 as a major contributor to ocular developmental anomalies and extends the SOX2 regulatory network.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE74598
Transcriptomic analysis after transfection in murine genetically modified stem cells overexpressing the RAX gene (CCE-Rx cells) of either a siRNA against SOX2 or a scramble siRNA
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

SOX2 is the main gene involved in anophthalmia. In order to identify genes regulated by SOX2 transcription factors (genes that could be good candidates to also be involved in ocular development), we studied transcriptomic profiles of murine genetically modified stem cells overexpressing the RAX gene (CCE-Rx cells) after transfection by a siRNA against SOX2 or a scramble siRNA.

Publication Title

Targeted resequencing identifies PTCH1 as a major contributor to ocular developmental anomalies and extends the SOX2 regulatory network.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE138236
Expression data in TDEC obtained from irradiated GBM stem cell
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Glioblastomas (GBM) are brain tumors which display a bad prognosis despite conventional treatment associating surgical resection and subsequent radio-chemotherapy. These tumors are defined by an abundant and abnormal vascularization as well as by an important cellular heterogeneity. GBM notably contain a subpopulation of GBM stem-like cells (GSC) which contribute to tumor aggressiveness, resistance, and recurrence. Moreover, GSC directly take part in the formation of new vessels via their transdifferentiation into tumor derived endothelial cells (TDEC). Considering the importance of the vascularization in the GBM, we postulate that radiation could enhance the transdifferentiation of GSC into TDEC. Here, we show that ionizing radiation potentiates endothelial features of TDEC obtained from 3 patient-derived primocultures of GSC. Indeed, TDEC obtained from irradiated GSC (TDEC IR+) migrate more towards VEGF, form more pseudotubes in Matrigel in vitro and develop more functional blood vessel in Matrigel plugs implanted in Nude mice than TDEC obtained from non-irradiated GSC. Transcriptomic analysis allows us to highlight an overexpression of Tie2 in TDEC IR+ which is associated with the activation of AKT signaling pathway. All radiation-induced effects on TDEC IR+ were abolished by using a Tie2 kinase inhibitor, confirming the role of Tie2 signaling pathway in this process. Finally, the number of Tie2+ vessels is increased in recurrent GBM compared with matched untreated tumors. In conclusion, we show that irradiation potentiates proangiogenic features of TDEC throught Tie2/AKT signaling pathway. New therapeutic stategies associating standard teatment and an inhibitor of Tie2 signaling pathway should be considered for forthcoming trials.

Publication Title

Ionizing radiation induces endothelial transdifferentiation of glioblastoma stem-like cells through the Tie2 signaling pathway.

Sample Metadata Fields

Specimen part

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accession-icon GSE40730
Genome-wide analysis of RNAs translationally regulated upon BRCA1 depletion in human mammary epithelial cells
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Loss of function of the tumor suppressor BRCA1 (Breast Cancer 1) protein is responsible for numerous familial and sporadic breast cancers. We previously identified PABP1 as a novel BRCA1 partner and showed that BRCA1 modulates translation through its interaction with PABP1. We showed that the global translation was diminished in BRCA1-depleted cells and increased in BRCA1-overexpressing cells. Our findings raised the question whether BRCA1 affects translation of all cytoplasmic cellular mRNAs or whether it specifically targets a subset of mRNAs.

Publication Title

BRCA1-Dependent Translational Regulation in Breast Cancer Cells.

Sample Metadata Fields

Cell line

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accession-icon GSE9098
Estrogen-modulated gene expression in c-kit+ stem cells and CD44+ stromal cells
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The recent interest in the role of bone marrow derived endothelial progenitor cells in the benefits of estrogen on cardiovascular health brought us to evaluate if estrogen could affect cardiac repair more broadly by regulating biological processes involved in the functional organization of the bone marrow stem cell niche.

Publication Title

Estrogen-induced gene expression in bone marrow c-kit+ stem cells and stromal cells: identification of specific biological processes involved in the functional organization of the stem cell niche.

Sample Metadata Fields

Sex, Age

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accession-icon GSE70302
Gene expression data of C57BL/6, Il1a-knockout and Il1b-knockout mice at 24 hours after spinal cord injury
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We have previously shown that Il1a-knockout (KO) mice exhibit rapid (at day 1) and persistent improvements in locomotion associated with reduced lesion volume compared with Il1b-KO mice and C57BL/6 controls after traumatic spinal cord injury (SCI). To investigate the mechanism by which Il1a mediates its detrimental effect, we analyzed the transcriptome of the injured spinal cord of Il1a-KO, Il1b-KO and C57BL/6 mice at 24 hours after SCI using GeneChip microarrays.

Publication Title

IL-1α Gene Deletion Protects Oligodendrocytes after Spinal Cord Injury through Upregulation of the Survival Factor Tox3.

Sample Metadata Fields

Specimen part

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accession-icon GSE29232
Identification of androgen-regulated genes in RWPE-1-AR cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Transcriptional profiling of RWPE-1 cells stably expressing human androgen receptor (as described in Altintas et al., Mol Cell Endocrinol 2011) treated with a non-metabolisable androgen, R1881

Publication Title

No associated publication

Sample Metadata Fields

Treatment

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accession-icon GSE44047
Secreted Frizzled-Related Protein 5 is Downregulated in Obesity and Promotes -Cell Proliferation
  • organism-icon Rattus norvegicus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Downregulation of Sfrp5 promotes beta cell proliferation during obesity in the rat.

Sample Metadata Fields

Specimen part

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accession-icon GSE43536
Effects of overexpressed Atoh8 on the transcriptional profile of mouse ductal cells mPAC in the absence or presence of co-expressed Neurogenin3
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The basic helix-loop-helix (bHLH) transcription factors of the Drosophilas atonal-related superfamily Neurogenin3 (Neurog3) and NeuroD1 promote endocrine differentiation in the gastrointestinal tract. Atonal Homolog 8 (Atoh8/Math6) is a newly identified member of the atonal-related family whose expression is induced by Neurog3 and NeuroD1 in cell culture, indicating a possible role for this gene in the endocrine differentiation program downstream of these two pro-endocrine factors. Intriguingly, available experimental evidence based on a reduced number of genes suggests that Atoh8 may negatively regulate Neurog3-targeting events. In this study, we have analyzed global changes in gene expression profiles upon exogenous expression of Atoh8 alone or in combination with Neurog3 in mouse pancreatic duct (mPAC) cells. These cells activate neuroendocrine-specific gene expression in response to Neurog3 and NeuroD1 and thus serve as an optimal model to evaluate the proendocrine activity of Atoh8. We have compared transcriptional profiles between mPAC cells treated with a recombinant adenovirus expressing Atoh8 (Ad-Atoh8) or a control adenovirus encoding B-galactosidase (Ad-Bgal), and between cells treated with Ad-Neurog3+Ad-Bgal or cells treated with Ad-Neurog3+Ad-Atoh8. The results obtained show that Atoh8 exhibits a very modest transcriptional activity in these cells thus confirming that Atoh8 does not function as a proendocrine gene. Furthermore, our data also confirm the ability of Atoh8 to block Neurog3-dependent transcriptional activation events. However, since repression is only seen for a small subset of Neurog3 gene targets, we discard a general role of Atoh8 as a negative regulator of Neurog3 pro-endocrine activity.

Publication Title

Characterization of the transcriptional activity of the basic helix-loop-helix (bHLH) transcription factor Atoh8.

Sample Metadata Fields

Cell line, Treatment

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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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