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accession-icon GSE104272
Combination effect of G-TPP and LXR623 on stem cell like glioma cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

We performed microarray analysis in order to evaluate the combination effect of the mitochondrial matrix chaperone inhibitor gamitrinib-triphenylphosphonium (G-TPP) and Liver X receptor agonist LXR623 on gene expression in stem cell like glioma cells (NCH644).

Publication Title

Activation of LXR Receptors and Inhibition of TRAP1 Causes Synthetic Lethality in Solid Tumors.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon SRP106312
Transcriptional profile of TL1A transgenic mice
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

To assess the effect of different forms of TL1A within different organs of the mouse we generated 2 different transgenic mouse lines where TL1A was expressed under the control of the CD2 promoter. 2 forms of TL1A was used. Either WT TL1A, which led to over expression of both membrane bound and soluble forms of TL1A (Refered to as Mem+Sol) or TL1A Delta 69-93 which only overexpressed membrane restricted TL1A (Refered to as Mem). Lungs and terminal ileums were taken from Either Mem, Mem+sol or WT litermate control mice at 12 weeks of age and the transcriptome assessed using RNAseq Through this we demonstrated enrichment of different transcripts and pathways both dependent on and independent of the form of TL1A and the site of action. This study is also the first to use RNASeq to assess the resualt of overexpression of TL1A within the mouse. Overall design: Poly-A purified mRNA profiles from the Ileum and Lung of Mem, Mem+Sol and WT mice generated using Illumina based RNASeq

Publication Title

Cleavage of TL1A Differentially Regulates Its Effects on Innate and Adaptive Immune Cells.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon E-MEXP-1443
Transcription profiling by array of Arabidopsis guard cells and mesophyll cells in response to ABA treatment
  • organism-icon Arabidopsis thaliana
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Transcriptional profiling of guard cells and mesophyll cells in response to ABA treatment

Publication Title

Isolation of a strong Arabidopsis guard cell promoter and its potential as a research tool.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Compound

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accession-icon GSE101291
Gene expression analysis of IDH1 wild type and IDH1 R132H mutated U87 cells
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

U87 cells were transduced with IDH1 WT or IDH1 R132H and stable clones were selected.

Publication Title

Induction of synthetic lethality in IDH1-mutated gliomas through inhibition of Bcl-xL.

Sample Metadata Fields

Specimen part

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accession-icon SRP056668
Foxc1 reinforces quiescence in hair follicle stem cells
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Illumina HiSeq 2500

Description

Quiescent stem cells are periodically activated to maintain tissue homeostasis or occasionally called into action upon injury. Molecular mechanisms that constitutively maintain stem cell identity or promote stem cell proliferation and differentiation upon activation have been extensively studied. However, it is unclear how quiescent stem cells maintain identity and reinforce quiescence when they transition from quiescence to activation. Here we show mouse hair follicle stem cell compartment induces a transcription factor, Foxc1, when activated. Importantly, deletion of Foxc1 in the activated but not quiescent stem cells compromises stem cell identity, fails to re-establish quiescence and subsequently drives premature stem cell activation.These findings uncover a dynamic, cell-intrinsic mechanism employed by hair follicle stem cells to reinforce stemness in response to activation. Overall design: Poly(A)-enriched transcriptome RNA-seq on HFSCs isolated in WT and K14Cre cKO mice at anagen and early telogen stage of hair cycle.

Publication Title

Foxc1 reinforces quiescence in self-renewing hair follicle stem cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE69131
Gene Expression of primary rat hippocampal neurons after Ncoa3 knockdown
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.0 ST Array (ragene20st)

Description

We identified Ncoa3 as a regulator of neuronal morphology and microRNA activity. In order to uncover target genes of this transcriptional coactivator we performed this microarray analysis.

Publication Title

A large-scale functional screen identifies Nova1 and Ncoa3 as regulators of neuronal miRNA function.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE69915
Expression profiling of 5 novel breast cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

The Fra-1 transcription factor promotes tumor cell growth, invasion and metastasis. While characterizing five breast cancer cell lines derived from primary human breast tumors, we identified BRC-31 as a novel basal-like cell model that expresses elevated Fra-1 levels. BRC-31 cells display elevated FAK, SRC and ERK2 phosphorylation relative to luminal breast cancer models. Inhibition of this signaling axis, through the use of pharmacological inhibitors, reduces the phosphorylation and stabilization of Fra-1. Elevated integrin V3 expression in these cells suggested that integrin receptors might activate this FAK-SRC-ERK2 signaling axis to enhance Fra-1 phosphorylation. These cells also express high levels of uPAR, a GPI-anchored receptor that has been shown to enhance integrin-mediated signaling initiated by Vitronectin engagement. Transient knockdown of uPAR in BRC31 cells grown on Vitronectin reduces Fra-1 phosphorylation and stabilization and uPAR and Fra-1 are required for Vitronectin-induced cell invasion. In clinical samples, a molecular component signature consisting of Vitronectin-uPAR-uPA-Fra-1 predicts poor overall survival in patients with breast cancer and correlates with a Fra-1 transcriptional signature. Taken together, we have identified a novel-signaling axis that leads to phosphorylation and stabilization of Fra-1, a transcription factor that is emerging as an important modulator of breast cancer progression and metastasis.

Publication Title

Integrin-uPAR signaling leads to FRA-1 phosphorylation and enhanced breast cancer invasion.

Sample Metadata Fields

Age, Disease, Disease stage

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accession-icon SRP083902
The Cdc42/Rac1 regulator CdGAP is a novel E-cadherin transcriptional co-repressor with Zeb2 in breast cancer
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The loss of E-cadherin causes dysfunction of the cell-cell junction machinery, which is an initial step in epithelial-to-mesenchymal transition (EMT), facilitating cancer cell invasion and the formation of metastases. A set of transcriptional repressors of E-cadherin (CDH1) gene expression, including Snail1, Snail2 and Zeb2 mediate E-cadherin down-regulation in breast cancer. However, the molecular mechanisms underlying the control of E-cadherin expression in breast cancer progression remain largely unknown. Here, by using global gene expression approaches, we uncover a novel function for Cdc42 GTPase-activating protein (CdGAP) in the regulation of expression of genes involved in EMT. We found that CdGAP used its proline-rich domain to form a functional complex with Zeb2 to mediate the repression of E-cadherin expression in ErbB2-transformed breast cancer cells. Conversely, knockdown of CdGAP expression led to a decrease of the transcriptional repressors Snail1 and Zeb2, and this correlated with an increase in E-cadherin levels, restoration of cell-cell junctions, and epithelial-like morphological changes. In vivo, loss of CdGAP in ErbB2-transformed breast cancer cells impaired tumor growth and suppressed metastasis to lungs. Finally, CdGAP was highly expressed in basal-type breast cancer cells, and its strong expression correlated with poor prognosis in breast cancer patients. Together, these data support a previously unknown nuclear function for CdGAP where it cooperates in a GAP-independent manner with transcriptional repressors to function as a critical modulator of breast cancer through repression of E-cadherin transcription. Targeting Zeb2-CdGAP interactions may represent novel therapeutic opportunities for breast cancer treatment. Overall design: Total RNA profiles of ErbB2-expressing control mammary tumor explants cells (shCON) and CdGAP-depleted cells (shCdGAP) were generated by deep sequencing, in triplicate, using Illumina HiSEq2000.

Publication Title

The Cdc42/Rac1 regulator CdGAP is a novel E-cadherin transcriptional co-repressor with Zeb2 in breast cancer.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE2603
Subpopulations of MDA-MB-231 and Primary Breast Cancers
  • organism-icon Homo sapiens
  • sample-icon 119 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Subpopulations of MDA-MB-231 that exhibit different metastatic tropisms when injected into immuno-deficient mice. Also, a cohort of primary breast cancers surgically resected at the Memorial Sloan-Kettering Cancer Center (MSKCC).

Publication Title

Genes that mediate breast cancer metastasis to lung.

Sample Metadata Fields

Specimen part

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accession-icon GSE18866
Expression data from doxycylin-inducible miR-15a/16-1 and empty vector (EV) expression in a 13q14-\- cell line
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Reexpression of microRNAs miR-15a/16-1 in a cell line deficient for these miRs (homozygous deletion of chromosomal region 13q14) results in the downregulation of certain mRNAs.

Publication Title

The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.

Sample Metadata Fields

Cell line

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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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