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accession-icon GSE53951
Gene expression after type-I interferon treatment in primary neurons, primary fibroblasts and L929 cells
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Microarray expression profilling of mouse primary mixed cortical/hippocampal neurons, primary fibroblasts and L929 cells to compare ISGs signature in disctinct cell types

Publication Title

Inefficient type I interferon-mediated antiviral protection of primary mouse neurons is associated with the lack of apolipoprotein l9 expression.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP073318
mRNA expression of breast cancer cell lines across different densities [SCRB-Seq]
  • organism-icon Homo sapiens
  • sample-icon 87 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

mRNA expression profiles for 3 breast cancer cell lines seeded at different density and grown for different duration Overall design: This experiment is part of a study fo the effect of cell density on drug sensitivity [1]. Cells plated at different densities in 384-well plates were harvested at the indicated times and RNA was extracted using the RNeasy mini kit (Qiagen). To ensure sufficient RNA amounts wells with low cell numbers were pooled. Some conditions have been tested in biollogical replicates grown at the same time. Libraries were prepared by the Broad Technology Labs (BTL) following the protocol for SCRB-Seq described in [2]. Transcripts were quantified by the BTL computational pipeline using Cuffquant version 2.2.1 [3]. [1] Hafner, M., Niepel, M., Chung, M., Sorger, P.K., Growth rate inhibition metrics correct for confounders in measuring sensitivity to cancer drugs. DOI:10.1038/NMETH.3853 [2] Soumillon, M., Cacchiarelli, D., Semrau, S., van Oudenaarden, A. & Mikkelsen, T.S. Characterization of directed differentiation by high-throughput single-cell RNA-Seq http://biorxiv.org/content/early/2014/03/05/003236 [3] Trapnell, C., Roberts, A., Goff, L., Pertea, G., Kim, D., Kelley, D.R., Pimentel, H., Salzberg, S.L., Rinn, J.L. & Pachter, L. Differential gene and transcript expression analysis of RNA-seq experiments with TopHat and Cufflinks, Nat. Protoc. 7, 562-578 (2012).

Publication Title

Growth rate inhibition metrics correct for confounders in measuring sensitivity to cancer drugs.

Sample Metadata Fields

Subject

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accession-icon GSE30516
Dynamic re-wiring of apoptotic signaling networks enhances tumor cell killing by DNA damage
  • organism-icon Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Crosstalk and complexity within signaling pathways has limited our ability to devise rational strategies for using network biology to treat human disease. This is particularly problematic in cancer where oncogenes that drive or maintain the tumorigenic state alter the normal flow of molecular information within signaling networks that control growth, survival and death. Understanding the architecture of oncogenic signaling pathways, and how these networks are re-wired by ligands or drugs, could provide opportunities for the specific targeting of oncogene-driven tumors. Here we use a systems biology-based approach to explore synergistic therapeutic strategies to optimize the killing of triple negative breast cancer cells, an incompletely understood tumor type with a poor treatment outcome. Using targeted inhibition of oncogenic signaling pathways combined with DNA damaging chemotherapy, we report the surprising finding that time-staggered EGFR inhibition, but not simultaneous co-administration, can dramatically sensitize the apoptotic response of a subset of triple-negative cells to conventional DNA damaging agents. A systematic analysis of the order and timing of inhibitor/genotoxin presentationusing a combination of high-density time-dependent activity measurements of signaling networks, gene expression profiles, cell phenotypic responses, and mathematical modelingrevealed an approach for altering the intrinsic oncogenic state of the cell through dynamic re-wiring of oncogenic signaling pathways. This process converts these cells to a less tumorigenic state that is more susceptible to DNA damage-induced cell death, through re-activation of an extrinsic apoptotic pathway whose function is suppressed in the oncogene-addicted state.

Publication Title

Sequential application of anticancer drugs enhances cell death by rewiring apoptotic signaling networks.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE148414
Eye-antenna early L3 disc expression profiling in combinations of COX7a-LoF, ATF4-LoF and Notch-GoF
  • organism-icon Drosophila melanogaster
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Gene expression in larval, early third instar eye-antenna discs was assessed to reveal an ATF4 contribution to target gene induction following COX7a knockdown. As hypothesised, these COX7a-RNAi induced target genes require the transcription factor ATF4 for induction, irrespective of concomitant Notch pathway activation through Delta over-expression.

Publication Title

ATF4-Induced Warburg Metabolism Drives Over-Proliferation in Drosophila.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE148407
Eye-antenna early L3 disc expression profiling in COX7a-LoF and Notch-GoF
  • organism-icon Drosophila melanogaster
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Gene expression in larval, early third instar eye-antenna discs was assesed in genotypes with Notch Gain-of-Function (UAS-Delta or UAS-Notch[intra2]) over-expression or mitochondrial COX7a Loss-of-function (UAS-COX7a-RNAi) or a combination of both (UAS-Delta, UAS-COX7a-RNAi). The analysis revealed that, despite a strong genetic interaction between Notch pathway activation and knockdown of COX7a, no transcriptional cooperation or synergy was detectable in early L3 eye-antenna discs. Rather, COX7a knockdown induced a unique transcriptional signature, which further experiments revealed to be mediated by the transcription factor ATF4.

Publication Title

ATF4-Induced Warburg Metabolism Drives Over-Proliferation in Drosophila.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE25595
The small RNA PhrS stimulates synthesis of the Pseudomonas aeruginosa quinolone signal
  • organism-icon Pseudomonas aeruginosa
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Pseudomonas aeruginosa Array (paeg1a)

Description

Quorum sensing, a cell-to-cell communication system based on small signal molecules, is employed by the human pathogen Pseudomonas aeruginosa to regulate virulence and biofilm development. Moreover, regulation by small trans-encoded RNAs has become a focal issue in virulence gene expression of bacterial pathogens. In this study, we have identified the small RNA PhrS as an activator of PqsR synthesis, one of the key quorum sensing regulators in P. aeruginosa. Genetic studies revealed a novel mode of regulation by a sRNA, whereby PhrS uses a base-pairing mechanism to activate a short upstream open reading frame to which the pqsR gene is translationally coupled. Expression of phrS is induced by the oxygen-responsive regulator ANR when the oxygen supply decreases. Thus, PhrS is the first bacterial sRNA that provides a regulatory link between oxygen availability and quorum sensing, which may impact on oxygen-limited growth in P. aeruginosa biofilms.

Publication Title

The small RNA PhrS stimulates synthesis of the Pseudomonas aeruginosa quinolone signal.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP148659
Total RNA profiles in response to four tyrosine kinase inhibitors in human induced pluripotent stem cell-derived cardiomyocytes
  • organism-icon Homo sapiens
  • sample-icon 671 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To define molecular markers of tyrosine kinase inhibitor-induced cardiotoxicity, we measured transcriptome changes in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) treated with one of four tyrosine kinase inhibitors (Erlotinib, Lapatinib, Sorafenib, or Sunitinib) displaying a range of mild to severe cardiotoxicity or a vehicle-only control (DMSO). Gene expression changes were assessed at the cell population level using total RNA-seq, which measured levels of both mRNAs and non-coding RNAs. hiPSC-CMs used in this study were the Cor.4U cells purchased from Ncardia. Overall design: hiPSC-CMs were treated with each TKI (Erlotinib, Lapatinib, Sorafenib or Sunitinib) at three doses (1, 3 and 10 µM) for 24 hours and the intermediate dose (3 µM) for an additional three time points (6h, 72h and 168h). hiPSC-CMs were also treated with the DMSO vehicle-only control at four time points (6h, 24h, 72h and 168h). Each treatment condition had three biological replicates, collected from three independent experiments using three different lots of hiPSC-CMs. Total RNA was collected from all these samples.

Publication Title

Adaptation of Human iPSC-Derived Cardiomyocytes to Tyrosine Kinase Inhibitors Reduces Acute Cardiotoxicity via Metabolic Reprogramming.

Sample Metadata Fields

Sex, Specimen part, Subject, Compound, Time

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accession-icon SRP131032
Small molecule screen identifies de novo nucleotide synthesis as a vulnerability of cells lacking SIRT3
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Sirtuin 3 (SIRT3) is an NAD+-dependent deacetylase downregulated in aging and age-associated diseases such as cancer and neurodegeneration, and high fat diet (HFD)-induced metabolic disorders. Thus, we performed a small molecule screen and identified an unexpected metabolic vulnerability associated with SIRT3 loss. Overall design: RNA sequencing in SV40T immortalized SIRT3 WT (triplicates) and SIRT3 KO MEF (duplicates) lines under normal conditions.

Publication Title

Small-Molecule Screen Identifies De Novo Nucleotide Synthesis as a Vulnerability of Cells Lacking SIRT3.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE2639
HUVEC gene profile after TNF-stimulation
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

HUVEC were left untreated or stimulated for 5h with 2 ng/ml TNF. Comparsion of the gene profiles revealed TNF-mediated gene expression changes in HUVEC.

Publication Title

TNF induces distinct gene expression programs in microvascular and macrovascular human endothelial cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE2638
HMEC gene profile after TNF-stimulation
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

HMEC cultures were left untreated or stimulated for 5h with 2 ng/ml TNF. Comparison of the gene expression profiles revealed the TNF-mediated gene expression changes.

Publication Title

TNF induces distinct gene expression programs in microvascular and macrovascular human endothelial cells.

Sample Metadata Fields

No sample metadata fields

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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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