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accession-icon GSE51498
Regulation of HSF1-mediated transcriptional programs by PGC-1alpha
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We examined global gene expression patterns in response to PGC-1 expression in cells derived from liver or muscle.

Publication Title

Direct link between metabolic regulation and the heat-shock response through the transcriptional regulator PGC-1α.

Sample Metadata Fields

Specimen part

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accession-icon GSE81171
Inhibition of adhesion molecule gene expression and cell adhesion by the metabolic regulator PGC-1alpha
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Cell adhesion plays an important role in determining cell shape and function in a variety of physiological and pathophysiological conditions. While links between metabolism and cell adhesion were previously suggested, the exact context and molecular details of such a cross-talk remain incompletely understood.

Publication Title

Inhibition of Adhesion Molecule Gene Expression and Cell Adhesion by the Metabolic Regulator PGC-1α.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE87100
Control of secreted protein gene expression and the mammalian secretome by the metabolic regulator PGC-1a
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Secreted proteins serve pivotal roles in the development of multicellular organisms, acting as structural matrix, extracellular enzymes and signal molecules. In this study we demonstrate, unexpectedly, that PGC-1, a critical transcriptional co-activator of metabolic gene expression, functions to down-regulate expression of diverse genes encoding secreted molecules and extracellular matrix (ECM) components to modulate the secretome. We show that both endogenous and exogenous PGC-1 down-regulate expression of numerous genes encoding secreted molecules. Mechanistically, results obtained using mRNA stability measurements as well as intronic RNA expression analysis are consistent with a transcriptional effect of PGC-1 on expression of genes encoding secreted proteins. Interestingly, PGC-1 requires the central heat shock response regulator HSF1 to affect some of its targets, and both factors co-reside on several target genes encoding secreted molecules in cells. Finally, using a mass spectrometric analysis of secreted proteins, we demonstrate that PGC-1 modulates the secretome of mouse embryonic fibroblasts (MEFs).

Publication Title

Control of Secreted Protein Gene Expression and the Mammalian Secretome by the Metabolic Regulator PGC-1α.

Sample Metadata Fields

Specimen part

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accession-icon GSE6342
Impact of Animal Strain on Gene Expression in a Rat Model of Acute Cardiac Rejection
  • organism-icon Rattus norvegicus
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

The expression levels of many genes show wide natural variation among strains or populations. This study investigated the potential for animal strain-related genotypic differences to confound gene expression profiles in acute cellular rejection (ACR). Additional analysis allowed for selection of 49 candidate genes uniquely associated with ACR, but only after accounting for the unexpectedly large effect of animal strain. Studies of ACR that examine gene expression in peripheral blood may be confounded by strain differences. These results indicate the need for study designs that eliminate or control for the large effect of genetic background on the transcriptome of immune cells.

Publication Title

Impact of animal strain on gene expression in a rat model of acute cardiac rejection.

Sample Metadata Fields

Specimen part

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accession-icon SRP099191
Mouse mammary fibroblast gene expression comparison between nulliparous and involution day 6.
  • organism-icon Mus musculus
  • sample-icon 57 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We tested the gene expression difference between PDGFRa+ fibroblasts FACS sorted from nulliparous balb/c mouse mammary glands and 6 days post-weaning mammary glands Overall design: 2 biological replicates of fibroblasts from nulliparous mammary glands and 3 biological replicates of fibroblasts from 6 days post-weaning mammary glands were used for comparison.

Publication Title

Physiologically activated mammary fibroblasts promote postpartum mammary cancer.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP119303
Endothelial Transcriptome Remodeling in a Mouse Model of Chronic Hypertension
  • organism-icon Mus musculus
  • sample-icon 104 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Aims: Hypertension poses a significant challenge to vasculature homeostasis and stands as the most common cardiovascular disease in the world. Its effects are especially profound on vasculature-lining endothelial cells that are directly exposed to the effects of excess pressure. Here, we characterize the in vivo transcriptomic response of cardiac endothelial cells to hypertension using the spontaneous hypertension mouse model BPH/2J. Methods and results: Verification of defective endothelial function in the BPH/2J hypertensive mouse strain was followed by acute isolation of cardiac endothelial cells and transcriptional profiling using RNA sequencing. Gene profiles from normotensive BPN/3J mice were compared to hypertensive animals. We observed over 3000 transcriptional differences between groups including pathways consistent with the cardiac fibrosis found in hypertensive animals. Importantly, many of the fibrosis-linked genes also differ between juvenile pre-hypertensive and adult hypertensive BPH/2J mice, suggesting that these transcriptional differences are hypertension-related. We also show that blood pressure normalization with amlodipine resulted in a subset of genes reversing their expression pattern, supporting the hypertension-dependency of altered gene expression. Yet, other transcripts were recalcitrant to therapeutic intervention illuminating the possibility that hypertension may irreversibly alter some endothelial transcriptional patterns. Conclusions: Hypertension has a profound effect on both function and transcription of endothelial cells, the latter of which was only partially restored with normalization of blood pressure. This study represents one of the first to quantify how endothelial cells are reprogrammed at the molecular level in cardiovascular pathology and advances our understanding of the transcriptional events associated with endothelial dysfunction. Overall design: Endothelium from hypertensive mice were acutely extracted at two different ages (4 weeks and 22 weeks) and compared to endothelium from 22 week old normotensive mice.

Publication Title

Endothelial transcriptomics reveals activation of fibrosis-related pathways in hypertension.

Sample Metadata Fields

Age, Cell line, Subject

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accession-icon SRP166768
Spatial chromosome folding and active transcription drive DNA fragility and formation of oncogenic MLL translocations [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

How spatial chromosome organization influences genome integrity is still poorly understood. Here we show that DNA double-strand breaks (DSBs) mediated by topoisomerase 2 (TOP2) activities, are enriched at chromatin loop anchors with high transcriptional activity. Recurrent DSBs occur at CTCF/cohesin bound sites at the bases of chromatin loops and their frequency positively correlates with transcriptional output and directionality. The physiological relevance of this preferential positioning is indicated by the finding that genes recurrently translocating to drive leukemias, are highly transcribed and are enriched at loop anchors. These genes accumulate DSBs at recurrent hot spots that give rise to chromosomal fusions relying on the activity of both TOP2 isoforms and on transcriptional elongation. We propose that transcription and 3D chromosome folding jointly pose a threat to genomic stability, and are key contributors to the occurrence of genome rearrangements that drive cancer. Overall design: Nuclear RNA profiling in lymphoblastoid TK6 cell line

Publication Title

Spatial Chromosome Folding and Active Transcription Drive DNA Fragility and Formation of Oncogenic MLL Translocations.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE4824
Analysis of lung cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 162 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

These arrays are used for various projects

Publication Title

DNA amplification is a ubiquitous mechanism of oncogene activation in lung and other cancers.

Sample Metadata Fields

Sex, Age, Race

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accession-icon SRP058107
Homo sapiens Raw sequence reads
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

RNA sequencing of tumor transcriptomes

Publication Title

Robust gene expression and mutation analyses of RNA-sequencing of formalin-fixed diagnostic tumor samples.

Sample Metadata Fields

No sample metadata fields

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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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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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