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accession-icon GSE71731
The impact of PPAR activation on whole genome gene expression in human precision-cut liver slices
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

Background: Studies in mice have shown that PPAR is an important regulator of lipid metabolism in liver and a key transcription factor involved in the adaptive response to fasting. However, much less is known about the role of PPAR in human liver. Here we set out to study the function of PPAR in human liver via analysis of whole genome gene regulation in human liver slices treated with the PPAR agonist Wy14643.

Publication Title

The impact of PPARα activation on whole genome gene expression in human precision cut liver slices.

Sample Metadata Fields

Sex, Specimen part, Treatment, Subject, Time

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accession-icon GSE23371
Transcriptomes of monocyte-derived DCs stimulated with various compounds
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Little is known about the early transcriptional events in innate immune signaling in immature and tolerogenic monocyte-derived dendritic cells (DCs), the professional antigen-presenting cells of our immune system. TLR ligands usually induce a proinflammatory transcriptional response, whereas IL10 and/or dexamethasone induce a more tolerogenic phenotype.

Publication Title

MicroRNA genes preferentially expressed in dendritic cells contain sites for conserved transcription factor binding motifs in their promoters.

Sample Metadata Fields

Specimen part

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accession-icon GSE18698
Functional differences among human postnatal stem cells of different origin are reflected by their transcriptome
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

GENES ASSOCIATED WITH THE CELL CYCLE, LINEAGE COMMITMENT AND IMMUNOMODULATORY POTENTIAL DISCRIMINATE HUMAN POSTNATAL STEM CELLS OF DIFFERENT ORIGIN.

Publication Title

Functional differences between mesenchymal stem cell populations are reflected by their transcriptome.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE54747
An intrahepatic gene expression signature of enhanced immune activity predicts response to peginterferon and adefovir in chronic hepatitis B patients
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

In this study we aimed to identify a baseline intrahepatic transcriptional signature associated with response in chronic hepatitis B patients treated with peginterferon-alfa-2a (peg-IFN) and adefovir.

Publication Title

An intrahepatic transcriptional signature of enhanced immune activity predicts response to peginterferon in chronic hepatitis B.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE50010
Modulation of NKG2D ligand expression and metastasis in tumors by spironolactone via RXR-gamma activation
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Tumor metastasis and lack of NKG2D ligand (NKG2DL) expression are associated with poor prognosis in patients with colon cancer. Here we found that spironolactone (SPIR), an FDA-approved diuretic drug with a long-term safety profile, can upregulate NKG2DL expression in multiple colon cancer cell lines by activating the ATM-Chk2-mediated checkpoint pathway, which in turn enhances tumor elimination by natural killer cells. SPIR can also upregulate the expression of metastasis-suppressor genes TIMP2 and TIMP3, thereby reducing tumor cell invasiveness. Although SPIR is an aldosterone antagonist, its anti-tumor effects are independent of the mineralocorticoid receptor pathway. Instead, by screening the human nuclear hormone receptor siRNA library, we identify retinoid X receptor gamma (RXR gamma) as being indispensable for the anti-tumor functions of SPIR. Collectively, our results strongly support the use of SPIR or other RXR gamma-agonists with minimal side effects for colon cancer prevention and therapy.

Publication Title

Modulation of NKG2D ligand expression and metastasis in tumors by spironolactone via RXRγ activation.

Sample Metadata Fields

Treatment

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accession-icon SRP028963
p53 shapes genome-wide changes in small non-coding RNA expression during the human DNA damage response
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Small RNA-seq on MCF10A, HCT116 and HCT116p53-/- cell lines after induction of DNA damage (5 Gy Irradiation). Overall design: Small RNA-seq on MCF10A, HCT116 and HCT116p53-/- at 4 and 24 hours after induction of DNA damage (5 Gy Irradiation), done in duplicate with respective control (0 hour) using illumina Genome Analyzer IIx

Publication Title

p53 shapes genome-wide and cell type-specific changes in microRNA expression during the human DNA damage response.

Sample Metadata Fields

Cell line, Treatment, Subject, Time

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accession-icon SRP026484
Oncogenic Hras-dependent epidermal growth is inhibited following RNAi-mediated depletion of Ctnnb1 and Mllt6
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Genome-wide RNAi screens in mice identified Ctnnb1 and Mllt6 as physiological regulators of HrasG12V-dependent epidermal hyperplasia. To probe the consequences of Ctnnb1 and Mllt6 on HrasG12V-dependent oncogenic growth, we examined how their depletion impacts gene expression in the HrasoncoX2 epidermis. We performed RNA-seq analysis of FACS-purified embryonic epidermal cells, followed by network analysis of differentially regulated transcripts. Whether Ctnnb1 or Mllt6, knockdown markedly enhanced activity of genes restricting growth, and decreased expression of genes promoting epidermal proliferation. This contrasted with known transcriptional changes that typically follow epidermal expression of oncogenic Hras. Moreover, there was a significant overlap in genes whose expression was affected by Mllt6 and ß-catenin, further implying a level of shared function. Overall design: Transcriptional profiles of epidermal progenitors of embryonic day 18.5 animals of wild-type, HrasG12V, and HrasG12V depleted of Ctnnb1 or Mllt6 backgrounds.

Publication Title

RNAi screens in mice identify physiological regulators of oncogenic growth.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE33634
Topoisomerase II inhibitors and histone eviction
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Drug-induced histone eviction from open chromatin contributes to the chemotherapeutic effects of doxorubicin.

Sample Metadata Fields

Age, Specimen part, Cell line, Treatment, Time

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accession-icon GSE33626
Tissue selective effects of topoisomerase II inhibitors in vivo
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

One major class of anti-cancer drugs targets topoisomerase II to induce DNA double-strand breaks and cell death of fast growing cells. In vitro experiments showed that doxorubicin can induce histone eviction as well as DNA damage, while etoposide can only induce DNA damage. Here, we compare the transcription responses of different tissues to doxorubicin or etoposide treatment in vivo.

Publication Title

Drug-induced histone eviction from open chromatin contributes to the chemotherapeutic effects of doxorubicin.

Sample Metadata Fields

Age, Specimen part, Treatment, Time

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accession-icon SRP108762
RNA sequencing to determine the contribution of kinase receptor transactivation to G protein coupled receptor signalling in vascular smooth muscle cells
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

G protein coupled receptor (GPCR) signalling covers three major mechanisms. GPCR agonist engagement allows for the G proteins to bind to the receptor leading to a classical downstream signalling cascade. The second mechanism is via the utilization of the ß-arrestin signalling molecule and thirdly via transactivation dependent signalling. GPCRs can transactivate protein tyrosine kinase receptors (PTKR) to activate respective downstream signalling intermediates. In the past decade GPCR transactivation dependent signalling was expanded to show transactivation of serine/threonine kinase receptors (S/TKR). Kinase receptor transactivation enormously broadens the GPCR signalling paradigm. This work utilizes next generation RNA-sequencing to study the contribution of transactivation dependent signalling to total protease activated receptor (PAR)-1 signalling. Transactivation, assessed as gene expression, accounted for 50 percent of the total genes regulated by thrombin acting through PAR-1 in human coronary artery smooth muscle cells. GPCR transactivation of PTKRs is approximately equally important as the transactivation of the S/TKR with 209 and 177 genes regulated respectively, via either signalling pathway. This work shows that genome wide studies can provide powerful insights into GPCR mediated signalling pathways Overall design: Human CASMCS cells were subject to various treatments: basal, thrombin, thrombin + SB, thrombin + AG and thrombin + SB + AG. Gene expression was studies after 30 minutes to assess genes that are differentially expressed by treat emnt with agonists and antagonists. The agonoists and antagonists are associated with transactivation of GPCRs and the gene expression results will help identify relevant genes.

Publication Title

RNA sequencing to determine the contribution of kinase receptor transactivation to G protein coupled receptor signalling in vascular smooth muscle cells.

Sample Metadata Fields

Specimen part, Treatment, Subject

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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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