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accession-icon GSE104859
Gene Expression of MCF10A cells expresing ERAS
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

ERAS (Embryonic stem (ES) cell-expressed Ras) is a constitutively active member of the Ras family that is not expressed in adult tissues, and has been involved in breast cancer.

Publication Title

The Ras-related gene ERAS is involved in human and murine breast cancer.

Sample Metadata Fields

Cell line

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accession-icon GSE69517
Expression in E. coli of hyper- and hypo-amyloidogenic RepA-WH1 variants
  • organism-icon Escherichia coli k-12
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

RepA-WH1 is a synthetic bacterial prionoid, i.e., a protein that aggregates as amyloid in bacteria leading to cell death

Publication Title

Outlining Core Pathways of Amyloid Toxicity in Bacteria with the RepA-WH1 Prionoid.

Sample Metadata Fields

Disease, Time

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accession-icon SRP162673
Caveolin-1 modulates mechanotransduction responses to substrate stiffness through actin-dependent control of YAP
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The transcriptional regulator YAP orchestrates important cell functions, determining tissue homeostasis, organ growth control, and tumorigenesis. Mechanical stimuli are a key input to YAP activity, but the mechanisms controlling this regulation remain largely uncharacterized. We show that CAV1 positively modulates the YAP mechanoresponse to substrate stiffness through actin cytoskeleton-dependent and Hippo kinase-independent mechanisms. RHO activity is necessary but not sufficient for CAV1-dependent mechanoregulation of YAP activity. Systematic quantitative interactomic studies and image-based siRNA screenings provide evidence that this actin-dependent regulation is determined by YAP interaction with the 14-3-3 protein YWHAH. Constitutive YAP activation rescued phenotypes associated with CAV1 loss, including defective ECM remodeling. CAV1-mediated control of YAP activity was validated in vivo in a model of pancreatitis-driven acinar-to-ductal metaplasia. We propose that this CAV1-YAP mechanotransduction system controls a significant share of cell programs linked to these two pivotal regulators, with potentially broad physiological and pathological implications. Overall design: RNA-Seq in WT and Cav1KO mouse embryonic fibroblasts (MEFs) cultured on stiff or soft polyacrylamide hydrogels

Publication Title

Caveolin-1 Modulates Mechanotransduction Responses to Substrate Stiffness through Actin-Dependent Control of YAP.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon SRP029466
Homeostatic skin contains two different subsets of resident macrophages with distinct origin and gene profile.
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

We have found the existence of two independent populations contributing to the skin-resident macrophage pool based on their different origin. We have analyzed their gene profile by deep-sequencing (RNA-Seq). Analysis of RNA-Seq data revealed a differential expression signature between both subsets of skin macrophages for 744 of 17741 genes compiled (198 of them showing similar normalized expression levels across replicates). We have further characterized their specialized functions related to their different gene profiles. Overall design: Examination of gene profile of 2 different macrophage subsets coexisting in skin under steady state.

Publication Title

Pivotal role for skin transendothelial radio-resistant anti-inflammatory macrophages in tissue repair.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE26807
The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mapping 250K Sty2 SNP Array (mapping250ksty), Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Preclinical activity of LBH589 alone or in combination with chemotherapy in a xenogeneic mouse model of human acute lymphoblastic leukemia.

Sample Metadata Fields

Sex, Specimen part, Cell line

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accession-icon GSE26790
The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (TOM-1 and MOLT-4)
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mapping 250K Sty2 SNP Array (mapping250ksty), Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Histone deacetylases (HDACs) have been identified as therapeutic targets due to regulatory function in DNA structure and organization. We have analyzed the role of the LBH589, a novel pan inhibitor of class I and II HDACs, in Acute Lymphoblastic Leukemia. In vitro, LBH589 was shown to induce a dose dependent antiproliferative and apoptotic effect which was associated with an increase in the acetylation of H3 and H4 histone acetylation which was uniformly in every genetic subgroup of ALL. In vivo administration of LBH589 in BALB/c-RAG2-/-c-/- mice in which T and B-cell leukemic cell lines were injected induced a significant reduction in tumor growth (TOM-1, p<0.01 and MOLT-4 p<0.05). Leukemic cells from patients were employed to establish a xenograft model of human leukemia in BALB/c-RAG2-/-c-/- mice and further transplanted in consecutive generations of mice. Treatment of these xenografts with LBH589 induced an increase in the acetylation of H3 and H4 and prolonged the survival of mice in comparison with the animals treated with Vincristine and Dexametasone (p<0.05) and this effect was significantly higher when LBH589 was combined with Vincristine and Dexametasone (p<0.001). Our results that the use of LBH589 in combination with standard chemotherapy represents an attractive option for treatment of patients with ALL.

Publication Title

Preclinical activity of LBH589 alone or in combination with chemotherapy in a xenogeneic mouse model of human acute lymphoblastic leukemia.

Sample Metadata Fields

Cell line

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accession-icon SRP064190
Chronic Activation of ?2 AMPK Induces Obesity and Reduces Beta Cell Function
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Despite significant advances in our understanding of the biology determining systemic energy homeostasis, the treatment of obesity remains a medical challenge. Activation of AMP-activated protein kinase (AMPK) has been proposed as an attractive strategy for the treatment of obesity and its complications. AMPK is a conserved, ubiquitously expressed, heterotrimeric serine/threonine kinase whose short-term activation has multiple beneficial metabolic effects. Whether these translate into long-term benefits for obesity and its complications is unknown. Here, we observe that mice with chronic AMPK activation, resulting from mutation of the AMPK ?2 subunit, exhibit ghrelin signalling-dependent hyperphagia, obesity and impaired pancreatic islet insulin secretion. Humans bearing the homologous mutation manifest a congruent phenotype. Our studies highlight that long-term AMPK activation can have adverse metabolic consequences with implications for pharmacological strategies seeking to chronically activate AMPK systemically to treat metabolic disease. Overall design: Transcriptomic profiling of the hypothalamic arcuate nucleus from AMPK ?2 R299Q knock-in mice

Publication Title

Chronic Activation of γ2 AMPK Induces Obesity and Reduces β Cell Function.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE117013
Gene expression array of brain, mandible and maxilla tissues from P0 FoxO6-/- and wildtype mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

FoxO6 is expressed in the brain, craniofacial region and somite, but the precise role of FoxO6 in craniofacial development remain unknown. We found that FoxO6 is expressed specifically in craniofacial tissues and FoxO6-/- mice undergo expansion of the face, frontal cortex, olfactory component and skull.

Publication Title

FoxO6 regulates Hippo signaling and growth of the craniofacial complex.

Sample Metadata Fields

Specimen part

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accession-icon GSE24768
Influence of Set7/9 on hESC differentiation
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We analyzed the role of the histone lysine methyltransferase Set7/9 in the differentiation of human embryonic stem (ES) cells. Human ES cell lines expressing a control short hairpin and a short hairpin against Set7/9 were established and the genome wide expression profile was compared between both cell lines at different days during differentiation. Analysis of both profiles indicates that in the absence of Set7/9 there is a delay in the silencing of self-renewal factors as well as in the induction of differentiation markers. These results indicate that Set7/9 plays an active role in the differentiation of human ES cells.

Publication Title

SETD7 Regulates the Differentiation of Human Embryonic Stem Cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP032541
Transcriptome analysis of yeast methyltransferase mutants set5?, set1? and set5?set1?
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: Understand the synergistic relationship between the methyltransferases Set1 and Set5 in the regulation of gene expression. Methods: Total mRNA was obtained from two independent biological replicates each of wildtype (WT), set1?, set5?, SET5 Y402A and set1?set5? S. cerevisiae strains. Libraries were generated and sequenced using an Illumina HiSeq2000 platform. The sequence reads that passed quality filters were mapped using TopHat and expression levels were quantified using Cufflinks. Results: We generated FPKM expression values for each transcript and identified the differentially expressed genes using an FDR-adjusted p-value of 0.05. Subsequent data analysis was restricted to genes with fold-change greater than 1.7 relative to WT. Our results show that Set1 and Set5 have roles primarily in transcription repression. Moreover, lack of both Set1 and Set5 results in a synergistic exhacerbation of the transcriptional derepression observed in the single mutants. Further analysis revealed a specific enrichment of the Set5/Set1-repressed genes near repetitive DNA sequences of the genome. Conclusions: Our study uncovers an unexpected synergistic role of Set1 and Set5 in transcription repression of telomeric regions and Ty retrotransposons. Overall design: mRNA profiles of wildtype (WT), set1?, set5?, SET5 Y402A and set1?set5? were generated by sequencing using an Illumina HiSeq2000 platform. Two biological replicates of each strain were used.

Publication Title

Transcriptome profiling of Set5 and Set1 methyltransferases: Tools for visualization of gene expression.

Sample Metadata Fields

Cell line, 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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