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accession-icon GSE66083
Widespread association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Illumina HiSeq 2500

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genome-wide association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE66082
Widespread association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth [gene expression]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The goal of this study was to identify YAP/TAZ direct transcriptional targets and transcriptional partners, through ChIP-sequencing and gene expression profiling.

Publication Title

Genome-wide association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE25012
WNT pathway activation promotes phenotypic reprogramming of glioblastoma derived cells in zebrafish nervous system microenvironment
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

phenotypic reprogramming ability of teh zebtafish brain microenviroment on GBM derived cells controlled by the activation of endogenous Wnt pathway

Publication Title

Wnt activation promotes neuronal differentiation of glioblastoma.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon SRP059699
Canonical Wnt signalling regulates nuclear export of Setdb1 during skeletal muscle terminal differentiation [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The histone 3 lysine 9 methyltransferase Setdb1 is essential for both stem cell pluripotency and terminal differentiation of different cell types. To shed light on Setdb1 roles in these mutually exclusive processes, we used mouse skeletal myoblasts as a model of terminal differentiation. Ex vivo studies on isolated single myofibres showed that Setdb1 is required for muscle adult stem cells expansion following activation. In vitro studies in skeletal myoblasts confirmed that Setdb1 suppresses terminal myoblast differentiation. Genomic binding analyses showed a release of Setdb1 from the promoter of selected target genes upon myoblast terminal differentiation, concomitant to a nuclear export of Setdb1 to the cytoplasm. Both genomic release and cytoplasmic Setdb1 relocalisation during differentiation were dependent on canonical Wnt signalling. Together, our findings revealed Wnt-dependent subcellular relocalisation of Setdb1 as a novel mechanism regulating Setdb1 functions and adult myogenesis. Overall design: RNA-seq of knockdown of Setdb1 in myoblast cells (C2C12).

Publication Title

Canonical Wnt signalling regulates nuclear export of Setdb1 during skeletal muscle terminal differentiation.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP100979
HSF1-dependent and -independent regulation of the mammalian in vivo heat shock response and its impairment in Huntington's disease
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The heat shock response (HSR) is a mechanism to cope with proteotoxic stress by inducing the expression of molecular chaperones and other heat shock response genes. The HSR is evolutionarily well conserved and has been widely studied in bacteria, cell lines and lower eukaryotic model organisms. However, mechanistic insights into the HSR in higher eukaryotes, in particular in mammals, are limited. We have developed an in vivo heat shock protocol to analyze the HSR in mice and dissected heat shock factor 1 (HSF1)-dependent and -independent pathways. Whilst the induction of proteostasis-related genes was dependent on HSF1, the regulation of circadian function related genes, indicating that the circadian clock oscillators have been reset, was independent of its presence. Furthermore, we demonstrate that the in vivo HSR is impaired in mouse models of Huntington's disease but we were unable to corroborate the general repression of transcription after a heat shock found in lower eukaryotes. Overall design: RNA-Seq was performed on mRNA isolated from quadriceps femoris muscle of 24 mice. These mice were of wild type, R6/2, and Hsf1-/- genotypes. Two mice of each genotype were tested in four conditions: (1) heat shock, (2) control heat shock, (3) HSP90 inhibition (NVP-HSP990), and (4) HSP90 inhibition vehicle.

Publication Title

HSF1-dependent and -independent regulation of the mammalian in vivo heat shock response and its impairment in Huntington's disease mouse models.

Sample Metadata Fields

Age, Specimen part, Treatment, Subject

View Samples
accession-icon SRP008430
Whole genome expression analysis in the third-instar larval midgut of Drosophila melanogaster
  • organism-icon Drosophila melanogaster
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Survival of insects on a substrate containing toxic substances such as plant secondary metabolites or insecticides is dependent on the metabolism or excretion of those xenobiotics. The primary sites of xenobiotic metabolism are the midgut, Malpighian tubules and fat body. In general, these organs are treated as single tissues by online databases, but several studies have shown that gene expression within subsections of the midgut is compartmentalized. In this article, RNA sequencing analysis was used to investigate whole-genome expression in subsections of the third-instar larval midgut. The results support functional diversification in subsections of the midgut. Analysis of the expression of gene families that are implicated in the metabolism of xenobiotics suggests that metabolism may not be uniform along the midgut. These data provide a starting point for investigating gene expression and xenobiotic metabolism in the larval midgut. Overall design: Examination of expression in eight samples corresponding to compartments of gene expression in the midgut

Publication Title

Whole-genome expression analysis in the third instar larval midgut of Drosophila melanogaster.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE10445
MERLION LUNG CANCER STUDY
  • organism-icon Homo sapiens
  • sample-icon 70 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Series of stage IB lung adenocarcinomas and large cell carcinomas. The aim of the study was to predict outcome using a Copy Number Driven Gene Expression signature.

Publication Title

Prediction of clinical outcome in multiple lung cancer cohorts by integrative genomics: implications for chemotherapy selection.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE30684
Stem Cell Antigen-1 (Sca-1) Regulates Mammary Tumor Development and Cell Migration
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Stem cell antigen-1 (Sca-1 or Ly6A) is a member of the Ly6 family of glycosyl phostidylinositol (GPI)-anchored cell surface proteins. To determine the potential mechanisms by which Sca-1 regulates cell migration, adhesion, and tumor development; we performed an Affymetrix mouse genome 430A 2.0 array on cDNA comparing shLuc and shSca-1 from cells grown in vitro.

Publication Title

Stem cell antigen-1 (sca-1) regulates mammary tumor development and cell migration.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE78753
A Preclinical Model for ER-Positive Breast Cancer Points to the Epithelial Microenvironment as Determinant of Luminal Phenotype and Hormone Response
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A Preclinical Model for ERα-Positive Breast Cancer Points to the Epithelial Microenvironment as Determinant of Luminal Phenotype and Hormone Response.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE74608
A Preclinical Model for ER-Positive Breast Cancer Points to the Epithelial Microenvironment as Determinant of Luminal Phenotype and Hormone Response [BT20 & HCC1806]
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A high percentage of potential oncology drugs fail in clinical trials, partly because preclinical models used to test them are inadequate. Breast cancer is the leading cause of cancer-related death among women worldwide but we lack appropriate in vivo models for the ER+ subtypes, which represent more than 75% of all cases. We address these issues by xenografting tumor cells to their site of origin, the milk ducts. All ER+ cell lines and patient-derived xenografts grow mimicking their clinical counterparts. Disease progresses with invasion and metastasis, which become amenable to study. The action of hormones, important in breast carcinogenesis, can now be studied in a relevant context. Importantly, these open opportunities for development and evaluation of therapies.

Publication Title

A Preclinical Model for ERα-Positive Breast Cancer Points to the Epithelial Microenvironment as Determinant of Luminal Phenotype and Hormone Response.

Sample Metadata Fields

Specimen part

View Samples
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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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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