refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 3078 results
Sort by

Filters

Technology

Platform

accession-icon GSE49373
Expression data from the lungs of Scnn1b-Transgenic and wild-type mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Airway mucus obstruction triggers macrophage activation and MMP12-dependent emphysema

Publication Title

Airway mucus obstruction triggers macrophage activation and matrix metalloproteinase 12-dependent emphysema.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE3860
Comparison of HutchinsonGilford Progeria Syndrome fibroblast cell lines to control fibroblast cell lines
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

HutchinsonGilford progeria syndrome (HGPS) is a rare genetic disease with widespread phenotypic features resembling premature aging. HGPS was recently shown to be caused by dominant mutations in the LMNA gene, resulting in the in-frame deletion of 50 amino acids near the carboxyl terminus of the encoded lamin A protein. Children with this disease typically succumb to myocardial infarction or stroke caused by severe atherosclerosis at an average age of 13 years. To elucidate further the molecular

Publication Title

Genome-scale expression profiling of Hutchinson-Gilford progeria syndrome reveals widespread transcriptional misregulation leading to mesodermal/mesenchymal defects and accelerated atherosclerosis.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE18639
Pluripotency Genes Overexpressed in Primate Embryonic Stem Cells Are Localized on Homologues of Human 16, 17, 19 and X
  • organism-icon Macaca mulatta
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Rhesus Macaque Genome Array (rhesus)

Description

While human embryonic stem cells (hESCs) are predisposed towards chromosomal aneploidities on 12, 17, 20 and X, rendering them susceptible to transformation, the specific genes expressed are not yet known. Here, by identifying the genes over expressed in pluripotent rhesus ESCs (nhpESCs) and comparing them to both their genetically-identical differentiated progeny (teratoma fibroblasts) as well as genetically-related differentiated parental cells (parental skin fibroblasts from whom gametes were used for ESC derivation), we find that some of those over expressed genes in nhpESCs cluster preferentially on rhesus chromosomes 16, 19, 20 and X, homologues of human chromosomes 17, 19, 16 and X respectively. Differentiated parental skin fibroblasts display gene expression profiles closer to nhpESC profiles than to teratoma cells, which are genetically identical to the pluripotent nhpESCs. Twenty over and under expressed pluripotency modulators, some implicated in neurogenesis, have been identified. The over expression of some of these genes discovered using pedigreed nhpESCs derived from prime embryos generated by fertile primates, which is impossible to perform with the anonymously donated clinically-discarded embryos from which hESCs are derived, independently confirms the importance of chromosome 17 and X regions in pluripotency and suggests specific candidates for targeting differentiation and transformation decisions.

Publication Title

Pluripotency genes overexpressed in primate embryonic stem cells are localized on homologues of human chromosomes 16, 17, 19, and X.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE7534
Pedigreed Primate Embryonic Stem Cells Express Homogeneous Familial Gene Profiles
  • organism-icon Macaca mulatta
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Rhesus Macaque Genome Array (rhesus)

Description

Pedigreed primate ESCs display homogeneous and reliable expression profiles.

Publication Title

Pedigreed primate embryonic stem cells express homogeneous familial gene profiles.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE26869
Regulation of myogenic progenitor proliferation in human fetal skeletal muscle by BMP4 and its antagonist Gremlin.
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Analysis of the transcriptome of mononuclear side population (SP) and main population (MP) cells of human fetal skeletal muscle from 12 human subjects of gestational age 14-18 weeks.

Publication Title

Regulation of myogenic progenitor proliferation in human fetal skeletal muscle by BMP4 and its antagonist Gremlin.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE38290
Functional analysis of ABCB5 in melanoma cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Functional analysis of ABCB5 in A375 and G3361 melanoma cells, by comparing stably-transfected controls to ABCB5-shRNA-targeted cells.

Publication Title

ABCB5 maintains melanoma-initiating cells through a proinflammatory cytokine signaling circuit.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE26569
VEGFR-1 expressed by malignant melanoma initiating cells is required for tumor growth
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Melanoma growth is driven by malignant melanoma initiating cells (MMIC) identified by expression of the ATP-binding cassette (ABC) member, ABCB5. ABCB5+ melanoma subpopulations have been shown to overexpress the vasculogenic differentiation markers CD144 (VE-cadherin) and TIE-1 and are associated with CD31-negative vasculogenic mimicry (VM), an established biomarker associated with increased patient mortality. Here we identify a critical role for VEGFR-1 signaling in ABCB5+ MMIC-dependent VM and tumor growth. Global gene expression analyses, validated by mRNA and protein determinations, revealed preferential expression of VEGFR-1 on ABCB5+ tumor cells purified from clinical melanomas and established melanoma lines. In vitro, VEGF induced in a VEGFR-1-dependent manner expression of CD144 in ABCB5+ subpopulations that constitutively expressed VEGFR-1, but not in ABCB5- bulk populations that were predominantly VEGFR-1-negative. In vivo, melanomaspecific shRNA-mediated knockdown of VEGFR-1 blocked the development of ABCB5+ VM morphology and inhibited ABCB5+ VM-associated production of the secreted melanoma mitogen, laminin. Moreover, melanoma-specific VEGFR-1 knockdown markedly inhibited tumor growth (by >90%). Our results demonstrate that VEGFR-1 function in MMIC regulates VM and associated laminin production, and show that this function represents one mechanism through which MMIC promote tumor growth.

Publication Title

VEGFR-1 expressed by malignant melanoma-initiating cells is required for tumor growth.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE92988
Expression data from microRNA-520f transfected PANC-1 pancreas carcinoma cells.
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

MicroRNA-520f regulates EMT, as it activates CDH1 (mRNA) and E-cadherin (protein) expression, and it suppresses tumor cell invasion. We have characterized miR-520f target genes through whole genome transcriptional profiling of miRNA transfected pancreas cancer cells (PANC-1).

Publication Title

miRNA-520f Reverses Epithelial-to-Mesenchymal Transition by Targeting <i>ADAM9</i> and <i>TGFBR2</i>.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE72149
Autism-like syndrome is induced in mice by pharmacological suppression of BET proteins
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Studies investigating the causes of autism spectrum disorder (ASD) point to genetic as well as epigenetic mechanisms of the disease. Identification of epigenetic processes that contribute to ASD development and progression is of major importance and may lead to the development of novel therapeutic strategies. Here we identify the bromodomain and extra-terminal domain containing transcriptional regulators (BETs) as epigenetic drivers of an ASD-like disorder in mice. We found that the pharmacological suppression of the BET proteins by a novel, highly selective and brain-permeable inhibitor, I-BET858, leads to selective suppression of neuronal gene expression followed by the development of an autism-like syndrome in mice. Many of the I-BET858 affected genes have been linked to ASD in humans thus suggesting the key role of the BET-controlled gene network in ASD. Our studies also suggest that environmental factors controlling BET proteins or their target genes may contribute to the epigenetic mechanism of ASD.

Publication Title

Autism-like syndrome is induced by pharmacological suppression of BET proteins in young mice.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE59557
Expression data of in vitro generated regulatory T cells overexpressing E47
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

E47 represses Foxp3 transcription, albeit indirectly through the activation of unknown negative regulatory of Foxp3 transcription.

Publication Title

Id3 Maintains Foxp3 Expression in Regulatory T Cells by Controlling a Transcriptional Network of E47, Spi-B, and SOCS3.

Sample Metadata Fields

Age, Specimen part

View Samples
...

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

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact