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accession-icon SRP102705
AKHR F1 heterozygous progeny of obese parents and controls, 10-11 days old adults
  • organism-icon Drosophila melanogaster
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Transgenerational effects of parental metabolic state have been shown, but the mechanism is still unclear. Here we present transcriptome sequencing data from AKHR heterozygous F1 progeny, either from obese maternal or paternal parents, compared to genetically matched heterozygous controls or to wild-type controls Overall design: 3 AKHR heterozygous samples descended from obese maternal parents, 3 AKHR heterozygous samples descended from obese paternal parents, 3 AKHR heterozygous samples descended from non-obese parents, and 3 wild-type controls, independent biological replicates and independent experimental replicates (1 set of samples from each experimental replicate)

Publication Title

Parental obesity leads to metabolic changes in the F2 generation in <i>Drosophila</i>.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE43830
Long Noncoding RNA MALAT1 Controls Cell Cycle Progression by Regulating the Expression of Oncogenic Transcription Factor B-MYB
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

Transcriptome analysis of control and MALAT1 lncRNA-depleted RNA samples from human diploid lung fibroblasts [WI38]

Publication Title

Long noncoding RNA MALAT1 controls cell cycle progression by regulating the expression of oncogenic transcription factor B-MYB.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE37458
Expression data from WT and VAChT KDHOM ventricles
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

VAChT KDHOM mice have a 70% decrease in the vesicular acetylcholine transporter (VAChT) and this leads to a systemic decrease in ACh release and cardiac dysfunction.

Publication Title

An analysis of the myocardial transcriptome in a mouse model of cardiac dysfunction with decreased cholinergic neurotransmission.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE98321
Epididymal white adipose tissue expression data from WT and Abhd15-ko mice on normal chow diet at refed state
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

Abhd15 is mainly expressed in white adipose tissues and highly upregulated upon adipogenesis. Abhd15 expression is correlated with insulin resistance in obese humans, however its physiological function remains unknown. We used the microarray technology to gain insight into ABHD15s physiological function by identifying dysregulated genes in eWAT from Abhd15-ko mice in comparison to WT mice.

Publication Title

Loss of ABHD15 Impairs the Anti-lipolytic Action of Insulin by Altering PDE3B Stability and Contributes to Insulin Resistance.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE154789
Gene expression profiles in SATB2-knockdown and control human glioblastoma stem cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Effects of SATB2 knockdown on gene expression were evaluated by microarray analysis in human glioblastoma stem cells

Publication Title

SATB2 drives glioblastoma growth by recruiting CBP to promote FOXM1 expression in glioma stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE41313
Expression data from breast cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 152 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Breast cancer is a genetically and phenotypically complex disease. To understand the role of microRNAs in this molecular complexity, we performed miRNA expression analysis in a cohort of molecularly well-characterized human breast cancer (BC) cell lines to discover miRNAs associated with the most common molecular subtypes and the most frequent genetic aberrations.Using a microarray carrying LNA modified oligonucleotide capture probes (Exiqon), expression levels of 725 human miRNAs were measured in 51 BC cell lines. MiRNA expression was explored by unsupervised cluster analysis and then associated with the molecular subtypes and genetic aberrations commonly present in breast cancer. Unsupervised cluster analysis using the most variably expressed miRNAs divided the 51 BC cell lines into a major and a minor cluster predominantly mirroring the luminal and basal intrinsic subdivision of BC cell lines. One hundred and thirteen miRNAs were differentially expressed between these two main clusters of which half were related to the ER-status of the cell lines. Forty miRNAs were differentially expressed between basal-like and normal-like/claudin-low cell lines. Within the luminal-group of cell lines, 39 miRNAs were associated with ERBB2 overexpression and 24 miRNAs with E-cadherin gene mutations, which are frequent in this subtype of BC cell lines. In contrast, 31 different miRNAs were associated with E-cadherin promoter hypermethylation, which, contrary to E-cadherin mutation, is exclusively observed in BC cell lines that are not of luminal origin. The differential expression of 30 miRNAs were associated with p16INK4 status while only a few differentially expressed miRNAs were associated with BRCA1, or PIK3CA/PTEN, TP53 mutation status of the cell lines (P-value < 0.05). Twelve miRNAs were associated with DNA copy number variation of the respective locus. Luminal-basal and epithelial-mesenchymal associated miRNAs determine the overall subdivision of miRNA transcriptome of BC cell lines. Specific sets of miRNAs were associated with ERBB2 overexpression, p16INK4aor E-cadherin mutation or E-cadherin methylation status, which implies that these miRNAs may contribute to the driver role of the genetic aberrations. Additionally, miRNAs, which are located in a genomic region showing recurrent genetic aberrations, may themselves play a driver role in breast carcinogenesis or contribute to a driver gene in their vicinity. In short, our study provides detailed molecular miRNA portraits of BC cell lines, which can be exploited for functional studies of clinically important miRNAs.

Publication Title

miRNA expression profiling of 51 human breast cancer cell lines reveals subtype and driver mutation-specific miRNAs.

Sample Metadata Fields

Cell line

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accession-icon GSE44636
LMO3 is a novel regulator of adipogenesis
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Human but not mouse adipogenesis is critically dependent on LMO3.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE41712
Expression data from mock- or LMO3 silenced differentiating adipose stem cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

In this study we aimed to gain further insight on the role of GCs in adipocyte differentiation. For the future drugability of candidate targets it is of utmost importance to find factors relevant to human biology. Thus, we analyzed the transcriptome of GC induced primary human adipose stem cells (hASC) to identify novel factors downstream of GC action

Publication Title

Human but not mouse adipogenesis is critically dependent on LMO3.

Sample Metadata Fields

Specimen part

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accession-icon GSE44626
Expression data from mock- or LMO3-silenced human preadipocytes isolated from SAT or VAT
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

In this study, we aimed to gain further insight on the role of glucocorticoids (GCs) in adipocyte differentiation. For the future drugability of candidate targets, it is of utmost importance to find factors relevant to human biology. Thus, we analyzed the transcriptome of GC-induced primary human adipose stem cells (hASCs) isolated from paired subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) to identify novel factors downstream of GC action.

Publication Title

Human but not mouse adipogenesis is critically dependent on LMO3.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE41683
Expression data from dexamethsone-treated human adipose stem cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

In this study we aimed to gain further insight on the role of GCs in adipocyte differentiation. For the future drugability of candidate targets it is of utmost importance to find factors relevant to human biology. Thus, we analyzed the transcriptome of GC induced primary human adipose stem cells (hASC) to identify novel factors downstream of GC action

Publication Title

Human but not mouse adipogenesis is critically dependent on LMO3.

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)

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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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