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accession-icon GSE58516
Effects of bisphenol A on gene expression in adipocytes from lean children: association to metabolic disorders
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Bisphenol A (BPA) is a xenobiotic endocrine disrupting chemical. In vitro and in vivo studies indicated that BPA alters endocrine-metabolic pathways in adipose tissue increasing the risk of developing metabolic disorders. BPA effects on human adipocytes, specifically in children, are poorly investigated. To investigate in childhood the effect of exposure to BPA on metabolic disorders we analyzed in vitro the effects of environmentally relevant doses of BPA on gene expression of mature human adipocytes from pre-pubertal lean patients and on related physiological outcomes. Adipocytes from children were treated in vitro with BPA and gene expression was evaluated by qRT-PCR. Genome wide analyses were performed using GeneChip Human Gene 1.0 ST array. Lipid content in adipocytes was estimated by ORO staining and Triglyceride Quantification Kit. Secreted IL-1, in adipocytes culture medium, and insulin, in PANC-1 culture medium, were performed using ELISA assays. BPA was found to promote up-regulation of ER and ERR, and down-regulation of GPR30 expression modulating estrogen signaling and following a non-linear dose-response. Microarray data analysis demonstrated that BPA increases the gene expression of pro-inflammatory cytokines and lipid metabolism-related FABP4 and CD36 in adipocytes. PCSK1 resulted the most interesting gene being down-regulated by BPA thus impairing insulin production in pancreas. BPA promotes inflammation and lipid metabolism dysregulation in adipocytes from lean children. Moreover, PCSK1 can be a key gene in BPA action modulating insulin production. Exposure to BPA in childhood may be an important risk factor in developing obesity and metabolic disorders.

Publication Title

Bisphenol A effects on gene expression in adipocytes from children: association with metabolic disorders.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE47920
Expression data from T lymphocytes derived from T-iPS and peripheral blood
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

T lymphocytes can be generated from T-cell-derived induced pluripotent stem cells (T-iPS). We used microarrays to better elucidate their phenotype and compare their gene expression profile to that of known lymhoid subsets from peripheral blood.

Publication Title

Generation of tumor-targeted human T lymphocytes from induced pluripotent stem cells for cancer therapy.

Sample Metadata Fields

Specimen part

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accession-icon GSE17584
Transcriptional effects of CRP* expression in Escherichia coli
  • organism-icon Escherichia coli
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Escherichia coli exhibits diauxic growth in sugar mixtures due to CRP-mediated catabolite repression and inducer exclusion related to phosphotransferase system enzyme activity. Replacement of the native crp gene with a catabolite repression mutant (referred to as crp*) alleviates diauxic effects in E. coli and enables co-utilization of glucose and other sugars. While previous studies have examined the effects of expressing CRP* mutants on the expression of specific catabolic genes, little is known about the global transcriptional effects of CRP* expression.

Publication Title

Transcriptional effects of CRP* expression in Escherichia coli.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP202546
The oncogenic action of NRF2 depends on de-glycation by Fructosamine-3-kinase (FN3K)
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We show that NRF2 activation drives hepatocellular carcinoma development in vivo. Moreover, NRF2 undergoes glucose dependent modification called glycation and requires the de-glycating enzyme FN3K to maintain NRF2' oncogenic functions. Overall design: Gene expression analysis in MYC-driven murine HCC with and without NRF2 activation. NRF2 is activated by targeting its negative regulators Keap1 or Cul3 or targeting NRF2 ETGE motif by sgRNA/Cas9 editing.

Publication Title

The Oncogenic Action of NRF2 Depends on De-glycation by Fructosamine-3-Kinase.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject

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accession-icon GSE37088
Follicular Lymphoma expression array
  • organism-icon Homo sapiens
  • sample-icon 71 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

We used microarrays to detail gene expression profile of several follicular lymphoma patient samples with different grades

Publication Title

Frequent disruption of the RB pathway in indolent follicular lymphoma suggests a new combination therapy.

Sample Metadata Fields

Specimen part

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accession-icon GSE14807
Investigation of over-expressing Annexin receptor cell line with and without agonists
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The therapeutic potential of pro-resolution factors in determining the outcome of inflammatory events has gained ground over the past decade. However, the attention has been focused on the non-genomic effects of these endogenous, anti-inflammatory substances. In this study, we have focused our attention on identifying specific annexin 1 (AnxA1) protein/ALX receptor mediated gene activation, in an effort to identify down-stream genomic targets of this well-known, glucocorticoid induced, pro-resolution factor.

Publication Title

Downstream gene activation of the receptor ALX by the agonist annexin A1.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE24392
Lhx1 is required for specification of renal progenitor cell field
  • organism-icon Xenopus laevis
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome Array (xenopuslaevis)

Description

The goal of this study is to investigate the molecular mechanism of lhx1 on regulation of pronephros formation during the early embryonic development. In the vertebrate embryo the kidney is derived from the intermediate mesoderm. The LIM-class homeobox transcription factor lhx1 is expressed early in the intermediate mesoderm and is one of the first genes to be expressed in the nephric mesenchyme. The animal cap cells can be induced by treatment of activin and retinoic acid to differentiate into pronephros tissue. In this study we investigated the role of Lhx1 in differentiation of pronephros by depleting lhx1 in the organ culture system. We generated the gene expression profile of early pronephros tissue, and demonstrated that expression of genes from all the kidney domains is affected by the absence of lhx1. Taken together our results highlight an essential role for Lhx1 in pronephros formation.

Publication Title

Lhx1 is required for specification of the renal progenitor cell field.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE69079
Expression data of sleeping, waking, and sleep deprived adult heterozygous aldh1l1 eGFP-L10a mice
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Transcriptomic studies revealed that hundreds of mRNAs show differential expression in the brains of sleeping versus awake rats, mice, flies, and sparrows. Although these results have offered clues regarding the molecular consequences of sleep and sleep loss, their functional significance thus far has been limited. This is because the previous studies pooled transcripts from all brain cells, including neurons and glia.

Publication Title

Transcriptome profiling of sleeping, waking, and sleep deprived adult heterozygous Aldh1L1 - eGFP-L10a mice.

Sample Metadata Fields

Disease

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accession-icon GSE23881
Kinetic gene expression profiles of chicken macrophage HD11 cells in response to endotoxin from Salmonella typhimurium-798
  • organism-icon Gallus gallus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Genome Array (chicken)

Description

HD11 cells were stimulated with 1 ug/ml endotoxin from ST-798 for 1, 2, 4 and 8 hours

Publication Title

Unique genome-wide transcriptome profiles of chicken macrophages exposed to Salmonella-derived endotoxin.

Sample Metadata Fields

Cell line, Time

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accession-icon SRP071252
Transcriptome of new DGCR8_KO mouse embryonic stem cells generated by paired CRISPR/Cas9 approach
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study was to obtain the trasncriptome of DGCR8_KO mESCs to compare it with the transcriptome of WT mESCs (deposit separately). Overall design: mRNA profiles of DGCR8_KO mouse embryonic stem cells were generated by deep sequencing, in duplicate, using Illumina HiSeq2000.

Publication Title

Noncanonical function of DGCR8 controls mESC exit from pluripotency.

Sample Metadata Fields

Specimen part, 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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