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accession-icon GSE24150
b-AP15, a novel proteasome inhibitor
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Microarray based mRNA profiling was used to identify the mechanism of action for the small molecule b-AP15.

Publication Title

Inhibition of proteasome deubiquitinating activity as a new cancer therapy.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE9121
Genome-wide effects of acute progressive feed restriction in liver and white adipose tissue
  • organism-icon Rattus norvegicus
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Acute progressive feed restriction (APFR) represents a specific form of caloric restriction in which feed availability is increasingly curtailed over a period of a few days to a few weeks. It is often used for control animals in toxicological and pharmacological studies on compounds causing body weight loss to equalize weight changes between experimental and control groups and thereby, intuitively, to also set their metabolic states to the same phase. However, scientific justification for this procedure is lacking. In the present study, we analyzed by DNA microarrays the impact on hepatic gene expression in rats of two APFR regimens that caused identical diminution of body weight (19%) but differed slightly in duration (4 vs. 10 days). In addition, white adipose tissue (WAT) was also subjected to the transcriptomic analysis on day-4. The data revealed that the two regimens led to distinct patterns of differentially expressed genes in liver, albeit some major pathways of energy metabolism were similarly affected (particularly fatty acid and amino acid catabolism). The reason for the divergence appeared to be entrainment by the longer APFR protocol of peripheral oscillator genes, which resulted in derailment of circadian rhythms and consequent interaction of altered diurnal fluctuations with metabolic adjustments in gene expression activities. WAT proved to be highly unresponsive to the 4-day APFR as only 17 mRNA levels were influenced by the treatment. This study demonstrates that body weight is a poor proxy of metabolic state and that the customary protocols of feed restriction can lead to rhythm entrainment.

Publication Title

Genome-wide effects of acute progressive feed restriction in liver and white adipose tissue.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE29859
Expression data from hypervitaminosis A rat diaphyseal bone
  • organism-icon Rattus norvegicus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Vitamin A is the only known compound that produces spontaneous fractures in rats. In an effort to resolve the molecular mechanism behind this effect, we fed young rats high doses of vitamin A and performed a global transcriptional analysis of diaphyseal bone after one week, i.e. just before the first fractures appeared. Microarray gene expression analysis revealed that 68 transcripts were differentially expressed in hypervitaminotic cortical bone and 118 transcripts were found when the bone marrow was also included. 98% of the differentially expressed genes in the bone marrow sample were up-regulated. In contrast, hypervitaminotic cortical bone without marrow showed reduced expression of 37% of differentially expressed genes. Gene Ontology (GO) analysis revealed that only samples containing bone marrow were associated to a GO term, which principally represented extracellular matrix (ECM). This is consistent with the histological findings of increased endosteal bone formation. Four of the genes in this ECM cluster and four other genes, including Cyp26b1 which is known to be up-regulated by vitamin A, were selected and verified by real-time PCR. In addition, immunohistochemical staining of bone sections confirmed that the bone-specific molecule, osteoadherin (Omd) was up-regulated. Further analysis of the major gene expression changes revealed distinct differences between cortical bone and bone marrow, e.g. there appeared to be augmented Wnt signaling in the bone marrow but reduced Wnt signaling in cortical bone. Moreover, induced expression of hypoxia-associated genes was only found in samples containing bone marrow. Together, these results corroborate our previous observations of compartment-specific effects of vitamin A, with reduced periosteal but increased endosteal bone formation, and suggest important roles for Wnt signaling and hypoxia in the processes leading to spontaneous fractures.

Publication Title

Microarray profiling of diaphyseal bone of rats suffering from hypervitaminosis A.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon GSE29169
Expression data of Hmg20 knock down I/11 cells and controls
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We performed microarray analysis to investigate the gene expression profile changes induced by Hmg20b knock down in I/11 cells.

Publication Title

The DNA binding factor Hmg20b is a repressor of erythroid differentiation.

Sample Metadata Fields

Specimen part

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accession-icon GSE61039
Transcriptional Profiling of rat hypothalamic response to TCDD
  • organism-icon Rattus norvegicus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

In many mammals, halogenated aromatic hydrocarbon (HAH) exposure causes wasting syndrome, defined as lethal weight loss as a result of severe and persistent hypophagia. The most potent HAH in causing wasting is 2,3,7,8-tetrachlorodibenzo--dioxin (TCDD), which exerts its toxic effects through the aryl hydrocarbon receptor (AHR) a transcription factor. Because TCDD toxicity is thought to predominantly arise from dysregulation of AHR-transcribed genes, we hypothesized that wasting syndrome is due to TCDD-induced dysregulation of genes involved in regulation of food-intake. We therefore focused on the hypothalamus, as it is the regulatory center of food-intake and energy balance in the central nervous system. We profiled mRNA abundance in hypothalamic tissue from two rat strains with widely differing sensitivities to wasting syndrome: TCDD-sensitive Long-Evans rats and TCDD-resistant Han/Wistar rats, 23 hours after exposure to TCDD (100 g/kg) or corn oil vehicle. We found that TCDD exposure caused minimal transcriptional dysregulation effects in the hypothalamus, with only 6 genes changed in Long-Evans rats and 15 genes in Han/Wistar rats. Two of the most dysregulated genes were Cyp1a1 and Nqo1, which are induced by TCDD across a wide range of tissues and are considered sensitive markers of TCDD exposure. The minimal response of the hypothalamic transcriptome to a lethal dose of TCDD at an early time-point suggests that the hypothalamus is not the predominant site of initial events leading to hypophagia and associated wasting. TCDD may affect feeding behaviour via events upstream or downstream of the hypothalamus, and further work is required to evaluate this at the level of individual hypothalamic nuclei and subregions.

Publication Title

Transcriptional profiling of rat hypothalamus response to 2,3,7,8-tetrachlorodibenzo-ρ-dioxin.

Sample Metadata Fields

Sex

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accession-icon GSE18301
Transcriptional profiling of the rat adipose tissue response to TCDD
  • organism-icon Rattus norvegicus
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Rodents exposed to the environmental contaminant, TCDD, suffer from a number of acute and chronic toxicities, including lethality and a wasting syndrome. Hypothesizing that the wasting syndrome may be caused by changes in adipose tissue -- either in its hormonal regulation or in homeostatic effects -- we profiled the transcriptional response of rat white adipose to TCDD. We employed two separate rat strains: the Long-Evans strain is sensitive to TCDD toxicities while the Han/Wistar strain is over four orders of magnitude more resistant. One day after TCDD exposure few genes were altered in either strain, but after four days a modest number of transcriptional alterations were observed. Strikingly, TCDD had far fewer effects than did a feed-restriction protocol intended to mimic the wasting syndrome itself. Notably several classic TCDD-responsive genes were modulated at all time-points, including Cyp1a1, Cyp1b1, and Nqo1. We therefore concluded that rat adipose tissue is unlikely to be the primary driver of the wasting syndrome, and that another tissue is likely involved.

Publication Title

Transcriptional profiling of rat white adipose tissue response to 2,3,7,8-tetrachlorodibenzo-ρ-dioxin.

Sample Metadata Fields

Sex

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accession-icon GSE98156
Expression data of Arabidopsis leaves during extended darkening of the whole plant or an individual leaf
  • organism-icon Arabidopsis thaliana
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Arabidopsis Gene 1.1 ST Array (aragene11st)

Description

In Arabidopsis, an individually darkened leaf (IDL) initiates senescence much quicker than a leaf from an entirely darkened plant (DP).

Publication Title

Darkened Leaves Use Different Metabolic Strategies for Senescence and Survival.

Sample Metadata Fields

Specimen part

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accession-icon GSE43928
Expression data from TNF-stimulated mouse glomeruli
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The specific contribution of the two TNF-receptors Tnfr1 and Tnfr2 to TNF-induced inflammation in the glomerulus is unknown. In mice, TNF exposure induces glomerular expression of inflammatory mediators like adhesion molecules and chemokines in vivo, and glomerular accumulation of leukocytes.

Publication Title

Distinct contributions of TNF receptor 1 and 2 to TNF-induced glomerular inflammation in mice.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE81653
Development of complete personalized treatment plans for early stage colorectal cancer patients
  • organism-icon Homo sapiens
  • sample-icon 251 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

593 FFPE colorectal cancer samples were used to generate three prediction models: Recurrence prediction, 5FU efficacy prediction, and FOLFOX efficacy prediction

Publication Title

Building personalized treatment plans for early-stage colorectal cancer patients.

Sample Metadata Fields

Specimen part

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accession-icon GSE27975
HL-1 cardiomyocyte response to hypoxia
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Expression profiling of cultured HL-1 cardiomyocytes subjected to hypoxia for 8 hours.

Publication Title

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction.

Sample Metadata Fields

Cell line

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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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