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accession-icon GSE21611
Oscillating gene expression determines competence for periodic branching in the Arabidopsis root
  • organism-icon Arabidopsis thaliana
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

The Oscillation Zone (OZ) of unsynchronized roots was disected and divided into an upper (OZ2) and lower (OZ1) half .

Publication Title

Oscillating gene expression determines competence for periodic Arabidopsis root branching.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE15876
The SHR/SCR pathway directly activates genes involved in asymmetric cell division in the Arabidopsis root
  • organism-icon Arabidopsis thaliana
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Asymmetric division of cortex/endodermal initials (CEI) in the Arabidopsis root generates two layers of ground tissue and is controlled by a finely orchestrated interplay between the transcription factors, SHORT ROOT (SHR) and SCARECROW (SCR). To understand the dynamics of the SHR/SCR regulatory network we performed microarray time course experiments using inducible versions of SHR and SCR and examined their transcriptional effects specifically in the ground tissue.

Publication Title

Spatiotemporal regulation of cell-cycle genes by SHORTROOT links patterning and growth.

Sample Metadata Fields

Treatment

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accession-icon GSE37749
Chronic inflammation and carcinogenesis caused by intestinal specific ablation of integrin alpha6 beta4
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Inflammatory bowel diseases (IBD) in humans are characterized by chronic inflammation and gastrointestinal tissue damage, caused by a combination of genetic and environmental factors. It has been largely documented that IBD frequently lead to colorectal cancers (CRC). The identification of causative factors of IBD is thus essential to understand CRC progression and develop therapeutical approaches. Models have been described in which molecular alterations are combined with inflammatory treatments in order to recapitulate IBD-associated CRC. Here, we describe a mouse line, 6fl/fl Villin-Cre, in which inactivation of the gene encoding the integrin alpha-6 subunit (ITGA6) specifically in the intestinal mucosa results into chronic inflammation and intestinal carcinogenesis. In these mice, the loss of integrin alpha-6 beta-4, a receptor mediating the attachment of epithelial cells to laminins, leads to epithelial detachment, hyperplasia, chronic inflammation, rectal prolapses, and ultimately adenocarcinomas. Alterations of differentiation affecting mucus secreting (goblet) cells as well as changes in expression of essential intestinal transcription factors were detected. Thus alpha-6 beta-4 integrin is a key factor for the maintenance of intestinal integrity and its loss may represent a risk factor for tumor progression associated with IBD.

Publication Title

Hemidesmosome integrity protects the colon against colitis and colorectal cancer.

Sample Metadata Fields

Specimen part

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accession-icon GSE70700
Characterization of the molecular signature associated with the ablation of integrin 6 in IECs in the 6IEC-TAM mouse model
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Transcriptome analysis of mRNAs extracted from the rectal mucosa of WT and 6IEC-TAM mice, 15 days after tamoxifen treatment

Publication Title

Hemidesmosome integrity protects the colon against colitis and colorectal cancer.

Sample Metadata Fields

Sex, Treatment

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accession-icon GSE93642
Intermittent calorie restriction largely counteracts the adverse health effects of a moderate-fat diet in aging C57BL/6J mice
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Calorie restriction (CR) has been shown to extend life- and health-span in model species. For most humans, a life-long CR diet is too arduous to adhere to. The aim of this study was to explore whether weekly intermittent CR can 1) provide long-term beneficial effects and 2) counteract diet-induced obesity in male aging mice. In this study, we have exposed C57Bl/6J mice for 24 months to an intermittent (INT) diet, alternating weekly between CR of a control diet and ad libitum moderate-fat (MF) feeding. This weekly intermittent CR significantly counteracted the adverse effects of the MF diet on mortality, body weight and liver health markers in male 24-month-old mice. Hepatic gene expression profiles of INT-exposed animals appeared much more comparable to CR than to MF-exposed mice. At 12 months of age, a subgroup of MF-exposed mice was transferred to the INT diet. Gene expression profiles in the liver of the 24-month-old diet switch mice were highly similar to the INT-exposed mice. However, a small subset of genes was consistently changed by the MF diet during the first phase of life. Weekly intermittent CR largely, but not completely, reversed adverse effects caused by a MF diet.

Publication Title

Intermittent calorie restriction largely counteracts the adverse health effects of a moderate-fat diet in aging C57BL/6J mice.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE44082
Hypothalamic gene expression of appetite regulators in a cancer-cachectic mouse model
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st), Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Hypothalamic food intake regulation in a cancer-cachectic mouse model.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE44081
Hypothalamic gene expression of appetite regulators in a cancer-cachectic mouse model [Dataset 2]
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st), Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Appetite is frequently affected in cancer patients, leading to anorexia and consequently insufficient food intake. In this study, we report on hypothalamic gene expression profile of a cancer cachectic mouse model with increased food intake. In this model, mice bearing C26 colon adenocarcinoma have an increased food intake subsequently to the loss of body weight. We hypothesize that in this model, appetite regulating systems in the hypothalamus, which apparently fail in anorexia, are still able to adapt adequately to changes in energy balance. Therefore studying the changes that occur on appetite regulators in the hypothalamus might reveal targets for treatment of cancer-induced eating disorders. By applying transcriptomics, many appetite regulating systems in the hypothalamus could be taken into account, providing an overview of changes that occur in the hypothalamus during tumour growth. We show that hypothalamic expression of orexigenic neuropeptides NPY and AgRP was higher, whereas expression of anorexigenic genes CCK and POMC were lower in TB compared to controls. In addition, serotonin and dopamine signalling pathways were found to be significantly altered in TB mice. Serotonin levels in brain showed to be lower in TB mice compared to control mice, while dopamine levels did not change. Moreover, serotonin levels inversely correlated with food intake. Transcriptomic analysis of the hypothalamus of cachectic TB mice with an increased food intake showed changes in NPY, AgRP and serotonin signalling. Serotonin levels in the brain showed to correlate with changes in food intake. Targeting these systems seems a promising strategy to avoid the development of cancer-induced eating disorders.

Publication Title

Hypothalamic food intake regulation in a cancer-cachectic mouse model.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE44080
Hypothalamic gene expression of appetite regulators in a cancer-cachectic mouse model [Dataset 1]
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Appetite is frequently affected in cancer patients, leading to anorexia and consequently insufficient food intake. In this study, we report on hypothalamic gene expression profile of a cancer cachectic mouse model with increased food intake. In this model, mice bearing C26 colon adenocarcinoma have an increased food intake subsequently to the loss of body weight. We hypothesize that in this model, appetite regulating systems in the hypothalamus, which apparently fail in anorexia, are still able to adapt adequately to changes in energy balance. Therefore studying the changes that occur on appetite regulators in the hypothalamus might reveal targets for treatment of cancer-induced eating disorders. By applying transcriptomics, many appetite regulating systems in the hypothalamus could be taken into account, providing an overview of changes that occur in the hypothalamus during tumour growth. We show that hypothalamic expression of orexigenic neuropeptides NPY and AgRP was higher, whereas expression of anorexigenic genes CCK and POMC were lower in TB compared to controls. In addition, serotonin and dopamine signalling pathways were found to be significantly altered in TB mice. Serotonin levels in brain showed to be lower in TB mice compared to control mice, while dopamine levels did not change. Moreover, serotonin levels inversely correlated with food intake. Transcriptomic analysis of the hypothalamus of cachectic TB mice with an increased food intake showed changes in NPY, AgRP and serotonin signalling. Serotonin levels in the brain showed to correlate with changes in food intake. Targeting these systems seems a promising strategy to avoid the development of cancer-induced eating disorders.

Publication Title

Hypothalamic food intake regulation in a cancer-cachectic mouse model.

Sample Metadata Fields

Sex, Specimen part, Treatment

View Samples
accession-icon GSE69151
TNFalpha and IL-6 induced anorexia: effects on serotonin turnover
  • organism-icon Mus musculus
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Anorexia can occur as a serious complication of chronic disease. Increasing evidence suggests that inflammation plays a major role, along with a hypothalamic dysregulation characterized by locally elevated serotonin levels. The present study was undertaken to further explore the connections between peripheral inflammation, anorexia and hypothalamic serotonin metabolism and signaling pathways. We studied transcriptomic changes and serotonergic activity in the hypothalamus of mice after an intraperitoneal injection with TNF, IL-6 or a combination of TNF and IL-6.

Publication Title

Increased hypothalamic serotonin turnover in inflammation-induced anorexia.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon E-MEXP-2452
Transcription profiling of human intestinal versus dermal lymphatic endothelial cells
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

In this analysis we have compared the gene expression profiles of lymphatic endothelial cells (LECs) isolated from human intestine (iLECs) versus LECs from human skin (dLECs).

Publication Title

Liprin (beta)1 is highly expressed in lymphatic vasculature and is important for lymphatic vessel integrity.

Sample Metadata Fields

Specimen part

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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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