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accession-icon GSE85682
Expression data from intestinal dendritic cells and macrophages of VDTR mice at 4 hours post diphtheria toxin administration
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Recognition and removal of apoptotic cells by professional phagocytes, including dendritic cells and macrophages, preserve self-tolerance and prevent chronic inflammation and autoimmune pathologies. However the diverse array of phagocytes residing within different tissues combined with the necessarily prompt nature of apoptotic cell clearance has made it difficult to study this process in situ. Thus, the full spectrum of functions executed by tissue resident phagocytes in response to homeostatic apoptosis remains unclear.

Publication Title

Different tissue phagocytes sample apoptotic cells to direct distinct homeostasis programs.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE47736
Interplay of host microbiota, genetic perturbations, and inflammation promotes local development of intestinal neoplasms in mice
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Interplay of host microbiota, genetic perturbations, and inflammation promotes local development of intestinal neoplasms in mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE47734
Interplay of host microbiota, genetic perturbations, and inflammation promotes local development of intestinal neoplasms in mice [BeadArray]
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

The preferential localization of some neoplasms, such as serrated polyps, in specific areas of the intestine suggests that non-genetic factors may be important for their development. To test this hypothesis, we took advantage of transgenic mice that expressed HB-EGF throughout the intestine, but develop serrated polyps only in the cecum.

Publication Title

Interplay of host microbiota, genetic perturbations, and inflammation promotes local development of intestinal neoplasms in mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE49970
Expression Data from 12 week old APCmin/+ and littermate matched Wildtype B6 mouse Terminal Ileum (TI)
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

APCmin/+ mice develop spontaneous gastrointestinal polyposis due to a dominantly inhereited germline loss-of-function mutation in the tumor suppressor adenomatous polyposis coli (APC). Changes in intestinal immune activity have been documented to occur prior to the development of fulminate polyposis. Such changes are thought to contribute to disease development.

Publication Title

Oral interleukin-10 alleviates polyposis via neutralization of pathogenic T-regulatory cells.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE66354
Investigation of the mechansim underlying the inflammatory phenotype in Group A ependymoma
  • organism-icon Homo sapiens
  • sample-icon 146 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Inflammatory response has been identified as a molecular signature of high-risk Group A ependymoma (EPN). To better understand the biology of this phenotype and aid therapeutic development, transcriptomic data from Group A and B EPN patient tumor samples, and additional malignant and normal brain data, were analyzed to identify the mechanism underlying EPN group A inflammation.

Publication Title

Interleukin-6/STAT3 Pathway Signaling Drives an Inflammatory Phenotype in Group A Ependymoma.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE63793
Rb family triple knock out liver progenitor cells
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This serie was performed on liver progenitor isolated based on their expression of the Sca1 surface marker. It contains two independent samples from Rb family deficient liver and three independent samples from control liver, all isolated 2 weeks after Tamoxifen-induced Rb family ablation. Hematopoietic (CD45, Ter119) and endothelial (CD31) markers were used as negative selection markers to exclude blood or endothelial cells from the isolated fraction.

Publication Title

Recruitment of Pontin/Reptin by E2f1 amplifies E2f transcriptional response during cancer progression.

Sample Metadata Fields

Specimen part

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accession-icon SRP065500
Downregulation of LATS kinases alters p53 to promote cell migration
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

p53 is a pivotal tumor suppressor and a major barrier against cancer. We now report that silencing of the Hippo pathway tumor suppressors LATS1 and LATS2 in non-transformed mammary epithelial cells reduces p53 phosphorylation and increases its association with the p52 NF-?B subunit. Moreover, it partly shifts p53’s conformation and transcriptional output towards a state resembling cancer-associated p53 mutants, and endow p53 with the ability to promote cell migration. Notably, LATS1 and LATS2 are frequently downregulated in breast cancer; we propose that such downregulation might benefit cancer by converting p53 from a tumor suppressor into a tumor facilitator. Overall design: MCF10A cells transfected with siRNA against LATS1/2 alone, p53 alone or LATS1/2 and p53 together. Two independent MCF10A batches provided biological replicates

Publication Title

Down-regulation of LATS kinases alters p53 to promote cell migration.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE11759
Role of HNF4alpha in the adult colon
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Background & Aims: HNF4 is an important transcriptional regulator of hepatocyte and pancreatic function. Hnf4 deletion is embryonically lethal with severe defects in visceral endoderm formation, liver maturation and colon development. However, the precise role of this transcription factor in maintaining homeostasis of the adult intestine remains unclear. Herein, we aimed to elucidate the adult intestinal functions of Hnf4. Methods: A conditional intestinal epithelial Hnf4 knockout mouse was generated. Histological abnormality of the colonic mucosa was assessed by immunodetection and Western. Changes in global gene expression and biological network were analyzed. Results: Hnf4 intestine null mice developed normally until reaching young adulthood. Crypt distortion became apparent in the Hnf4 null colon at 3 months of age followed by focal areas of crypt dropout, increased immune cell infiltrates, crypt hyperplasia and early signs of polyposis later in life. A gene profiling analysis identified cell death and cell cycle related to cancer as the most significant sets of genes altered in the Hnf4 colon null mice. Expression levels of the tight junction proteins claudin 4, 8 and 15 were altered early in the colon epithelium of Hnf4 mutants and correlated with increased barrier permeability to a molecular tracer that does not normally penetrate normal mucosa. Conclusion: These observations support a functional role for Hnf4 in protecting the colonic mucosa against the initiation of the changes resembling inflammatory bowel diseases and polyp formation.

Publication Title

Loss of hepatocyte-nuclear-factor-4alpha affects colonic ion transport and causes chronic inflammation resembling inflammatory bowel disease in mice.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE58095
Dissecting the heterogeneity of skin gene expression patterns in systemic sclerosis.
  • organism-icon Homo sapiens
  • sample-icon 59 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

We identified fibro-inflammatory and keratin gene expression signatures in systemic sclerosis skin.

Publication Title

Dissecting the heterogeneity of skin gene expression patterns in systemic sclerosis.

Sample Metadata Fields

Age, Specimen part, Race, Subject, Time

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accession-icon GSE47162
Skin gene expression correlates of severity of interstitial lung disease in systemic sclerosis
  • organism-icon Homo sapiens
  • sample-icon 59 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

We identified eighty two skin transcripts significantly correlated with the severity of interstitial lung disease (ILD) in systemic sclerosis.

Publication Title

Skin gene expression correlates of severity of interstitial lung disease in systemic sclerosis.

Sample Metadata Fields

Age, Specimen part, Race, 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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