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accession-icon GSE43396
Comparison of gene expression in NOD versus B6 splenic B cell subsets.
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon

Description

NOD mice are an inbred strain that display enhanced MZ B cell differentiation from an early age. Interestingly, several lines of evidence implicate MZ B cells in this strain as important contributors to the T cell mediated beta cell destruction associated with the development of type 1 diabetes (T1D). In order to develop a better understanding of the underlying causes for augmented MZ B cell production in NOD mice, we obtained the transcriptional profiles of FO and MZ subsets and TR precursors from NOD mice and compared them to those of the B6 strain.

Publication Title

Intrinsic molecular factors cause aberrant expansion of the splenic marginal zone B cell population in nonobese diabetic mice.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE30684
Stem Cell Antigen-1 (Sca-1) Regulates Mammary Tumor Development and Cell Migration
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

Stem cell antigen-1 (Sca-1 or Ly6A) is a member of the Ly6 family of glycosyl phostidylinositol (GPI)-anchored cell surface proteins. To determine the potential mechanisms by which Sca-1 regulates cell migration, adhesion, and tumor development; we performed an Affymetrix mouse genome 430A 2.0 array on cDNA comparing shLuc and shSca-1 from cells grown in vitro.

Publication Title

Stem cell antigen-1 (sca-1) regulates mammary tumor development and cell migration.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE13333
Srf conditional knockout in the mouse liver
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

Serum response factor (SRF) is a transcription factor that binds to the serum response element (SRE) of genes that are expressed in response to mitogens. SRF plays essential roles in muscle and nervous system development; however, little is known about the role of SRF during liver growth and function. To examine the function of SRF in the liver, we generated mice in which the Srf gene was specifically disrupted in hepatocytes. The survival of mice lacking hepatic SRF activity was lower than that of control mice; moreover, surviving mutant mice were smaller and had lower blood glucose and triglyceride levels compared with control mice. Srf-deficient livers were also smaller than control livers, hepatocyte morphology was abnormal, and liver-cell proliferation and viability was compromised. Gene array and quantitative RT-PCR analysis of SRF depleted livers revealed a reduction in mRNAs encoding components of the growth hormone/IGF1 pathway, cyclins, several metabolic regulators, and cytochrome p450 enzymes. Conclusion: SRF is essential for hepatocyte proliferation and survival, liver function, and control of postnatal body growth by regulating hepatocyte gene expression.

Publication Title

Hepatocyte expression of serum response factor is essential for liver function, hepatocyte proliferation and survival, and postnatal body growth in mice.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE11194
GATA4 conditional knockout in the small intestine
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
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Description

Background and Aims: Although the zinc finger transcription factor GATA4 has been implicated in regulating jejunal gene expression, the contribution of GATA4 in controlling jejunal physiology has not been addressed. Methods: We generated mice in which the Gata4 gene was specifically deleted in the small intestinal epithelium. Measurements of plasma cholesterol and phospholipids, intestinal absorption of dietary fat and cholesterol, and gene expression were performed on these animals. Results: Mice lacking GATA4 in the intestine displayed a dramatic block in their ability to absorb cholesterol and dietary fat. Comparison of the global gene expression profiles of control jejunum, control ileum, and GATA4 null jejunum by gene array analysis demonstrated that GATA4 null jejunum lost expression of 53% of the jejunal-specific gene set and gained expression of 47% of the set of genes unique to the ileum. These alterations in gene expression included a decrease in mRNAs encoding lipid and cholesterol transporters as well as an increase in mRNAs encoding proteins involved in bile acid absorption. Conclusion: Our data demonstrate that GATA4 is essential for jejunal function including fat and cholesterol absorption and confirm that GATA4 plays a pivotal role in determining jejunal versus ileal identity.

Publication Title

GATA4 is essential for jejunal function in mice.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE3126
Comparison of HNF4 null mouse embryonic livers with control mouse embryonic livers
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

To study the role of hepatic nuclear factor alpha (HNF4a in hepatogenesis, we used loxP-Cre technology to eliminate it from developing mouse livers.

Publication Title

Hepatocyte nuclear factor 4alpha orchestrates expression of cell adhesion proteins during the epithelial transformation of the developing liver.

Sample Metadata Fields

Specimen part

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accession-icon GSE10964
Virus-Induced Airway Disease in Mice (C57BL/6J, d21/d49)
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
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Description

Analysis of gene expression in lungs of C57BL/6J mice that develop chronic airway disease phenotypes after a single Sendai virus infection, compared with mice treated with UV-inactivated virus.

Publication Title

Persistent activation of an innate immune response translates respiratory viral infection into chronic lung disease.

Sample Metadata Fields

Sex, Time

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accession-icon GSE12367
Deaf-1 regulated genes in the mouse mammary gland
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
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Description

Microarray analysis was used to compare the gene expression profiles of Deaf-1-transduced mouse mammary epithelial cells (MECs) relative to Deaf-1-deficient MECs.

Publication Title

Deaf-1 regulates epithelial cell proliferation and side-branching in the mammary gland.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE55489
Liver expression data from 31 mouse strains treated with vehicle or isoniazid for 3 days
  • organism-icon Mus musculus
  • sample-icon 215 Downloadable Samples
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Description

Isoniazid induced varying degrees of hepatic steatosis in an inbred strain Mouse Diversity Panel (MDP) study. RNA was isolated from all animals for analysis of gene expression changes in the liver. The objective of this study was to identify gene expression changes that drive isoniazid-induced steatosis.

Publication Title

A systems biology approach utilizing a mouse diversity panel identifies genetic differences influencing isoniazid-induced microvesicular steatosis.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE27605
The intestinal stem cell signature identifies colorectal cancer stem cells and predicts disease relapse
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Using EphB2 or the ISC marker Lgr5, we have FACS-purified and profiled intestinal stem cells (ISCs), crypt proliferative progenitors and late transient amplifying cells to define a gene expression program specific for normal ISCs.

Publication Title

The intestinal stem cell signature identifies colorectal cancer stem cells and predicts disease relapse.

Sample Metadata Fields

Specimen part

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accession-icon GSE9857
Striatal gene expression data from 12 weeks-old R6/2 mice and control mice
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Mutant huntingtin's effects on striatal gene expression in mice recapitulate changes observed in human Huntington's disease brain and do not differ with mutant huntingtin length or wild-type huntingtin dosage.

Sample Metadata Fields

No sample metadata fields

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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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