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.
Intrinsic molecular factors cause aberrant expansion of the splenic marginal zone B cell population in nonobese diabetic mice.
Sex, Age, Specimen part
View SamplesStem 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.
Stem cell antigen-1 (sca-1) regulates mammary tumor development and cell migration.
Specimen part, Cell line
View SamplesSerum 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.
Hepatocyte expression of serum response factor is essential for liver function, hepatocyte proliferation and survival, and postnatal body growth in mice.
No sample metadata fields
View SamplesBackground 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.
GATA4 is essential for jejunal function in mice.
No sample metadata fields
View SamplesTo study the role of hepatic nuclear factor alpha (HNF4a in hepatogenesis, we used loxP-Cre technology to eliminate it from developing mouse livers.
Hepatocyte nuclear factor 4alpha orchestrates expression of cell adhesion proteins during the epithelial transformation of the developing liver.
Specimen part
View SamplesAnalysis 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.
Persistent activation of an innate immune response translates respiratory viral infection into chronic lung disease.
Sex, Time
View SamplesMicroarray analysis was used to compare the gene expression profiles of Deaf-1-transduced mouse mammary epithelial cells (MECs) relative to Deaf-1-deficient MECs.
Deaf-1 regulates epithelial cell proliferation and side-branching in the mammary gland.
No sample metadata fields
View SamplesIsoniazid 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.
A systems biology approach utilizing a mouse diversity panel identifies genetic differences influencing isoniazid-induced microvesicular steatosis.
Sex, Specimen part, Treatment
View SamplesUsing 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.
The intestinal stem cell signature identifies colorectal cancer stem cells and predicts disease relapse.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
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.
No sample metadata fields
View Samples