Differential expression in human peripheral blood monocytes between F. novicida-infected and uninfected, and between Francisella tularensis tularensis isolate Schu S4 and uninfected.
Microarray analysis of human monocytes infected with Francisella tularensis identifies new targets of host response subversion.
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View SamplesWe hypothesized that tissue genome-wide gene expression analysis, coupled with gene network analyses of differentially expressed genes, would provide novel insights into the pathogenesis of pulmonary sarcoidosis.
Gene expression profiling identifies MMP-12 and ADAMDEC1 as potential pathogenic mediators of pulmonary sarcoidosis.
Specimen part, Disease, Disease stage
View SamplesSingle O-GlcNAc modification orchestrate by O-GlcNAc Transferase (OGT) and O-GlcNAcase (OGA alias MGEA5) enzymes, affects signal transduction and gene expression by chromatin modulation. We developed Oga deleted MEF (mouse embryonic fibroblast) cells to investigate effects of O-GlcNAc modification in mice. RNA isolated from Mouse Embryonic Fibroblast cells generated from Oga Knock out (KO) Heterozygous (Het) and wild type (WT) cells and subjected to microarray analysis.
Conditional knock-out reveals a requirement for O-linked N-Acetylglucosaminase (O-GlcNAcase) in metabolic homeostasis.
Sex, Specimen part
View SamplesPPARg and C/EBPa cooperate to control preadipocyte differentiation (adipogenesis). However, the factors that regulate PPARg and C/EBPa expression during adipogenesis remain largely unclear. Here we show PTIP, a protein that associates with histone H3K4 methyltransferases, regulates PPARg and C/EBPa expression in mouse embryonic fibroblasts (MEFs) and during preadipocyte differentiation. PTIP deletion in MEFs leads to marked decreases of PPARg expression and PPARg-stimulated C/EBP expression. Further, PTIP is essential for induction of PPARg and C/EBPa expression during preadipocyte differentiation. Deletion of PTIP impairs the enrichment of H3K4 trimethylation and RNA polymerase II on PPARg and C/EBPa promoters. Accordingly, PTIP-/- MEFs and preadipocytes all show striking defects in adipogenesis. Furthermore, rescue of the adipogenesis defect in PTIP-/- MEFs requires co-expression of PPARg and C/EBPa. Finally, deletion of PTIP in brown adipose tissue significantly reduces tissue weight in mice. Thus, by regulating PPARg and C/EBPa expression, PTIP plays a critical role in adipogenesis.
Histone methylation regulator PTIP is required for PPARgamma and C/EBPalpha expression and adipogenesis.
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Xanthine oxidoreductase is a regulator of adipogenesis and PPARgamma activity.
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View Samples3T3-L1 fibroblasts are a commonly used in vitro model for adipogenesis. When induced with hormones, they differentiate into mature fat cells. Here, microarrays were used to study 3T3-L1 adipose differentiation through time.
Xanthine oxidoreductase is a regulator of adipogenesis and PPARgamma activity.
No sample metadata fields
View SamplesSphingosine-1-phosphate (S1P) is a sphingolipid metabolite that regulates basic cell functions through metabolic and signaling pathways. Intracellular metabolism of S1P is controlled, in part, by two homologous S1P phosphatases, 1 and 2, which are encoded by Sgpp1 and Sgpp2, respectively. S1P phosphatase activity is needed for efficient recycling of sphingosine into the sphingolipid synthesis pathway. S1P phosphatase 1 is important for skin homeostasis, but little is known about the functional role of S1P phosphatase 2. To identify the functions of S1P phosphatase 2 in vivo, we studied mice with the Sgpp2 gene deleted. In contrast to Sgpp1-/- mice, Sgpp2-/- mice had normal skin and were viable into adulthood. Unexpectedly, WT mice expressed Sgpp2 mRNA at high levels in pancreatic islets when compared with other tissues. Sgpp2-/- mice had normal blood insulin levels and pancreatic islet size; however, Sgpp2-/- mice treated with a high-fat diet (HFD) had significantly lower blood insulin levels and smaller pancreatic islets compared with WT mice. The smaller islets in the HFD-treated Sgpp2-/- mice had a significantly lower adaptive -cell proliferation rate in response to the diet compared with HFD-treated WT mice. Importantly, -cells from Sgpp2-/- mice fed a normal diet showed significantly increased expression of proteins characteristic of the endoplasmic reticulum (ER) stress response compared with -cells from WT mice. Our results suggest that Sgpp2 deletion causes -cell ER stress, which is a known cause of -cell dysfunction, and reveal a novel juncture in the sphingolipid recycling pathway that could impact the development of diabetes.
Sphingosine-1-phosphate Phosphatase 2 Regulates Pancreatic Islet β-Cell Endoplasmic Reticulum Stress and Proliferation.
No sample metadata fields
View SamplesGene expression was studied from different mouse tissues
Xanthine oxidoreductase is a regulator of adipogenesis and PPARgamma activity.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A tissue-specific landscape of sense/antisense transcription in the mouse intestine.
Specimen part
View SamplesGenome wide expression profiling to determine the overlap of Affymetrix-signals with SOLID sequencing
A tissue-specific landscape of sense/antisense transcription in the mouse intestine.
Specimen part
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