These arrays contain data from the livers of 10 week old L-Pex5 -/- male mice
Carbohydrate metabolism is perturbed in peroxisome-deficient hepatocytes due to mitochondrial dysfunction, AMP-activated protein kinase (AMPK) activation, and peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) suppression.
Sex, Age, Specimen part
View SamplesThe prostate represents a complex mix of cell types and there is a need to analyze distinct cell populations to better understand their potential interactions. This study of cell-type specific gene expression patterns will contribute to understanding of how tumor epithelial cells may be affected by adjacent interstitial stromal cells within the tumor microenvirnonment.
Analysis of gene expression in prostate cancer epithelial and interstitial stromal cells using laser capture microdissection.
Specimen part, Disease, Disease stage
View SamplesMicroRNA-155 (miR-155) is upregulated in primary effector CD8 T cells but is expressed at low amounts in nave cells. Anti-viral CD8 T cell responses and viral clearance were impaired in miR-155 deficient (bic-/-) mice, and this defect was intrinsic to CD8 T cells, as adoptively transferred bic-/- CD8 T cells generated greatly reduced primary and memory responses during infection. To understand the mechanism by which miR-155 regulates CD8 T cell activation, we analyzed the gene expression profiles of naive and in vitro activated wild-type and bic-/- CD8 T cells.
The microRNA miR-155 controls CD8(+) T cell responses by regulating interferon signaling.
Specimen part
View SamplesRationale: The Id1 and Id3 genes play major roles during cardiac development, despite their expression being confined to non-myocardial layers (endocardium endothelium - epicardium). We previously described that Id1/Id3/ double knockout (dKO) mouse embryos die at mid-gestation from multiple cardiac defects, but early demise precluded the studies of the roles of Id in the adult mice.
Developmental ablation of Id1 and Id3 genes in the vasculature leads to postnatal cardiac phenotypes.
Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Trichostatin A enhances vascular repair by injected human endothelial progenitors through increasing the expression of TAL1-dependent genes.
Treatment
View SamplesEndothelial colony-forming cells (ECFCs) have been reported as promising cells for regenerative medicine thanks to their angiorepair properties. Transcription factors are primary determinants of the functional capacity of the cells and TAL1 has been shown as a critical regulator of endothelial lineage in both development and adult life. However, only few (three) TAL1 targets have been identified so far in mouse and human endothelial cells. This microarray experiment, where TAL1 expression was knocked-down, was designed to identify TAL1-dependent genes in primary human endothelial stem/progenitor cells.
Trichostatin A enhances vascular repair by injected human endothelial progenitors through increasing the expression of TAL1-dependent genes.
Treatment
View SamplesDuchenne muscular dystrophy (DMD) is an incurable neuromuscular degenerative disease, caused by a mutation in the dystrophin gene. Mdx mice recapitulate DMD features. Here we show that injection of wild-type (WT) embryonic stem cells (ESCs) into mdx blastocysts produces mice with improved pathology. A small fraction of WT ESCs incorporates into the mdx mouse nonuniformly to upregulate protein levels of dystrophin in the skeletal muscle. The chimeric muscle shows reduced regeneration and restores dystrobrevin, a dystrophin-related protein, in areas with high and with low dystrophin content. WT ESC injection also normalizes the amount of fat, a tissue that does not express dystrophin. ESC injection without dystrophin does not prevent the appearance of phenotypes in the skeletal muscle or in the fat. Thus, dystrophin supplied by the ESCs reverses disease in mdx mice globally.
Blastocyst injection of wild type embryonic stem cells induces global corrections in mdx mice.
No sample metadata fields
View SamplesIt is still unclear that how obesity increases the risk of breast cancer. To address this question, we used mRNA microarrays to characterize mouse breast tumor EO771 cells treated with mouse recombinant A-FABP protein and compared the data from their controls.
Circulating Adipose Fatty Acid Binding Protein Is a New Link Underlying Obesity-Associated Breast/Mammary Tumor Development.
Cell line
View SamplesStress constantly challenges plant adaptation to the environment. Of all stress types, arsenic was a major threat during the early evolution of plants. The most prevalent chemical form of arsenic is arsenate, whose similarity to phosphate renders it easily incorporated into cells via the phosphate transporters. Here we found that arsenate stress provokes a notable transposon burst in plants, in coordination with arsenate/phosphate transporter repression, which immediately restricts arsenate uptake. This repression was accompanied by delocalization of the phosphate transporter from the plasma membrane. When arsenate was removed, the system rapidly restored transcriptional expression and membrane localization of the transporter. We identify WRKY6 as an arsenate-responsive transcription factor that mediates arsenate/phosphate transporter gene expression and restricts arsenate-induced transposon activation. Plants therefore have a dual WRKY-dependent signaling mechanism that modulates arsenate uptake and transposon expression, providing a coordinated strategy for arsenate tolerance and transposon gene silencing.
WRKY6 transcription factor restricts arsenate uptake and transposon activation in Arabidopsis.
Time
View SamplesWe sought to obtain gene signature specific of high oxidative phsophorylation function.
Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism.
Cell line, Treatment
View Samples