These arrays contain data from hypthalamus tissue of nestin-Pex5 -/- male mice
Peroxisome deficiency but not the defect in ether lipid synthesis causes activation of the innate immune system and axonal loss in the central nervous system.
Specimen part
View SamplesWe characterize histone crotonylation in intestinal epithelium-derived cells through Mass spectrometry, ChIp-Seq and RNA-Seq approaches and show that this modification is removed by class I histone deacetylases, HDAC1, 2 and 3. Overall design: RNA-Seq profile from mouse colon epithelium. ChIP-Seq experiments for H3K18crotonylation and H3K4me3 on mouse colon epithelium. ChIP-Seq experiments for H3K18 crotonylation and H3K18 acetylation on HCT116 cell line treated or not with the HDAC inhibitor MS275 (5 µM) for 18h. All the experiments were performed in triplicate.
Microbiota derived short chain fatty acids promote histone crotonylation in the colon through histone deacetylases.
No sample metadata fields
View SamplesRecent observations about how cells sense amino acids have argued for preeminent roles of mTOR and the stress kinase GCN2 in allowing cells to estimate their amino acid needs. Here we used models of programmed immune microenvironments where helper T cells have to sense how much amino acids are available to engage in antigen-fueled proliferation. Contrary to current models, T cells activate mTOR in the competency phase of the cell cycle regardless of amino acid amounts, GCN2 or surface TCR. Instead, we found T cells use an amino acid sensing system to target IL-2-induced STAT5 phosphorylation at the restriction point of cell cycle commitment. mTOR activity is subsequently reduced and specifically connected to SREBP activation. T cells can be pushed into cycle by increasing IL-2 even when no amino acids are available. Collectively, our studies reveal helper T cells use sequential and distinct pathways to measure local amino acid concentrations.
Proliferating Helper T Cells Require Rictor/mTORC2 Complex to Integrate Signals from Limiting Environmental Amino Acids.
Specimen part, Treatment
View SamplesIntegrins facilitate intercellular movement and communication. Unlike the promiscuous activities of many integrins, 6 integrin is restricted to epithelia and partners exclusively with integrin V to modulate acute lung injury (ALI). Given that ALI is a complication of respiratory infection, we used mice lacking 6 integrin (6 KO) to probe the role of the epithelial layer in controlling the lung microenvironment during infection. We found 6 KO mice were protected from disease caused by influenza and Sendai virus infections. They were also protected from disease caused by Streptococcus pneumoniae infection alone and after prior influenza virus infection, the co-infection representing an often-lethal condition in humans. Resistance in the absence of epithelial 6 integrin was caused by intrinsic priming of the lung microenvironment by type I interferons through a mechanism involving transforming growth factor- regulation. Expression of 6 on epithelia suppresses the production of interferons, providing an advantage to the pathogen. Acute inhibition of 6 function may therefore provide a means to improve outcomes in lung microbial infections.
An Epithelial Integrin Regulates the Amplitude of Protective Lung Interferon Responses against Multiple Respiratory Pathogens.
Specimen part
View SamplesLong term exposure to incretin hormones is known to have salutory effects on beta cell function and viability. While short-term cAMP induction is known to have a signature CREB-CRTC target gene response, the long-term effects of cAMP on beta cell gene expression are less well understood.
mTOR links incretin signaling to HIF induction in pancreatic beta cells.
Cell line, Time
View SamplesStudy on gene expression in multifunctional protein 2 deficient mice. Liver samples of two days old mice in normal conditions are used. In total 8 arrays were hybridized corresponding to 4 KO mice and 4 WT mice Results: Cholesterol synthesis is induced and ppar alpha targets also differentially expressed between KO and WT.
Coordinate induction of PPAR alpha and SREBP2 in multifunctional protein 2 deficient mice.
No sample metadata fields
View SamplesThe liver is one of the most sexually dimorphic organs as measured by gene expression differences. About 80% of the sexually dimorphic genes are known to be regulated by growth hormone (GH). Somatostatin (SST) inhibits the release of GH.
Somatostatin is essential for the sexual dimorphism of GH secretion, corticosteroid-binding globulin production, and corticosterone levels in mice.
Sex, Specimen part
View SamplesThese 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 results of this study indicate that stenotic fibroblasts exhibit an aberrant response to tissue stiffness with reduced MMP activity, leading to a perpetuous vicious circle of ever more fibrosis formation. Altering the microenvironment by LOX inhibition increases MMP activity and decreases ECM contraction, resulting in a potential anti-fibrotic agent for Crohns disease.
Fibrostenotic Phenotype of Myofibroblasts in Crohn's Disease is Dependent on Tissue Stiffness and Reversed by LOX Inhibition.
Sex, Specimen part, Disease, Subject
View SamplesSurfactant deficiency, diffuse alveolar damage and respiratory failure caused by loss of Abca3 in AT2 cells was followed by remarkable proliferation of alveolar cells and selective survival of ABCA3 sufficient cells resulting in regeneration of alveolar structure and function, providing the conceptual framework for the development of therapies to ameliorate lung diseases caused by mutations in ABCA3 and other genes critical for AT2 cell function or surfactant homeostasis. Overall design: Control and Abca3 cKO AT2 cell RNA-seq at 6 days post tamoxifen in adult mice.
Alveolar injury and regeneration following deletion of ABCA3.
Specimen part, Subject
View Samples