Brown adipose tissue dissipates energy through heat and functions as a defense against cold and obesity. PPAR ligands have been shown to induce the browning of white adipocytes; however, the underlying mechanisms remain unclear. Here we show that PPAR ligands require full agonism to induce a brown fat gene program preferentially in subcutaneous white adipose. These effects require expression of PRDM16, a factor that controls the development of classical brown fat. Depletion of PRDM16 blunts the effects of the PPAR agonist rosiglitazone on the induced brown fat gene program. Conversely, PRDM16 and rosiglitazone synergistically activate the brown fat gene program in vivo. This synergy is tightly associated with an increased accumulation of PRDM16 protein, due in large measure to an increase in the half-life of the protein in agonist treated cells. Identifying compounds that stabilize PRDM16 protein may represent a novel therapeutic pathway for the treatment of obesity and diabetes.
PPARγ agonists induce a white-to-brown fat conversion through stabilization of PRDM16 protein.
Sex
View SamplesWe used microarray analysis to identify specific molecular mechanisms controlling Th17 cell differentiation in HFD mice
Obesity Drives Th17 Cell Differentiation by Inducing the Lipid Metabolic Kinase, ACC1.
Specimen part
View SamplesDrought is an important environmental factor affecting plant growth and biomass production. Despite this importance little is known on the molecular mechanisms regulating plant growth under water limiting conditions. The main goal of this work was to investigate, using a combination of growth and molecular profiling techniques, how stress arrests CELl proliferation in Arabidopsis thaliana leaves upon osmotic stress imposition.
Pause-and-stop: the effects of osmotic stress on cell proliferation during early leaf development in Arabidopsis and a role for ethylene signaling in cell cycle arrest.
Specimen part
View SamplesThe purpose of this study is to determine the changes in gene expression by a human retinal pigment epithelium (RPE) cell line (ARPE-19) in response to combination treatment of TGF and TNF, which induces phenotypic changes in vitro that mimic the EMT (Epithelial-to-Mesenchymal Transition).
Tumor necrosis factor-alpha regulates transforming growth factor-beta-dependent epithelial-mesenchymal transition by promoting hyaluronan-CD44-moesin interaction.
No sample metadata fields
View SamplesFollowing antigen encounter by CD4 T cells, polarizing cytokines induce the expression of master regulators that control differentiation. Inactivation of the histone methyltransferase Ezh2 was found to specifically enhance T-helper (Th)1 and Th2 cell differentiation and plasticity. Ezh2 directly bound and facilitated correct expression of Tbx21 and Gata3 in differentiating Th1 and Th2 cells, accompanied by substantial tri-methylation at lysine 27 of histone 3 (H3K27-Me3). In addition, Ezh2 deficiency resulted in spontaneous generation of discrete IFN- and Th2 cytokine-producing populations in non-polarizing cultures, and under these conditions IFN- expression was largely dependent on enhanced expression of the transcription factor Eomesodermin. In vivo, Loss of Ezh2 caused increased pathology in a model of allergic asthma and resulted in progressive accumulation of memory phenotype Th2 cells. This study establishes a functional link between Ezh2 and transcriptional regulation of lineage-specifying genes in terminally differentiated CD4 T cells.
The polycomb protein Ezh2 regulates differentiation and plasticity of CD4(+) T helper type 1 and type 2 cells.
Specimen part
View SamplesWe found that CITED2 is highly expressed in metastatic prostate cancer, and its expression is correlated with poor survival in pateints. In this study, we used an siRNA to decrease CITED2 expression in PC3 cells. A RNA-seq approach was utilized in order to determine global gene expression changes in CITED2 knockdown cells compared to control cells. Overall design: PC3 cells transfected with control siRNAs were used as controls. Cells transfected with siRNAs targeting CITED2 were used as experimental group. Cells were transfected for 72 hr and the analyses were done.
Aberrant expression of CITED2 promotes prostate cancer metastasis by activating the nucleolin-AKT pathway.
Cell line, Subject
View SamplesMemory helper T (Th) cells are crucial for secondary immune responses against infectious microorganisms but also drive the pathogenesis of chronic inflammatory diseases. Therefore, it is of fundamental importance to understand how memory T cells are generated. However, the molecular mechanisms governing memory Th cell generation remain incompletely understood. Here, we identified CD30 as a molecule heterogeneously expressed on effector Th1 and Th17 cells, and CD30hi effector Th1 and Th17 cells preferentially generated memory Th1 and Th17 cells. We found that CD30 mediated signal induced Transglutaminase-2 (TG2) expression, and that the TG2 expression in effector Th cells is essential for memory Th cell generation. In fact, Cd30-deficiency resulted in the impaired generation of memory Th1 and Th17 cells, which can be rescued by overexpression of TG2. Furthermore, transglutaminase-2 (Tgm2)-deficient CD4 T cells failed to become memory Th cells. As a result, T cells from Tgm2-deficient mice displayed impaired antigen-specific antibody production and attenuated Th17-mediated allergic responses. Our data indicate that CD30-induced TG2 expression in effector Th cells is essential for the generation of memory Th1 and Th17 cells, and that CD30 can be a marker for precursors of memory Th1 and Th17 cells.
Essential Role for CD30-Transglutaminase 2 Axis in Memory Th1 and Th17 Cell Generation.
Specimen part
View SamplesOur previous investigation indicated that high-virulence C. gattii (C. gattii TIMM 4097) tend to reside in the alveoli, whereas low-virulence C. gattii (C. gattii TIMM 4903) tend to be washed out from the alveoli and move into the central side of the respiratory system. To test this hypothesis, we performed microarray assay.
How histopathology can contribute to an understanding of defense mechanisms against cryptococci.
Sex, Specimen part
View SamplesExperiment design
Glucose-dependent cell size is regulated by a G protein-coupled receptor system in yeast Saccharomyces cerevisiae.
No sample metadata fields
View SamplesThe NGS-associated mRNA-seq analysis was conducted to survey transcriptome changes responding to three UPR inducers (tunicamycin, DTT, & Azetidine-2-cytosine) by four double mutant of three UPR-associated transcription factors (bZIP17, bZIP28, & bZIP60) and two activators (S1P & S2P). Overall design: Four double mutant lines (bz17/28, bz28/60, bz17/60, and s1p/s2p) were subjected to the analysis.
ER-Anchored Transcription Factors bZIP17 and bZIP28 Regulate Root Elongation.
Age, Specimen part, Subject
View Samples