Knockdowns of c-JUN and JUND had opposite effects on PC3 prostate cell migration. We predicted that c-JUN and JUND control the same set of cell migration genes, but in opposite directions. To test this hypothesis, mRNA with expression changes in c-JUN and JUND knockdown PC3 cell lines were compared to mRNA levels in control (luciferase knockdown) PC3 cells by RNA-seq. Overall design: mRNA profiles of luciferase knockdown (WT), c-Jun knockdown, and Jun-D knockdown in PC3 cells were generated using deep sequencing, in triplicate, using Illumina HiSeq. Knockdowns were stable shRNA expression from a lentiviral construct selected with puromycin.
Extracellular signal-regulated kinase signaling regulates the opposing roles of JUN family transcription factors at ETS/AP-1 sites and in cell migration.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Up-regulation of expression of the ubiquitin carboxyl-terminal hydrolase L1 gene in human airway epithelium of cigarette smokers.
Sex, Age, Race
View SamplesUpregulation of Expression of the Ubiquitin Carboxyl Terminal Hydrolase L1 Gene in Human Airway Epithelium of Cigarette Smokers
Up-regulation of expression of the ubiquitin carboxyl-terminal hydrolase L1 gene in human airway epithelium of cigarette smokers.
Sex, Age
View SamplesNOD mice deficient in the transcription factor Batf3 never develop diabetes. The goal of this study was to determine if NOD.Batf3-/- mice islets had any inflammatory signature associated with type 1 diabetes. Islets of Langerhans were isolated from NOD, NOD.Batf3-/-, and NOD.Rag1-/- and then compared to determine inflammatory gene profiles. At 6 and 8 weeks of age, NOD.Batf3-/- islets had an absence of inflammatory gene expression and were almost identical to uninflamed NOD.Rag1-/- islets. This work shows that absence of the Batf3 transcription factor is sufficient to prevent all the inflammatory sequelae of autoimmune diabetes.
A minor subset of Batf3-dependent antigen-presenting cells in islets of Langerhans is essential for the development of autoimmune diabetes.
Sex, Specimen part
View SamplesModification of Gene Expression of the Small Airway Epithelium in Response to Cigarette Smoking
Modification of gene expression of the small airway epithelium in response to cigarette smoking.
Sex, Age
View SamplesThe mammary gland develops mainly postnatally, when during pregnancy the epithelium grows out into the mammary fat pad and forms a network of epithelial ducts. During pregnancy, these ducts branch and bud to form alveoli. These alveoli produce the milk during lactation. After 7 days of lactation, involution was induced by force weaning the pups. The newly formed epithelium undergoes apoptosis and is removed from the tissue by neighbouring epithelial cells. Tissue remodelling leads to a morphology resembling a gland of a pre-pregnant mouse. Microarray analysis was used to measure mRNA expression of genes during puberty, pregnancy, lactation and involution in a Balb/c mouse strain.
Involution of the mouse mammary gland is associated with an immune cascade and an acute-phase response, involving LBP, CD14 and STAT3.
No sample metadata fields
View SamplesGamma-aminobutyric acid (GABA) is a multifunctional mediator that functions as a neurotransmitter in the central nervous system and a trophic factor during nervous system development, affecting proliferation, differentiation and cell death [1-3].GABA is synthesized from glutamate, catalyzed by GAD65 and GAD67, glutamic acid decarboxylase {Tillakaratne, Medina-Kauwe, et al. 1995 21 /id}{Owens & Kriegstein 2002 3 /id}{Watanabe, Maemura, et al. 2002 73 /id}. In the CNS transporters and catabolic enzymes work in a coordinated fashion to control the availability of GABA {Tillakaratne, Medina-Kauwe, et al. 1995 21 /id}{Owens & Kriegstein 2002 3 /id}{Watanabe, Maemura, et al. 2002 73 /id} It is now recognized that GABA also functions in a variety of organs outside of the CNS [1,3,4]. In the lung, a series of recent studies suggest that the GABAergic signaling system plays a role in the control of asthma related-airway constriction and mucin secretion [5-9]. In the context that goblet cell hyperplasia and mucin overproduction is associated with cigarette smoking [10-12], we hypothesized that components of the GABAergic system may also be altered in the airway epithelium of cigarette smokers. To assess this hypothesis, we evaluated the expression of the entire GABAergic system in the large and small airway epithelium of healthy nonsmokers and healthy smokers. The data demonstrates there is expression of genes for a complete GABAergic system in the airway epithelium. Interestingly, the expression of GAD67 was markedly modified by smoking, with increased expression in healthy smokers compared to healthy nonsmokers at the mRNA and protein levels. In the context that mucus overproduction is commonly associated with cigarette smoking, GAD67 may be a pharmacologic target for treatment of smoking-related disorders.
Smoking-mediated up-regulation of GAD67 expression in the human airway epithelium.
Sex, Age
View SamplesWe examined the transcriptional profiles of macrophages that reside in the islets of Langerhans of NOD, NOD.Rag1-/-, and B6.g7 mice at three weeks of age. Islet macrophages expressed an activation signature with high expression of Tnf, Il1b, and MHC-II both at the transcript and protein levels. These features are common with barrier macrophages of the lung and gastrointestinal tract. Moreover, injection of lipopolysaccharide induced a rapid inflammatory gene expression, indicating that blood stimulants are accessible to the macrophages and that these macrophages can sense them. In NOD mice, the autoimmune process imparted an increased inflammatory signature, including elevated expression of chemokines, chemokine receptors, and an oxidative response. The elevated inflammatory signature indicates that the autoimmune program was active at the time of weaning. Thus, the macrophages of the islets of Langerhans are poised to mount an immune response even at steady state, while the presence of the adaptive immune system elevates their activation state. Overall design: We examined the transcriptional profiles of macrophages that reside in the islets of Langerhans of NOD, NOD.Rag1-/-, and B6.g7 mice at three weeks of age. Lung macrophages and pancreatic LN dendritic cells of NOD mice were also examined.
The islet-resident macrophage is in an inflammatory state and senses microbial products in blood.
Age, Specimen part, Cell line, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Discovery of drug mode of action and drug repositioning from transcriptional responses.
Specimen part, Cell line, Treatment
View SamplesThe effects of several compounds on the MCF7 human adenocarcinoma mammary cell line were analysed by gene expression profiling.
Discovery of drug mode of action and drug repositioning from transcriptional responses.
Specimen part, Cell line, Treatment
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