This SuperSeries is composed of the SubSeries listed below.
MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state.
Sex, Specimen part
View SamplesWe address the molecular mechanisms through which MYC promotes loss of cell identity and acquisition of stem cell-like traits, favouring the onset of tumorigenesis, by performing gene expression profile analyses in a transition from WT IMEC, IMEC over-expressing MYC and mammospeheres formed from IMEC-MYC (named M2). We then investigated the global gene expression profile of the fraction of cells hyper-activating the WNT pathway in M2 spheres, compared to the ones with low activation
MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state.
Sex, Specimen part
View SamplesKnockdowns 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 SamplesP1 encodes an R2R3-MYB transcription factor responsible for the accumulation of insecticidal flavones in maize silks and red phlobaphene pigments in pericarps and other floral tissues, which contributed to making P1 an important visual marker since the dawn of modern genetics. We conducted RNA-Seq using pericarps at two different stages, 14 and 25 days after pollination (DAP). High-throughput sequencing using the Illumina platform resulted in the generation of ~20 million high quality reads, from which ~90% aligned to the recently completed maize genome sequence corresponding to ~5 million reads for each one of the four samples. Overall design: Examination of two different RNA samples from two different stages of maize pericarp tissues.
A genome-wide regulatory framework identifies maize pericarp color1 controlled genes.
Specimen part, Subject
View SamplesP1 encodes an R2R3-MYB transcription factor responsible for the accumulation of insecticidal flavones in maize silks and red phlobaphene pigments in pericarps and other floral tissues, which contributed to making P1 an important visual marker since the dawn of modern genetics. We conducted RNA-Seq using from maize silks obtained at 2-3 days after emergence. High-throughput sequencing using the Illumina platform resulted in the generation of ~14 million high quality reads, corresponding to ~7 million reads for each sample, from which 76% aligned to the maize genome. Overall design: Examination of two different RNA samples from maize silks obtained at 2-3 days after emergence
A genome-wide regulatory framework identifies maize pericarp color1 controlled genes.
Specimen part, Subject
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
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