ZnO nanoparticles can elicit a range of perturbed cell responses in vitro. Exposure to topically applied sunscreens containing ZnO particles may or may not elicit a biological effect in mice.
Dermal absorption and short-term biological impact in hairless mice from sunscreens containing zinc oxide nano- or larger particles.
Specimen part
View SamplesZnO and TiO2 nanoparticles can elicit a range of perturbed cell responses in vitro. Exposure to topically applied sunscreens containing ZnO or TiO2 particles may or may not elicit a biological effect in mice. We aimed to compare the biological responses of immune-competent hairless mice receiving topical applications of commercially available sunscreens with or without metal oxide nanoparticles, with the responses of mice receiving no sunscreen.
Long-term exposure to commercially available sunscreens containing nanoparticles of TiO2 and ZnO revealed no biological impact in a hairless mouse model.
Specimen part, Time
View SamplesWe compared the seedling transcription profiles to determine the effects of loss-of-function of the BRX gene of Arabidopsis. BRX is required for optimal root growth. We compared seedlings of a loss-of-function line (brx) with its control background (Sav-0). Because the loss-of-function line was derived from introgression, a brx line that was complemented by a transgenic wild type copy of BRX was also included as a control. This line (rescued brx) allows the identification of expression differences that are due to introgression drag. See Mouchel et al. 2004, Genes & Dev. Vol. 18, p. 700 for a detailed description. We also compared to response of the different genotypes to the application of the phytohormones brassinolide (BL) and indole acetic acid (IAA)
BRX mediates feedback between brassinosteroid levels and auxin signalling in root growth.
Age, Compound, Time
View SamplesMyocardial infarction (MI) is one of the most severe manifestations of coronary artery disease (CAD) and the leading cause of death from non-infectious diseases worldwide. It is known, that the central component of CAD pathogenesis is a chronic vascular inflammation. However, the mechanisms underlying the changes that occur in T, B and NK-lymphocytes, monocytes and other immune cells during CAD and MI are still poorly understood. One of those pathogenic mechanisms might be the dysregulation of intracellular signaling pathways in the immune cells.
Collapsing the list of myocardial infarction-related differentially expressed genes into a diagnostic signature.
Sex, Specimen part, Disease stage
View SamplesWe report the identification of stable intronic sequence RNAs (sisRNAs) in Drosophila. Overall design: RNA was obtained from unfertilized eggs and subjected to deep sequencing.
Generation of Drosophila sisRNAs by Independent Transcription from Cognate Introns.
Subject
View SamplesWe report the identification of stable intronic sequence RNAs (sisRNAs) in Drosophila. Overall design: RNA was obtained from 0-2 hr embryos and subjected to deep sequencing.
Stable intronic sequence RNAs have possible regulatory roles in Drosophila melanogaster.
Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Ets transcription factor GABP controls T cell homeostasis and immunity.
Specimen part
View SamplesEts family transcription factor GA-binding protein (GABP) regulates gene expression in CD4 and CD8 T cells.
Ets transcription factor GABP controls T cell homeostasis and immunity.
Specimen part
View SamplesThe combination of JQ1 and Vemurafenib acted synergistically in BRAF-mutant cell lines, resulting in marked apoptosis in vitro, with up-regulation of pro-apoptotic proteins. In vivo, combination treatment suppressed tumor growth and significantly improved survival compared to either drug alone. RNA sequencing of tumor tissues revealed almost four thousand genes that were uniquely modulated by the combination, with several anti-apoptotic genes significantly down-regulated. Overall design: 16 samples analyzed from 8 mice (each mouse was bearing two tumors, one on each flank) in 4 treatment groups (control, vemurafenib alone, JQ1 alone, JQ1+vemurafenib)
BET and BRAF inhibitors act synergistically against BRAF-mutant melanoma.
Cell line, Treatment, Subject
View SamplesG protein coupled receptor (GPCR) signalling covers three major mechanisms. GPCR agonist engagement allows for the G proteins to bind to the receptor leading to a classical downstream signalling cascade. The second mechanism is via the utilization of the ß-arrestin signalling molecule and thirdly via transactivation dependent signalling. GPCRs can transactivate protein tyrosine kinase receptors (PTKR) to activate respective downstream signalling intermediates. In the past decade GPCR transactivation dependent signalling was expanded to show transactivation of serine/threonine kinase receptors (S/TKR). Kinase receptor transactivation enormously broadens the GPCR signalling paradigm. This work utilizes next generation RNA-sequencing to study the contribution of transactivation dependent signalling to total protease activated receptor (PAR)-1 signalling. Transactivation, assessed as gene expression, accounted for 50 percent of the total genes regulated by thrombin acting through PAR-1 in human coronary artery smooth muscle cells. GPCR transactivation of PTKRs is approximately equally important as the transactivation of the S/TKR with 209 and 177 genes regulated respectively, via either signalling pathway. This work shows that genome wide studies can provide powerful insights into GPCR mediated signalling pathways Overall design: Human CASMCS cells were subject to various treatments: basal, thrombin, thrombin + SB, thrombin + AG and thrombin + SB + AG. Gene expression was studies after 30 minutes to assess genes that are differentially expressed by treat emnt with agonists and antagonists. The agonoists and antagonists are associated with transactivation of GPCRs and the gene expression results will help identify relevant genes.
RNA sequencing to determine the contribution of kinase receptor transactivation to G protein coupled receptor signalling in vascular smooth muscle cells.
Specimen part, Treatment, Subject
View Samples