Expression data from β-globin let7 HeLa tet off cells treated with doxycycline
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE66541 | GEO | 2016/03/15
SECONDARY ACCESSION(S): PRJNA277230
REPOSITORIES: GEO
Similar Datasets
Project description:We used microarray to determine the genes whose expression was changed at six hours after doxycycline treatment Cells were transfected with β-globin let7 wt constructs. Two-condition experiment; HeLa tet off cells overexpressed control vs HeLa tet off cells treated with doxycycline for six hours
2016-03-15 | E-GEOD-66541 | biostudies-arrayexpress
Project description:Purpose is to examine the effect of SmN expression to gene expression in HeLa Compare the differences between the transcriptome of untreated and doxycycline-treated HeLa/TO-SmN in which expression of SmN is under doxycycline control
2015-01-16 | E-GEOD-54136 | biostudies-arrayexpress
Project description:Tet-on and tet-off systems are among the most popular vector systems for inducible transgene expression in mammalian cells. In tet-regulated systems the expression of the transgene depends on the presence or absence of the antibiotic tetracycline or its derivative doxycycline, which are added to the cell culture medium in concentrations considered to be far below cytotoxic levels. Therefore, potential effects on the treated cells, which are exerted by the antibiotic itself and unrelated to transgene expression, are often ignored. We examined the influence of low dose doxycycline on the transcriptional profile of two independent clones of MCF7 human breast carcinoma cells, transfected with tet-off regulator and response plasmids but not harboring any transgene. Treatment with 80 ng/ml doxycycline for 12 days markedly altered gene expression in these cells. Many genes associated with interferon-signaling were up-regulated while cell cycle-associated genes were down-regulated, which was also accompanied by a reduction of cell growth. These results highlight the importance of appropriate controls when working with tet-regulated gene expression systems, to allow distinction between the effects of transgene expression and potential “side effects” of the antibiotic used for its regulation.
2011-05-20 | GSE13926 | GEO
Project description:We used microarray to determine the genes whose expression was changed at three or six hours after Y27632 treatment.
2014-04-21 | GSE32024 | GEO
Project description:Mice with mitochondrial complex I deficiency (Ndufs4-/-) suffer from severe energy impairment primarily affecting the brain and die at P55. A small molecule screen developed by our lab using cells harboring human mitochondrial disease mutations identified antibiotics targeting mitochondrial translation as potent inhibitors of cell death under nutrient stress conditions. Doxycycline, which was identified amongst these antibiotics, was administered in the diet of Ndufs4-/- mice after weaning at P21. Mice fed with doxycycline showed improved motor function and significantly increased lifespan relative to untreated Ndufs4-/- mice. In order to investigate the molecular changes promoted by doxycycline in the brains of these mice, Ndufs4-/- doxycycline treated (DOX), Ndufs4-/- untreated (KO), and Ndufs4+/+ (WT) control mice were sacrificed at P55 and their brains harvested. Proteomic analysis revealed doxycycline treatment largely prevented the neuroimmune and inflammatory profile identified in the Ndufs4-/- mice. These findings implicate a potentially causality of these proteins in the neuronal cell death ultimately leading to the observed brain pathology.
2021-09-09 | PXD022860 | Pride
Project description:The tetracycline-controlled Tet-Off and Tet-On gene expression systems are used to regulate the activity of genes in eukaryotic cells in diverse settings, varying from basic biological research to biotechnology and gene therapy applications. These systems are based on regulatory elements that control the activity of the tetracycline-resistance operon in bacteria. The Tet-Off system allows silencing of gene expression by administration of tetracycline (Tc) or tetracycline-derivatives like doxycycline (dox), whereas the Tet-On system allows activation of gene expression by dox. Since the initial design and construction of the original Tet-system, these bacterium-derived systems have been significantly improved for their function in eukaryotic cells. We here review how a dox-controlled HIV-1 variant was designed and used to greatly improve the activity and dox-sensitivity of the rtTA transcriptional activator component of the Tet-On system. These optimized rtTA variants require less dox for activation, which will reduce side effects and allow gene control in tissues where a relatively low dox level can be reached, such as the brain.
| S-EPMC5070417 | biostudies-literature
Project description:Recent work in immunometabolism has emphasised the role of mitochondria in both the innate and adaptive immune system. Mitochondria are important in T cell development and differentiation, but less is known about their role in CD8+ effector T cells (CTLs). We found that CTLs that lack the mitochondrial deubiquitinase USP30 undergo promiscuous mitophagy, destroying most of the cellular mitochondria. Surprisingly, this results in a markedly diminished killing capacity, while motility, signalling and secretion remain intact. This study uses quantitative DIA proteomics to measure the impact of USP30 deficiency on the global proteome of IL-2 maintained, 4.5 h TCR retriggered and 4.5 h TCR retriggered + cycloheximide CTL. We also measured the impact of pharmacologically inhibiting mitochondrial translation by performing Quantitative DIA proteomics on IL2 maintained or TCR retriggered CTL treated with the mitochondrial translation inhibitor doxycycline for 4.5 hrs. Unexpectedly, inhibition of mitochondrial translation, through genetic or pharmacologic methods, was the mechanism by which CTL killing was impaired. Reduced mitochondrial translation triggered attenuated cytosolic translation which precluded replenishment of secreted effector molecules thereby limiting the capacity of CTLs to serially kill multiple targets. Thus, mitochondria emerge as a previously unappreciated homeostatic regulator of protein translation required for serial CTL killing.
2022-06-09 | PXD026948 | Pride
Project description:We used microarray to determine the genes whose expression was changed at three or six hours after Y27632 treatment. Three-condition experiment; 293T control vs 293T treated with Y27632 for three hours, 293T control vs 293T treated with Y27632 for six hours.
2014-04-21 | E-GEOD-32024 | biostudies-arrayexpress
Project description:Undifferentiated mouse embryonic stem cells stably expressing the HOXB1 transcription factor under doxycycline tet-on control were differentiated into embryoid bodies. Nestin+ neuroepithelial cells were selected by transfer of the embryoid bodies to ISTFn media. Expression of HOXB1 was induced by addition of doxycycline or not induced on the seventh day of selection and also for one day after trypsination and transfer to laminin/polyornithine substrate on matrigel substrate.
2008-06-30 | E-MIMR-441 | biostudies-arrayexpress
Project description:To characterize the mitochondrial stress response induced by Doxycycline in vivo in liver and kidneys, we administered doxycycline (Dox) at 500 mg/kg/day (mpkd) in the drinking water to 9 weeks-old germ-free C57BL/6J mice for 16 days, hence eliminating the potential confounding impacts of Doxycycline on the microbiome.
2022-09-14 | GSE202754 | GEO