Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA295321 | ENA |
REPOSITORIES: ENA
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Project description:We integrate experimental data and mathematical modelling to unveil how ERK signal duration is relayed to mRNA dynamics. HEK293 cells were transfected with an inducible form of RAF (âRAF1:ER) and induced with tamoxifen (4OHT) or stimulated with different growth factors (EGF, FGF, iGF). Effects of RAF signalling were perturbed subsequently or in parallel with MEK inhibtor U0126, translation inhibtor cycloheximide (CYHX) and actinomycin D (ActD).
2017-04-28 | E-GEOD-72919 | biostudies-arrayexpress
Project description:Time-course expression data from HEK293∆RAF1:ER cells stimulated with 4OHT, U0126, CYHX, ActD, EGF, FGF, or IGF and labelled with 4SU
| PRJNA361281 | ENA
Project description:Time-course expression data from HEK293∆RAF1:ER cells stimulated with 4OHT and labelled with 4SU
| PRJNA361293 | ENA
Project description:An inducible oncogenic cell line ZFL-?Raf1-ER was established, in which oncogenic human Raf-1(?Raf1) can be activated in zebrafish liver cells by administration of 4-hydroxytamoxifen (4HT). Transcriptional profilling of the ZFL-?Raf1-ER cells with and without administration of 4HT and/or the MEK inhibitor U0126 defined the gene signatures transcriptionally regulated by hyperactive Raf/MEK/MAPK signaling in zebrafish liver cells. The ZFL-?Raf1-ER cells were cultured in 12-well plates till confluence. Cell were starved for 4h in plain medium and susequently treated with or without 1µM 4HT and/or 30µM U0126 for 12h. Biological triplications were taken for each condition.
2011-07-07 | E-GEOD-29308 | biostudies-arrayexpress
Project description:To investigate the mechansims that underly astrocyte dedifferentiation, we performed single cell RNA sequencing analysis of primary astrocytes after p53 loss and exposure to mitogens, EGF and and FGF. Primary astrocytes were isolated from postnatal day 3 inducible p53 knockout mice (GFAP-CreERT2;p53flox/flox;LSL-tdTomato), whereby treatment with 4-hydroxytamoxifen (4OHT) induces p53 loss and tdTomato labelling in GFAP+ astrocytes. Astrocytes were treated with 4OHT in media supplemented with EGF and FGF to induce recombination and astrocyte dedifferentiation in vitro.
2023-02-23 | GSE196408 | GEO
Project description:To investigate the mechansims that underlie astrocyte dedifferentiation, we performed single cell RNA sequencing analysis of primary astrocytes isolated from adult mouse cortex after p53 loss and exposure to mitogens, EGF and and FGF. Primary astrocytes were isolated from cortices of 2-3month old inducible p53 knockout mice (GFAP-CreERT2;p53flox/flox;LSL-tdTomato) using Miltenyi Adult Brain Dissociation kit and ACSA-2 beads. Treatment with 4-hydroxytamoxifen (4OHT) induces p53 loss and tdTomato labelling in GFAP+ astrocytes. Astrocytes were treated with 4OHT in media supplemented with EGF and FGF to induce recombination and astrocyte dedifferentiation in vitro.
2023-02-23 | GSE220477 | GEO
Project description:Background: Striatum is the crucial unit in brain involved in higher-level organizational learning, motor control and cognitive finctions. It also produces dopaminergic neurons, which play an important role in the control of multiple brain functions including voluntary movement and a span of neurobehavioral processes such as, mood, reward, addiction, and stress. Traumatic brain injury (TBI) lead to striatum related persistent cognitive dysfunctions. A number of cell based therapies such as; induced pluripotent stem cells (ips), neural stem cells (NSCs) and mesenchymal stem cells (MSCs), have been investigated so far for their potential application in TBI. But the journey from bench-to-bedside has not yet been covered sucessfully. As their survival and long-term maintenance in vivo has been huddle so far. So to understand the fate of embryonic striatal stem cells (ESSCs) in long-term neurogenesis in vitro, we have studied the neurogenic potential of rat embryonic striatal stem cells from E18th day embryos under conditioned microenvironments. Objectives: To evaluate the neuro-regenerative potential striatum-derived stem cells, we have employed synergestic effects of certain neurotrophins, such as ; EGF, IGF, FGF and LIF as in four combinations (Control/untreated-A, EGF+FGF-B, EGF+FGF+LIF-C, EGF+FGF+IGF-D and EGF+FGF+ IGF +LIF –E) in the microenvironment . To decipher the regulatory miRNAs involved in ESSC-derived neurogenesis, we have performed detailed miRNA profiling for ESSCs at passage 3 for groupD and group E derived ESSCs (based on their performance in vitro). Out data has explored cruicial mIRNAs involved in strital neurogenesis .
2011-08-25 | GSE30276 | GEO
Project description:Molecular responses to MEK inhibition in cancer cells are complex and dynamic. We performed a time-series experiment to measure global RNA expression changes following treatment with the MEK inihibor U0126 MDA-MB-231 human breast cancer cells were grown in low-serum conditions. Treatment with U0126 was initiated in the presence of EGF. RNA was harvested at multiple time points during the course of 48 hours.
2015-04-01 | E-GEOD-61364 | biostudies-arrayexpress
Project description:To elucidate mechanisms of cancer progression, we generated inducible human neoplasia in 3-dimensionally intact epithelial tissue. Gene expression profiling of both epithelia and stroma at specific time points during tumor progression revealed sequential enrichment of genes mediating discrete biologic functions in each tissue compartment. A core cancer progression signature was distilled using the increased signaling specificity of downstream oncogene effectors and subjected to network modeling. Network topology predicted that tumor development depends upon specific ECM-interacting network hubs. Blockade of one such hub, the b1 integrin subunit, disrupted network gene expression and attenuated tumorigenesis in vivo. Thus, integrating network modeling and temporal gene expression analysis of inducible human neoplasia provides an approach to prioritize and characterize genes functioning in cancer progression. There are 3 experiments in this study: (1a) a time course of human epidermal tissue transformed by oncogenic ER:H-Ras and IkBaM comprising days 0, 5, 20, and 35 post Ras activation using 4OHT; (1b) a matched time course of adjacent mouse stromal tissue during tumor progression; (2) Arrays comparing 4OHT-induced, Raf-1:ER/IkBaM transformed epidermal tissue and -4OHT controls; and (3) Arrays comparing Ras:ER/IkBaM grafts co-treated with 4OHT and either IgG control antibody or an anti-b1 integrin blocking antibody, P5D2 for 30 days. All arrays were done in biologic duplicate. Epidermal tissue co-expressing ER:H-RasG12V (ER:Ras) and IkBaM was regenerated on female scid/scid mouse recipients. Grafts were allowed to heal for at least 3 weeks before Ras activation via daily i.p. injections of 730ug of 4OHT (in 110ul of a corn oil/ethanol mixture). Duplicate grafts were harvested after 0, 5, 20, and 35 days of 4OHT treatment. Laser capture microdissection was utilized to independently isolate epithelial cells of the basal most layers and adajacent stromal tissue for each time point. RNA was subjected to one round of T7-based linear amplification (Ambion Message Amp II enhanced kit) and hybridized to either HG-U133A 2.0 or MG-430A affymetrix oligonucleotide arrays. Arrays from this experiment are labeled Ras and Stroma, respectively. The second experment was performed on Raf-1:ER/IkBaM expressing grafts with and without 4OHT treament for 30 days. The third experiment was done comparing ER:Ras/IkBaM grafts concomitantly treated with 4OHT and 1.5mg/week of either IgG control antibody or a mouse monoclonal blocking antibody against b1 integrin for 30 days. For experiments 2 and 3, HG-U133A 2.0 GeneChips were used; 4OHT treatment and RNA isolation/amplification was performed as above.
2009-06-02 | E-GEOD-15299 | biostudies-arrayexpress
Project description:Characterization of gene expression changes 72 hours after withdrawal of tamoxifen in murine hematopoietic progenitors transformed by Hoxa9-ER/Meis1 using RNAseq. In the presence of tamoxifen (4OHT), Hoxa9-ER localizes to the nucleus of cells allowing for transformation, while withdrawal of 4OHT (culture in EtOH) leads to loss of nuclear Hoxa9-ER. Loss of Hoxa9-ER leads to a decrease in cellular proliferation and differentiation along the myeloid lineage.
2014-06-11 | GSE58359 | GEO