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: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:Time-course expression data from HEK293∆RAF1:ER cells stimulated with 4OHT and labelled with 4SU
| PRJNA361293 | ENA
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:A fundamental facet of cell signaling is the conversion of extracellular signals into adaptive transcriptional responses. The role of RNA modifications in this process is poorly understood. We found that epidermal growth factor (EGF) promotes ERK-dependent phosphorylation of the m6A writer enzyme METTL3 at serine-43. Serine-43 phosphorylation increased METTL3-mediated methylation of the small nuclear RNA 7SK. Here we performed of phosphorylation mass spectrometry based on Data independent acquisition (DIA) of Hela cells stimulated with EGF in the absence or presence of the inhibitor U0126. Additionally, we validated known interactions between the 7SK-associated protein LARP7. Our findings establish a novel function for the m6A modification in converting growth-factor signaling events to a transcriptional elongation regulatory response via an RNA-methylation-dependent switch mediated by ERK signaling.
2023-06-27 | PXD036344 | Pride
Project description:MCF-7:PF is a a new in vitro model of antihormone resistant breast cancer that exhibits the characteristics of acquired tamoxifen resistance in vivo. It is well known that estrogen (E2) induces apoptosis in long-term estrogen-deprived breast cancer cells, MCF-7:5C (PubMed References PMID:15862958, PMID:16333030). MCF-7:PF was derived from MCF-7:5C through inhibition of c-Src, which blocks E2-induced apoptosis, coverts E2 responses from apoptosis to proliferation. MCF-7:PF cell growth is stimulated by E2 and SERMS in an ERα-dependent manner. Abstract: A c-Src inhibitor blocks estrogen (E2)-induced stress and converts E2 responses from inducing apoptosis to stimulating growth in E2-deprived breast cancer cells. A resulting cell line, MCF-7:PF, is reprogrammed with features of functional estrogen receptor (ER) and over-expression of insulin-like growth factor-1 receptor beta (IGF-1Rβ). We addressed the question of whether the antiestrogenic selective ER modulator 4-hydroxytamoxifen (4-OHT) could target ER to prevent E2-stimulated growth in MCF-7:PF cells. Unexpectedly, 4-OHT stimulated cell growth in an ER-dependent manner. However, unlike E2, 4-OHT suppressed classic ER-target genes as does the pure antiestrogen ICI 182,780, even during growth stimulation. Chromatin-immunoprecipitation (ChIP) assay indicated that 4-OHT did not recruit ER or nuclear receptor coactivator 3 (SRC3) to the promoter of ER-target gene, pS2. Paradoxically, 4-OHT reduced total IGF-1Rβ but increased phosphorylation of IGF-1Rβ, which was responsible for the activation of the phosphatidylinositol-3 kinases (PI3K)/Akt signaling pathway. Mechanistic studies revealed that 4-OHT rapidly activated the non-genomic pathway through ER, but other membrane-associated proteins such as IGF-1Rβ and c-Src participated. Furthermore, 4-OHT was more potent than E2 to up-regulate membrane remodeling molecules and activated focal adhesion molecules to promote cell growth. Therefore, disruption of membrane-associated signaling completely abolished 4-OHT-stimulated cell growth, but not E2-stimulated cell growth. Despite continued suppression of classic ER-target genes, 4-OHT activated the complex network of cytoskeleton remodeling and extracellular matrix-related signaling which facilitated 4-OHT-stimulated cell growth. This study is the first to recapitulate a cellular model in vitro of acquired tamoxifen (TAM) resistance developed in athymic mice in vivo.
2014-07-14 | GSE54171 | GEO
Project description:Substantial evidence implicates IGF-I signaling in the development and progression of breast cancer. To identify transcriptional targets of IGF action in breast cancer cells, we performed gene expression profiling (>22,000 RNA transcripts) of IGF-I-stimulated MCF-7 cells, a well characterized breast cancer cell line that is highly responsive to IGFs. We defined an IGF-I gene signature pattern of hundreds of genes either up-regulated or down-regulated at both 3 and 24 hrs in vitro. After removing genes considered generic to cell proliferation, the signature was examined in four different public profile datasets of clinical breast tumors (representing close to 1000 patients), as well as in profile datasets of experimental models for various oncogenic signaling pathways. Genes with early and sustained regulation by IGF-I were highly enriched for transcriptional targets of the estrogen, Ras, and PI3K/Akt/mTOR pathways. The IGF-I signature appeared activated in most estrogen receptor-negative (ER-) clinical breast tumors and in a substantial subset (~25%) of ER+ breast tumors. Patients with tumors showing activation of the IGF-I signature tended to have a shorter time to disease recurrence (including patients not receiving adjuvant therapy), both when considering all patients and the subset of ER+ patients. We found evidence for cross-talk and common transcriptional endpoints between the IGF-I and estrogen systems. Our results support the idea that the IGF-I pathway is one mechanism by which breast tumors may acquire hormone independence and a more aggressive phenotype. Keywords: two group comparison
2008-11-20 | GSE7561 | GEO
Project description:Comparison of genomic data from astrocytes and non-astrocyte cells from mice with or without FGF+EGF after SCI. We conducted genome-wide RNA sequencing of (i) immunoprecipitated astrocyte-specific ribosome-associated RNA (ramRNA) and (ii) the non-precipitated (flow-through) RNA deriving from non-astrocyte cells, from spinal cord tissue of mice recieving i) SCI alone, ii) SCI+hydrogel depot containing FGF+EGF, or iii) SCI+empty hydrogel depot.
2018-09-20 | GSE111529 | GEO