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Time-course expression data from HEK293∆RAF1:ER cells stimulated with 4OHT, U0126, CYHX, ActD, EGF, FGF, or IGF

ABSTRACT: We integrate experimental data and mathematical modelling to unveil how ERK signal duration is relayed to mRNA dynamics.

ORGANISM(S): Homo sapiens

PROVIDER: GSE72919 | GEO | 2017/04/28

SECONDARY ACCESSION(S): PRJNA295321

REPOSITORIES: GEO

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Time-course expression data from HEK293âRAF1:ER cells stimulated with 4OHT, U0126, CYHX, ActD, EGF, FGF, or IGF

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

Time-course expression data from HEK293∆RAF1:ER cells stimulated with 4OHT, U0126, CYHX, ActD, EGF, FGF, or IGF and labelled with 4SU

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-04-28 | GSE93611 | GEO

Time-course expression data from HEK293∆RAF1:ER cells stimulated with 4OHT and labelled with 4SU

Project description:We integrate experimental data and mathematical modelling to unveil how ERK signal duration is translated to mRNA dynamics.

2017-04-28 | GSE93610 | GEO

Time-course expression data from HEK293∆RAF1:ER cells stimulated with 4OHT, U0126, CYHX, ActD, EGF, FGF, or IGF and labelled with 4SU

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

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Localization dynamics of endogenous fluorescently labeled RAF1 in EGF-stimulated cells.

Project description:Activation of the epidermal growth factor (EGF) receptor (EGFR) at the cell surface initiates signaling through the RAS-RAF-MAPK/ERK1/2 pathway and receptor endocytosis. Whether this signaling continues from endosomes remains unclear, because RAS is predominantly located on the plasma membrane, and the localization of endogenous RAF kinases, downstream effectors of RAS, is not defined. To examine RAF localization, we labeled endogenous RAF1 with mVenus using gene editing. From 10 to 15% of RAF1-mVenus (<2000 molecules/cell), which was initially entirely cytosolic, transiently translocated to the plasma membrane after EGF stimulation. Following an early burst of translocation, the membrane-associated RAF1-mVenus was undetectable by microscopy or subcellular fractionation, and this pool was estimated to be <200 molecules per cell. In contrast, persistent EGF-dependent translocation of RAF1-mVenus to the plasma membrane was driven by the RAF inhibitor sorafenib, which increases the affinity of Ras-GTP:RAF1 interactions. RAF1-mVenus was not found in EGFR-containing endosomes under any conditions. Computational modeling of RAF1 dynamics revealed that RAF1 membrane abundance is controlled most prominently by association and dissociation rates from RAS-GTP and by RAS-GTP concentration. The model further suggested that the relatively protracted activation of the RAF-MEK1/2-ERK1/2 module, in comparison with RAF1 membrane localization, may involve multiple rounds of cytosolic RAF1 rebinding to active RAS at the membrane.

| S-EPMC6594441 | biostudies-literature

FGF/EGF signaling regulates the renewal of early nephron progenitors during embryonic development.

Project description:Recent studies indicate that nephron progenitor cells of the embryonic kidney are arranged in a series of compartments of an increasing state of differentiation. The earliest progenitor compartment, distinguished by expression of CITED1, possesses greater capacity for renewal and differentiation than later compartments. Signaling events governing progression of nephron progenitor cells through stages of increasing differentiation are poorly understood, and their elucidation will provide key insights into normal and dysregulated nephrogenesis, as well as into regenerative processes that follow kidney injury. In this study, we found that the mouse CITED1(+) progenitor compartment is maintained in response to receptor tyrosine kinase (RTK) ligands that activate both FGF and EGF receptors. This RTK signaling function is dependent on RAS and PI3K signaling but not ERK. In vivo, RAS inactivation by expression of sprouty 1 (Spry1) in CITED1(+) nephron progenitors results in loss of characteristic molecular marker expression and in increased death of progenitor cells. Lineage tracing shows that surviving Spry1-expressing progenitor cells are impaired in their subsequent epithelial differentiation, infrequently contributing to epithelial structures. These findings demonstrate that the survival and developmental potential of cells in the earliest embryonic nephron progenitor cell compartment are dependent on FGF/EGF signaling through RAS.

| S-EPMC3210493 | biostudies-literature

ELONGATED HYPOCOTYL 5 mediates blue light signalling to the Arabidopsis circadian clock

Project description:Circadian clocks are gene networks producing 24-h oscillations at the level of clock gene expression that is synchronized to environmental cycles via light signals. The ELONGATED HYPOCOTYL 5 (HY5) transcription factor is a signalling hub acting downstream of several photoreceptors and is a key regulator of photomorphogenesis. Here we describe a mechanism by which light quality could modulate the pace of the circadian clock through controlling abundance of HY5. We show that hy5 mutants display remarkably shorter period rhythms in blue but not in red light or darkness and blue light is more efficient than red to induce accumulation of HY5 at transcriptional and post-transcriptional levels. We demonstrate that the pattern and level of HY5 accumulation modulates its binding to specific promoter elements of majority of clock genes, but only a few of these show altered transcription in the hy5 mutant. Mathematical modelling suggests that the direct effect of HY5 on the apparently non-responsive clock genes could be masked by feed-back from the clock gene network. We conclude that the information on the ratio of blue and red components of the white light spectrum is decoded and relayed to the circadian oscillator, at least partially, by HY5.

2018-09-05 | GSE117797 | GEO

Project description:Nanodynamo: studying the dynamics of RNA metabolism through mathematical modelling and native RNA profiling.

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Novel role of cannabinoid receptor 2 in inhibiting EGF/EGFR and IGF-I/IGF-IR pathways in breast cancer.

Project description:Breast cancer is the second leading cause of cancer deaths among women. Cannabinoid receptor 2 (CNR2 or CB2) is an integral part of the endocannabinoid system. Although CNR2 is highly expressed in the breast cancer tissues as well as breast cancer cell lines, its functional role in breast tumorigenesis is not well understood. We observed that estrogen receptor-? negative (ER?-) breast cancer cells highly express epidermal growth factor receptor (EGFR) as well as insulin-like growth factor-I receptor (IGF-IR). We also observed IGF-IR upregulation in ER?+ breast cancer cells. In addition, we found that higher CNR2 expression correlates with better recurrence free survival in ER?- and ER?+ breast cancer patients. Therefore, we analyzed the role of CNR2 specific agonist (JWH-015) on EGF and/or IGF-I-induced tumorigenic events in ER?- and ER?+ breast cancers. Our studies showed that CNR2 activation inhibited EGF and IGF-I-induced migration and invasion of ER?+ and ER?- breast cancer cells. At the molecular level, JWH-015 inhibited EGFR and IGF-IR activation and their downstream targets STAT3, AKT, ERK, NF-kB and matrix metalloproteinases (MMPs). In vivo studies showed that JWH-015 significantly reduced breast cancer growth in ER?+ and ER?- breast cancer mouse models. Furthermore, we found that the tumors derived from JWH-015-treated mice showed reduced activation of EGFR and IGF-IR and their downstream targets. In conclusion, we show that CNR2 activation suppresses breast cancer through novel mechanisms by inhibiting EGF/EGFR and IGF-I/IGF-IR signaling axes.

| S-EPMC5444694 | biostudies-other

Stromal EGF and igf-I together modulate plasticity of disseminated triple-negative breast tumors.

Project description:The causes for malignant progression of disseminated tumors and the reasons recurrence rates differ in women with different breast cancer subtypes are unknown. Here, we report novel mechanisms of tumor plasticity that are mandated by microenvironmental factors and show that recurrence rates are not strictly due to cell-intrinsic properties. Specifically, outgrowth of the same population of incipient tumors is accelerated in mice with triple-negative breast cancer (TNBC) relative to those with luminal breast cancer. Systemic signals provided by overt TNBCs cause the formation of a tumor-supportive microenvironment enriched for EGF and insulin-like growth factor-I (IGF-I) at distant indolent tumor sites. Bioavailability of EGF and IGF-I enhances the expression of transcription factors associated with pluripotency, proliferation, and epithelial-mesenchymal transition. Combinatorial therapy with EGF receptor and IGF-I receptor inhibitors prevents malignant progression. These results suggest that plasticity and recurrence rates can be dictated by host systemic factors and offer novel therapeutic potential for patients with TNBC.

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