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Genome wide extracellular signal-regulated kinase (ERK) pathway components interaction with human genome

ABSTRACT: Several recent studies, including ours, show that most components of signal transduction cascades including the extracellular signal-regulated protein kinase (ERK), that once were thought to act predominantly in cytoplasm, are in fact recruited to chromatin and are integral components of transcriptional complexes. However, their distribution along whole genome remains uncovered. Here we investigate genome wide recruitment of the ERK pathway components using chromatin immunoprecipitations (ChIP) followed by deep sequencing, ChIP-Seq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE65323 | GEO | 2016/08/18

SECONDARY ACCESSION(S): PRJNA273670

REPOSITORIES: GEO

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Genome wide extracellular signal-regulated kinase (ERK) pathway components interaction with human genome

Project description:Several recent studies, including ours, show that most components of signal transduction cascades including the extracellular signal-regulated protein kinase (ERK), that once were thought to act predominantly in cytoplasm, are in fact recruited to chromatin and are integral components of transcriptional complexes. However, their distribution along whole genome remains uncovered. Here we investigate genome wide recruitment of the ERK pathway components using chromatin immunoprecipitations (ChIP) followed by deep sequencing, ChIP-Seq. Hela-S3 cells were starved for 48 hours (control) and stimulated with EGF at concentration of 100ng/mL for 20 minutes. Cells were fixed with formaldehyde, chromatin isolated and subjected to ChIP reaction. Two technical replicates of ChIP reaction followed by sequencing were performed.

2015-08-01 | E-GEOD-65323 | biostudies-arrayexpress

RNAi of signal transduction components in HCT116 cells

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Protein abundance of AKT and ERK pathway components governs cell-type-specific regulation of proliferation

Project description:Activation of the AKT and ERK signaling pathway is a major contributor to cell proliferation. However, the integrated regulation of this multistep process, involving signal processing, cell growth and cell-cycle progression, is poorly understood. Here we study three cell types of hematopoietic origin, in which AKT and ERK signaling is triggered by erythropoietin (Epo). We find that the different cell types exhibit distinct proliferative responses, despite sharing the molecular network for pro-proliferative signaling. Iterating quantitative experiments and mathematical modeling, we show that the cell-type-specific regulation of proliferation emerges from two sources: (1) the protein abundance patterns of signaling components that cause differential flow of signals along the AKT and ERK pathways, and (2) the differential impact of the downstream regulators for protein synthesis and for cell-cycle progression on proliferation. Our integrated mathematical model of Epo-driven proliferation explains cell-type-specific effects of targeted AKT and ERK inhibitors and correctly predicts whether their combined application results in synergy.

2017-01-20 | GSE72317 | GEO

Protein abundance of AKT and ERK pathway components governs cell-type-specific regulation of proliferation

Project description:Signaling through the AKT and ERK pathways controls cell proliferation. However, the integrated regulation of this multistep process, involving signal processing, cell growth and cell-cycle progression, is poorly understood. Here we study different murine hematopoietic cell types, in which AKT and ERK signaling is triggered by erythropoietin (Epo). Although these cell types share the molecular network topology for pro-proliferative Epo signaling, they exhibit distinct proliferative responses. Iterating quantitative experiments and mathematical modeling, we identify two molecular sources for cell-type-specific proliferation. First, cell-type-specific protein abundance patterns cause differential signal flow along the AKT and ERK pathways. Second, downstream regulators of both pathways have differential effects on proliferation, suggesting that protein synthesis is rate-limiting for faster-cycling cells while slower cell-cycles are controlled at the G1-S progression. The integrated mathematical model of Epo-driven proliferation explains cell-type-specific effects of targeted AKT and ERK inhibitors and faithfully predicts based on the protein abundance anti-proliferative effects of inhibitors in primary human erythroid progenitor cells. Our findings suggest that the effectiveness of targeted cancer therapy might become predictable from protein abundance patterns.

2017-01-30 | PXD004816 | Pride

RNAi of signal transduction components in HCT116 cells

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Protein abundance of AKT and ERK pathway components governs cell-type-specific regulation of proliferation

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Characterization of RAS/RAF/ERK signal cascade as a novel regulating factor in alpha-amanitin-induced liver injury

Project description:The well-known hepatotoxicity mechanism resulting from alpha-amanitin (-AMA) exposure arises from RNA polymerase II (RNAP II) inhibition. RNAP Ⅱ inhibition occurs through the dysregulation of mRNA synthesis. However, the signaling pathways in hepatocytes that arise from -AMA have not yet been fully elucidated. Here, we identified that the RAS/RAF/ERK signaling pathway was activated through quantitative phosphoproteomic and molecular biological analyses. Bioinformatics analysis showed that AMA exposure increased protein phosphorylation in a time-dependent AMA AMA exposure. In addition, phosphorylation increased not only the components of the ERK signaling pathway but also U2AF65 and SPF45, known splicing factors. Therefore, we propose a novel mechanism of -AMA as follows. The RAS/RAF/ERK signaling pathway involved in aberrant splicing events is activated by -AMA exposure followed by aberrant splicing events leading to cell death.

2023-03-11 | PXD035758 | Pride

Characterization of RAS/RAF/ERK signal cascade as a novel regulating factor in alpha-amanitin-induced liver injury

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RNA-seq of Drosophila S2 cells after RNAi knock-down of signal transduction components

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2011-07-08 | E-MTAB-315 | biostudies-arrayexpress

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