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Homo sapiens

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

PROVIDER: PRJNA273670 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1773230.fastq.gz	Fastqsanger.gz
	SRR1773231.fastq.gz	Fastqsanger.gz
	SRR1773222.fastq.gz	Fastqsanger.gz
	SRR1773232.fastq.gz	Fastqsanger.gz
	SRR1773223.fastq.gz	Fastqsanger.gz

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

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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.

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Splicing factor Ybx1 maintains persistent Jak2-mutated neoplasms via Mknk1-ERK-signaling persistent clones in Jak2-mutated neoplasms

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An ERK biosensor identifies phosphatases regulating ERK pathway in tissue development and carcinoma cells

Project description:Extracellular signal-regulated kinases (ERKs) play essential roles in development and are implicated in numerous diseases. Phosphatases act as key regulators of ERK activation. To obtain a view of the phosphorylation network regulating ERK activity, we describe a binary approach using mammalian cell culture and forward genetic screens in a model organism. We analyzed a spectrum of phosphatases in human cells with ERK-SPARK reporters. Further validation of selected components in Drosophila revealed a functional map of ERK pathway phosphatases. EYA family phosphatases were selected and characterized as novel and critical regulators of ERK signaling in vivo and in mammalian cells. Chemical screens using phosphatase inhibitors showed that pharmacological inhibition of Drosophila Eyes Absent Homologue 2 (EYA2) promotes the progression of ERK-dependent carcinoma. The kinase reporter enabled high-throughput screening of genetic and pharmacological regulators under physiological and pathological condition, an important approach for investigating the regulation of kinase signaling.

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Project description:Kwang2003 - The influence of RKIP on the ERK signaling pathway This model is described in the article: Mathematical Modeling of the Influence of RKIP on the ERK Signaling Pathway Kwang-Hyun Cho, Sung-Young Shin, Hyun-Woo Kim, Olaf Wolkenhauer, Brian McFerran and Walter Kolch Computational Methods in Systems Biology: First International Workshop, CMSB 2003 Rovereto, Italy, February 24â??26, 2003 Proceedings Abstract: This paper investigates the influence of the Raf Kinase Inhibitor Pro- tein (RKIP) on the Extracellular signal Regulated Kinase (ERK) signaling pathway through mathematical modeling and simulation. Using nonlinear ordi- nary differential equations to represent biochemical reactions in the pathway, we suggest a technique for parameter estimation, utilizing time series data of proteins involved in the signaling pathway. The mathematical model allows the simulation the sensitivity of the ERK pathway to variations of initial RKIP and ERK-PP (phosphorylated ERK) concentrations along with time. Throughout the simulation study, we can qualitatively validate the proposed mathematical model compared with experimental results. This model is hosted on BioModels Database and identified by: BIOMD0000000647. To cite BioModels Database, please use: Chelliah V et al. BioModels: ten-year anniversary. Nucl. Acids Res. 2015, 43(Database issue):D542-8. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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