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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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The Possible Protective Role of Omeprazole Against Oxaliplatin Induced Neuropathy in Cancer Patients

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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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A Study of LY3214996 Administered Alone or in Combination With Other Agents in Participants With Advanced/Metastatic Cancer

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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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ERK Oscillation-Dependent Gene Expression Patterns and Deregulation By The Stress-Response

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ERK Oscillation-Dependent Gene Expression Patterns and Deregulation By The Stress-Response

Project description:Studies were undertaken to determine whether oscillatory behavior in the extracellular signal regulated kinase (ERK) pathway results in unique gene regulation patterns. Microarray analysis was performed on three subcloned populations of human keratinocytes with distinct ERK signaling/oscillation phenotypes. Microarray analysis identified 45 genes that overlapped between 2 subclones with oscillation phenotypes but not in the subclone which is non-oscillatory. Transcription factor networks revealed a role for MED1 in mediating ERK oscillation-dependent gene expression, which was confirmed with Western blot analysis. Further experimentation confirmed a role for p38 in the mediation of MED1 phosphorylation and ERK oscillatory behavior. hTERT-immortalized normal human keratinocytes (provided by Dr. Jerry Shay, The University of Texas Southwestern Medical Center) were stably transfected with ERK1-green fluorescent protein chimera and stable subclones were isolated with distinct ERK activation/oscillation patterns: Clone #1 exhibits transient ERK activation with ligand activation but does not oscillate; Clone #2 exhibits persistent ERK oscillations that are dependent on ligand activation; and Clone #3 exhibits spontaneous ERK oscillations in the absence of ligand activation.

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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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ChIP-Seq for ERK2/MAPK1 and ELK1 in human embryonic stem cells

Project description:The ERK/MAPK signal transduction cascade is one of the key pathways regulating proliferation and differentiation in development and disease. In human embryonic stem cells (hESCs), ERK signaling is required for their self-renewing property. Here we studied the convergence of the ERK signaling cascade at the DNA by mapping genome-wide kinase-chromatin interactions for ERK2 in hESCs. We observe that ERK2 targets genes coding for small RNAs, histones, and genes involved in cellular metabolism and cell cycle. We find that the transcription factor ELK1 is essential in hESCs and that ERK2 co-occupies promoters bound by ELK1. Strikingly, promoters bound by ELK1 without ERK2 are occupied by Polycomb group proteins that repress genes involved in lineage commitment. In summary, we propose a model where extracellular signaling-stimulated proliferation and intrinsic repression of differentiation is integrated to maintain the identity of hESCs.

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