Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

Project description:RNAi of signal transduction components in HCT116 cells

| PRJEB2536 | ENA

RNAi of signal transduction components in Drosophila S2 cells

Project description:RNAi of signal transduction components in Drosophila S2 cells

| PRJEB2222 | ENA

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

Project description:We performed RNAi knockdown experiments on 7 different signal transduction components of the Wnt pathway in HCT116 colon cancer cells and prepared RNA libraries from the poly-adenylated fraction of the RNA. SOLiD sequencing of strand-specific, barcoded transcriptome libraries yielded expression profiles allowing us to extract common pathway signatures and enabeling us to perform susequent nested effects modelling. the resulting pathway models yields new insight in the pathway topology in colon cancer.

2014-04-18 | E-MTAB-651 | biostudies-arrayexpress

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

2017-03-31 | MSV000080844 | MassIVE

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.

2024-08-07 | PXD054658 |

CCL2/CCR2/Erk signal induced by interaction between cancer cells and macrophages contributes to hepatocellular carcinoma progression

Project description:Macrophages infiltrating into tumors are known as tumor-associated macrophages (TAMs) and play a central role in tumor progression. In immunohistochemistry, intra-tumoral CD68-positive macrophages correlated with poor prognosis and clinicopathological factors of patients with hepatocellular carcinoma (HCC). Next, we established an indirect co-culture assay between HCC cells and peripheral blood-derived macrophages. cDNA microarray analysis revealed that C-C motif chemokine ligand 2 (CCL2) was highly expressed in HCC cells co-cultured with macrophages. CCL2 bound to CCR2, known as a main receptor of CCL2, and promoted the proliferation and migration of HCC cells and macrophages. The Erk pathway as a downstream signal of the CCL2/CCR2 axis contributed to controlling these phenotypes of HCC cells and macrophages. In the ELISA using serum samples, the serum CCL2 levels of patients with HCC were significantly elevated compared with healthy volunteer donors. The survival outcomes of patients with intra-tumoral CCL2 expression Positive based on immunohistochemistry tended to be worse, without statistical significance. Consequently, the CCL2 upregulated through the interactions between HCC cells and macrophages contributed to HCC progression and the CCL2/CCR2/Erk signal might be an effective candidate for the treatment target of HCC and macrophages.

2024-12-18 | GSE274406 | GEO

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data