ArticleIET systems biology2009
Sensitivity analysis predicts that the ERK-pMEK interaction regulates ERK nuclear translocation.
Article in IET systems biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- An integrated modelling approach for targeted degradation: insights on optimization, data requirements and PKPD predictions from semi- or fully-mechanistic models and exact steady state solutions.Journal of pharmacokinetics and pharmacodynamics · 2023Article
- Computational investigation of the dynamic control of cAMP signaling by PDE4 isoform types.Biophysical journal · 2022Article
- Structure-activity relationship study of DEL-22379: ERK dimerization inhibitors with increased safety.Molecular diversity · 2021Article
- Revealing hidden information in osteoblast's mechanotransduction through analysis of time patterns of critical events.BMC bioinformatics · 2020Article
- Reverse engineering gene regulatory networks: coupling an optimization algorithm with a parameter identification technique.BMC bioinformatics · 2014Article
- Cellular compartments cause multistability and allow cells to process more information.Biophysical journal · 2013Article
- Mathematical simulation of membrane protein clustering for efficient signal transduction.Annals of biomedical engineering · 2012Review
- Inferring robust gene networks from expression data by a sensitivity-based incremental evolution method.BMC bioinformatics · 2012Article
- Monomeric and dimeric models of ERK2 in conjunction with studies on cellular localization, nuclear translocation, and in vitro analysis.Molecules and cells · 2012Review
- Quantitative understanding of cell signaling: the importance of membrane organization.Current opinion in biotechnology · 2010Review
- Analytical solution of steady-state equations for chemical reaction networks with bilinear rate laws.IEEE/ACM transactions on computational biology and bioinformaticsArticle
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Following phosphorylation, nuclear translocation of the mitogen-activated protein kinases (MAPKs), ERK1 and ERK2, is critical for both gene expression and DNA replication induced by growth factors. ERK nuclear translocation has therefore been studied extensively, but many details remain unresolved, including whether or not ERK dimerisation is required for translocation. Here, we simulate ERK nuclear translocation with a compartmental computational model that includes systematic sensitivity analysis. The governing ordinary differential equations are solved with the backward differentiation formula and decoupled direct methods. To better understand the regulation of ERK nuclear translocation, we use this model in conjunction with a previously published model of the ERK pathway that does not include an ERK dimer species and with experimental measurements of nuclear translocation of wild-type ERK and a mutant form, ERK1-4, which is unable to dimerise. Sensitivity analysis reveals that the delayed nuclear uptake of ERK1-4 compared to that of wild-type ERK1 can be explained by the altered interaction of ERK1-4 with phosphorylated MEK (MAPK/ERK kinase), and so may be independent of dimerisation. Our study also identifies biological experiments that can verify this explanation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.