ArticlePloS one2011
A computational analysis of the dynamic roles of talin, Dok1, and PIPKI for integrin activation.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Leukocyte arrest: Biomechanics and molecular mechanisms of β2 integrin activation.Biorheology · 2015Review
- Investigation of the essential role of platelet-tumor cell interactions in metastasis progression using an agent-based model.Theoretical biology & medical modelling · 2014Article
- Prediction stability in a data-based, mechanistic model of σF regulation during sporulation in Bacillus subtilis.Scientific reports · 2013Article
- The Process-Interaction-Model: a common representation of rule-based and logical models allows studying signal transduction on different levels of detail.BMC bioinformatics · 2012Article
- Hybrid spatial Gillespie and particle tracking simulation.Bioinformatics (Oxford, England) · 2012Article
- Specification, annotation, visualization and simulation of a large rule-based model for ERBB receptor signaling.BMC systems biology · 2012Article
- Plasticity of TGF-β signaling.BMC systems biology · 2011Article
- Inferring Biological Mechanisms by Data-Based Mathematical Modelling: Compartment-Specific Gene Activation during Sporulation in Bacillus subtilis as a Test Case.Advances in bioinformatics · 2011Article
- A computational analysis of the dynamic roles of talin, Dok1, and PIPKI for integrin activation.PloS one · 2011Article
- Rule-based modeling: a computational approach for studying biomolecular site dynamics in cell signaling systems.Wiley interdisciplinary reviews. Systems biology and medicineReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Integrin signaling regulates cell migration and plays a pivotal role in developmental processes and cancer metastasis. Integrin signaling has been studied extensively and much data is available on pathway components and interactions. Yet the data is fragmented and an integrated model is missing. We use a rule-based modeling approach to integrate available data and test biological hypotheses regarding the role of talin, Dok1 and PIPKI in integrin activation. The detailed biochemical characterization of integrin signaling provides us with measured values for most of the kinetics parameters. However, measurements are not fully accurate and the cellular concentrations of signaling proteins are largely unknown and expected to vary substantially across different cellular conditions. By sampling model behaviors over the physiologically realistic parameter range we find that the model exhibits only two different qualitative behaviors and these depend mainly on the relative protein concentrations, which offers a powerful point of control to the cell. Our study highlights the necessity to characterize model behavior not for a single parameter optimum, but to identify parameter sets that characterize different signaling modes.
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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.