ArticleThe Biochemical journal2006
Quantitative model of Ras-phosphoinositide 3-kinase signalling cross-talk based on co-operative molecular assembly.
Article in The Biochemical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Prognostic biomarkers in phase II trial of cetuximab-containing induction and chemoradiation in resectable HNSCC: Eastern cooperative oncology group E2303.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Trial
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- A phase field model with stochastic input simulates cellular gradient sensing, morphodynamics, and fidelity of haptotaxis.bioRxiv : the preprint server for biology · 2026Article
- Insight from the maximal activation of the signal transduction excitable network inProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Excitable Signal Transduction Networks in Directed Cell Migration.Annual review of cell and developmental biology · 2017Review
- Exosomal miRs in Lung Cancer: A Mathematical Model.PloS one · 2016Article
- Dimerization-based control of cooperativity.Molecular bioSystems · 2014Article
- Computational model of VEGFR2 pathway to ERK activation and modulation through receptor trafficking.Cellular signalling · 2013Article
- Coordinate direct input of both KRAS and IGF1 receptor to activation of PI3 kinase in KRAS-mutant lung cancer.Cancer discovery · 2013Article
- Article
- A mathematical model of CR3/TLR2 crosstalk in the context of Francisella tularensis infection.PLoS computational biology · 2012Article
- Data-driven modelling of receptor tyrosine kinase signalling networks quantifies receptor-specific potencies of PI3K- and Ras-dependent ERK activation.The Biochemical journal · 2012Article
- Allosteric modulation of Ras-GTP is linked to signal transduction through RAF kinase.The Journal of biological chemistry · 2011Article
- Systematic quantification of negative feedback mechanisms in the extracellular signal-regulated kinase (ERK) signaling network.The Journal of biological chemistry · 2010Article
- Spontaneous phosphoinositide 3-kinase signaling dynamics drive spreading and random migration of fibroblasts.Journal of cell science · 2009Article
- PI3K-dependent cross-talk interactions converge with Ras as quantifiable inputs integrated by Erk.Molecular systems biology · 2009Article
- Signal transduction at point-blank range: analysis of a spatial coupling mechanism for pathway crosstalk.Biophysical journal · 2008Article
- Computational models of tandem SRC homology 2 domain interactions and application to phosphoinositide 3-kinase.The Journal of biological chemistry · 2008Article
- Sensing and integration of Erk and PI3K signals by Myc.PLoS computational biology · 2008Article
- A mathematical model for neutrophil gradient sensing and polarization.PLoS computational biology · 2007Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In growth-factor-stimulated signal transduction, cell-surface receptors recruit PI3Ks (phosphoinositide 3-kinases) and Ras-specific GEFs (guanine nucleotide-exchange factors) to the plasma membrane, where they produce 3'-phosphorylated phosphoinositide lipids and Ras-GTP respectively. As a direct example of pathway networking, Ras-GTP also recruits and activates PI3Ks. To refine the mechanism of Ras-PI3K cross-talk and analyse its quantitative implications, we offer a theoretical model describing the assembly of complexes involving receptors, PI3K and Ras-GTP. While the model poses the possibility that a ternary receptor-PI3K-Ras complex forms in two steps, it also encompasses the possibility that receptor-PI3K and Ras-PI3K interactions are competitive. In support of this analysis, experiments with platelet-derived growth factor-stimulated fibroblasts revealed that Ras apparently enhances the affinity of PI3K for receptors; in the context of the model, this suggests that a ternary complex does indeed form, with the second step greatly enhanced through membrane localization and possibly allosteric effects. The apparent contribution of Ras to PI3K activation depends strongly on the quantities and binding affinities of the interacting molecules, which vary across different cell types and stimuli, and thus the model could be used to predict conditions under which PI3K signalling is sensitive to interventions targeting Ras.
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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.