ArticleBiophysical journal2015
Use of mechanistic models to integrate and analyze multiple proteomic datasets.
Article in Biophysical journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 24 citations in OpenAlex.
- Visualizing mechanistic models by integrating site-specific molecular details into reaction networks.Frontiers in molecular biosciences · 2025Article
- Mathematical Modeling and Inference of Epidermal Growth Factor-Induced Mitogen-Activated Protein Kinase Cell Signaling Pathways.International journal of molecular sciences · 2024Review
- A scalable, open-source implementation of a large-scale mechanistic model for single cell proliferation and death signaling.Nature communications · 2022Article
- An Optimized Single-Molecule Pull-Down Assay for Quantification of Protein Phosphorylation.Journal of visualized experiments : JoVE · 2022Article
- Validation Through Collaboration: Encouraging Team Efforts to Ensure Internal and External Validity of Computational Models of Biochemical Pathways.Neuroinformatics · 2022Review
- New analysis pipeline for high-throughput domain-peptide affinity experiments improves SH2 interaction data.The Journal of biological chemistry · 2020Article
- Multisite EGFR phosphorylation is regulated by adaptor protein abundances and dimer lifetimes.Molecular biology of the cell · 2020Article
- Generalizing Gillespie's Direct Method to Enable Network-Free Simulations.Bulletin of mathematical biology · 2019Article
- New insights into RAS biology reinvigorate interest in mathematical modeling of RAS signaling.Seminars in cancer biology · 2019Review
- Modeling cell line-specific recruitment of signaling proteins to the insulin-like growth factor 1 receptor.PLoS computational biology · 2019Article
- A mechanistic pan-cancer pathway model informed by multi-omics data interprets stochastic cell fate responses to drugs and mitogens.PLoS computational biology · 2018Article
- How low can you go?eLife · 2018Article
- Protein abundance of AKT and ERK pathway components governs cell type-specific regulation of proliferation.Molecular systems biology · 2017Article
- Conservation of protein abundance patterns reveals the regulatory architecture of the EGFR-MAPK pathway.Science signaling · 2016Article
- Mathematics in modern immunology.Interface focus · 2016Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Proteins in cell signaling networks tend to interact promiscuously through low-affinity interactions. Consequently, evaluating the physiological importance of mapped interactions can be difficult. Attempts to do so have tended to focus on single, measurable physicochemical factors, such as affinity or abundance. For example, interaction importance has been assessed on the basis of the relative affinities of binding partners for a protein of interest, such as a receptor. However, multiple factors can be expected to simultaneously influence the recruitment of proteins to a receptor (and the potential of these proteins to contribute to receptor signaling), including affinity, abundance, and competition, which is a network property. Here, we demonstrate that measurements of protein copy numbers and binding affinities can be integrated within the framework of a mechanistic, computational model that accounts for mass action and competition. We use cell line-specific models to rank the relative importance of protein-protein interactions in the epidermal growth factor receptor (EGFR) signaling network for 11 different cell lines. Each model accounts for experimentally characterized interactions of six autophosphorylation sites in EGFR with proteins containing a Src homology 2 and/or phosphotyrosine-binding domain. We measure importance as the predicted maximal extent of recruitment of a protein to EGFR following ligand-stimulated activation of EGFR signaling. We find that interactions ranked highly by this metric include experimentally detected interactions. Proteins with high importance rank in multiple cell lines include proteins with recognized, well-characterized roles in EGFR signaling, such as GRB2 and SHC1, as well as a protein with a less well-defined role, YES1. Our results reveal potential cell line-specific differences in recruitment.
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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.