ArticlePloS one2010
Phosphoproteomics-based modeling defines the regulatory mechanism underlying aberrant EGFR signaling.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Mathematical Modeling and Inference of Epidermal Growth Factor-Induced Mitogen-Activated Protein Kinase Cell Signaling Pathways.International journal of molecular sciences · 2024Review
- 8-Br-cGMP suppresses tumor progression through EGFR/PLC γ1 pathway in epithelial ovarian cancer.Molecular biology reports · 2024Article
- Analytical reduction of combinatorial complexity arising from multiple protein modification sites.Journal of the Royal Society, Interface · 2015Article
- Functional aspects of the EGF-induced MAP kinase cascade: a complex self-organizing system approach.PloS one · 2014Article
- PKIS: computational identification of protein kinases for experimentally discovered protein phosphorylation sites.BMC bioinformatics · 2013Article
- Systematic parameter estimation in data-rich environments for cell signalling dynamics.Bioinformatics (Oxford, England) · 2013Article
- Research resource: identification of novel growth hormone-regulated phosphorylation sites by quantitative phosphoproteomics.Molecular endocrinology (Baltimore, Md.) · 2012Article
- Article
- Phosphoproteomics-based systems analysis of signal transduction networks.Frontiers in physiology · 2011Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMutation of the epidermal growth factor receptor (EGFR) results in a discordant cell signaling, leading to the development of various diseases. However, the mechanism underlying the alteration of downstream signaling due to such mutation has not yet been completely understood at the system level. Here, we report a phosphoproteomics-based methodology for characterizing the regulatory mechanism underlying aberrant EGFR signaling using computational network modeling. METHODOLOGY/PRINCIPAL
findingsOur phosphoproteomic analysis of the mutation at tyrosine 992 (Y992), one of the multifunctional docking sites of EGFR, revealed network-wide effects of the mutation on EGF signaling in a time-resolved manner. Computational modeling based on the temporal activation profiles enabled us to not only rediscover already-known protein interactions with Y992 and internalization property of mutated EGFR but also further gain model-driven insights into the effect of cellular content and the regulation of EGFR degradation. Our kinetic model also suggested critical reactions facilitating the reconstruction of the diverse effects of the mutation on phosphoproteome dynamics. CONCLUSIONS/SIGNIFICANCE: Our integrative approach provided a mechanistic description of the disorders of mutated EGFR signaling networks, which could facilitate the development of a systematic strategy toward controlling disease-related cell signaling.
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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.