Fibroblast growth factor is predicted to dominate MAPK activation by pro-angiogenic factors
This study develops a mathematical model to predict how FGF and VEGF interact to activate MAPK signaling, finding that FGF dominates ERK phosphorylation.
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University of Southern CaliforniaORCID 0000-0001-6901-3692Unclaimed ORCID profile · follow to get notified of new preprints
37 papers
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This study develops a mathematical model to predict how FGF and VEGF interact to activate MAPK signaling, finding that FGF dominates ERK phosphorylation.
Jennifer A. Rohrs, Dongqing Zheng, Nicholas Alexander Graham…·Stacey D. Finley
The paper develops a computational model to explain site-specific phosphorylation kinetics of CARs using phospho-proteomic data and mechanistic modeling.
Qianhui Wu, Alyssa D. Arnheim, Stacey D. Finley
The paper uses a computational model to identify tumor growth kinetic parameters as prognostic biomarkers for anti-angiogenic treatment outcomes.
Jennifer A. Rohrs, Sahak Z. Makaryan, Stacey D. Finley
This paper outlines an approach for parameterizing and validating systems biology models to create predictive tools that generate testable hypotheses and expand biological understanding.
This study constructs a systems biology model to investigate how tumor receptor heterogeneity affects responses to combination anti-angiogenic therapy in cancer patients.
Thomas D. Gaddy, Qianhui Wu, Alyssa D. Arnheim, Stacey D. Finley
This study uses computational modeling to show that tumor growth kinetics influence the response to anti-VEGF treatment, with nonlinear dependence on VEGF receptor expression.
The paper develops a mathematical model to predict strategies enhancing TSP1-mediated apoptosis in endothelial cells by simulating signaling perturbations and identifying molecular targets.