Publications
Vascular endothelial growth factor (VEGF) and platelet (PF-4) factor 4 inputs modulate human microvascular endothelial signaling in a three-dimensional matrix migration context. Mol Cell Proteomics. 2013;12(12):3704-18.
. Understanding resistance to combination chemotherapy. Drug Resist Updat. 2012;15(5-6):249-57.
. Understanding effects of matrix protease and matrix organization on directional persistence and translational speed in three-dimensional cell migration. Ann Biomed Eng. 2007;35(1):91-100.
. Training signaling pathway maps to biochemical data with constrained fuzzy logic: quantitative analysis of liver cell responses to inflammatory stimuli. PLoS Comput Biol. 2011;7(3):e1001099.
. Three-kinase inhibitor combination recreates multipathway effects of a geldanamycin analogue on hepatocellular carcinoma cell death. Mol Cancer Ther. 2009;8(8):2183-92.
. Signaling network state predicts twist-mediated effects on breast cell migration across diverse growth factor contexts. Mol Cell Proteomics. 2011;10(11):M111.008433.
. Robust co-regulation of tyrosine phosphorylation sites on proteins reveals novel protein interactions. Mol Biosyst. 2012;8(10):2771-82.
. Receptor tyrosine kinases fall into distinct classes based on their inferred signaling networks. Sci Signal. 2013;6(284):ra58.
. The receptor AXL diversifies EGFR signaling and limits the response to EGFR-targeted inhibitors in triple-negative breast cancer cells. Sci Signal. 2013;6(287):ra66.
. RAS mutations affect tumor necrosis factor-induced apoptosis in colon carcinoma cells via ERK-modulatory negative and positive feedback circuits along with non-ERK pathway effects. Cancer Res. 2009;69(20):8191-9.
. Rapid phospho-turnover by receptor tyrosine kinases impacts downstream signaling and drug binding. Mol Cell. 2011;43(5):723-37.
. Quantitative modeling perspectives on the ErbB system of cell regulatory processes. Exp Cell Res. 2009;315(4):717-25.
. Quantitative analysis of gradient sensing: towards building predictive models of chemotaxis in cancer. Curr Opin Cell Biol. 2012;24(2):284-91.
. Qualitatively different T cell phenotypic responses to IL-2 versus IL-15 are unified by identical dependences on receptor signal strength and duration. J Immunol. 2014;192(1):123-35.
. PTMScout, a Web resource for analysis of high throughput post-translational proteomics studies. Mol Cell Proteomics. 2010;9(11):2558-70.
. Proteolytic Activity Matrix Analysis (PrAMA) for simultaneous determination of multiple protease activities. Integr Biol (Camb). 2011;3(4):422-38.
. Protein kinases display minimal interpositional dependence on substrate sequence: potential implications for the evolution of signalling networks. Philos Trans R Soc Lond B Biol Sci. 2012;367(1602):2574-83.
. Predicting cancer drug mechanisms of action using molecular network signatures. Mol Biosyst. 2013;9(7):1604-19.
. O6-Methylguanine DNA lesions induce an intra-S-phase arrest from which cells exit into apoptosis governed by early and late multi-pathway signaling network activation. Integr Biol (Camb). 2012;4(10):1237-55.
. Networks inferred from biochemical data reveal profound differences in toll-like receptor and inflammatory signaling between normal and transformed hepatocytes. Mol Cell Proteomics. 2010;9(9):1849-65.
. Network analysis of differential Ras isoform mutation effects on intestinal epithelial responses to TNF-α. Integr Biol (Camb). 2013;5(11):1355-65.
. Multiplexed protease activity assay for low-volume clinical samples using droplet-based microfluidics and its application to endometriosis. J Am Chem Soc. 2013;135(5):1645-8.
. Multiple reaction monitoring for robust quantitative proteomic analysis of cellular signaling networks. Proc Natl Acad Sci U S A. 2007;104(14):5860-5.
. Multipathway model enables prediction of kinase inhibitor cross-talk effects on migration of Her2-overexpressing mammary epithelial cells. Mol Pharmacol. 2008;73(6):1668-78.
. Molecular network analysis of phosphotyrosine and lipid metabolism in hepatic PTP1b deletion mice. Integr Biol (Camb). 2013;5(7):940-63.
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