Publications
A Pleiotropic RNA-Binding Protein Controls Distinct Cell Cycle Checkpoints to Drive Resistance of p53-Defective Tumors to Chemotherapy. Cancer Cell. 2015;28(5):623-37.
. Polo-like kinase-1 is activated by aurora A to promote checkpoint recovery. Nature. 2008;455(7209):119-23.
. Is post-transcriptional stabilization, splicing and translation of selective mRNAs a key to the DNA damage response?. Cell Cycle. 2011;10(1):23-7.
. Predicting cancer drug mechanisms of action using molecular network signatures. Mol Biosyst. 2013;9(7):1604-19.
. Profiles of Basal and stimulated receptor signaling networks predict drug response in breast cancer lines. Sci Signal. 2013;6(294):ra84.
. Protein 4.1B suppresses prostate cancer progression and metastasis. Proc Natl Acad Sci U S A. 2007;104(31):12784-9.
. 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.
. Proteolytic Activity Matrix Analysis (PrAMA) for simultaneous determination of multiple protease activities. Integr Biol (Camb). 2011;3(4):422-38.
. 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.
. Quantitative analysis of EGFRvIII cellular signaling networks reveals a combinatorial therapeutic strategy for glioblastoma. Proc Natl Acad Sci U S A. 2007;104(31):12867-72.
. Quantitative analysis of gradient sensing: towards building predictive models of chemotaxis in cancer. Curr Opin Cell Biol. 2012;24(2):284-91.
. Quantitative analysis of signaling networks across differentially embedded tumors highlights interpatient heterogeneity in human glioblastoma. J Proteome Res. 2014;13(11):4581-93.
. Quantitative modeling perspectives on the ErbB system of cell regulatory processes. Exp Cell Res. 2009;315(4):717-25.
. Quantitative phospho-proteomics to investigate the polo-like kinase 1-dependent phospho-proteome. Mol Cell Proteomics. 2011;10(11):M111.008540.
. Quantitative Profiling of Lysine Acetylation Reveals Dynamic Crosstalk between Receptor Tyrosine Kinases and Lysine Acetylation. PLoS One. 2015;10(5):e0126242.
. Rapid phospho-turnover by receptor tyrosine kinases impacts downstream signaling and drug binding. Mol Cell. 2011;43(5):723-37.
. A rapid survival assay to measure drug-induced cytotoxicity and cell cycle effects. DNA Repair (Amst). 2012;11(1):92-8.
. 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.
. 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.
. Robust co-regulation of tyrosine phosphorylation sites on proteins reveals novel protein interactions. Mol Biosyst. 2012;8(10):2771-82.
. SAMNet: a network-based approach to integrate multi-dimensional high throughput datasets. Integr Biol (Camb). 2012;4(11):1415-27.
. SAMNetWeb: identifying condition-specific networks linking signaling and transcription. Bioinformatics. 2015;31(7):1124-6.
. Sequential application of anticancer drugs enhances cell death by rewiring apoptotic signaling networks. Cell. 2012;149(4):780-94.
. Serendipitous alkylation of a Plk1 ligand uncovers a new binding channel. Nat Chem Biol. 2011;7(9):595-601.
. Signaling network state predicts twist-mediated effects on breast cell migration across diverse growth factor contexts. Mol Cell Proteomics. 2011;10(11):M111.008433.
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