Publications
EGFRvIV: a previously uncharacterized oncogenic mutant reveals a kinase autoinhibitory mechanism. Oncogene. 2010;29(43):5850-60.
. Epidermal growth factor-induced enhancement of glioblastoma cell migration in 3D arises from an intrinsic increase in speed but an extrinsic matrix- and proteolysis-dependent increase in persistence. Mol Biol Cell. 2008;19(10):4249-59.
. An integrated comparative phosphoproteomic and bioinformatic approach reveals a novel class of MPM-2 motifs upregulated in EGFRvIII-expressing glioblastoma cells. Mol Biosyst. 2009;5(1):59-67.
. Linking proteomic and transcriptional data through the interactome and epigenome reveals a map of oncogene-induced signaling. PLoS Comput Biol. 2013;9(2):e1002887.
. MARQUIS: a multiplex method for absolute quantification of peptides and posttranslational modifications. Nat Commun. 2015;6:5924.
. Minor Changes in Expression of the Mismatch Repair Protein MSH2 Exert a Major Impact on Glioblastoma Response to Temozolomide. Cancer Res. 2015;75(15):3127-38.
. Molecular characterization of EGFR and EGFRvIII signaling networks in human glioblastoma tumor xenografts. Mol Cell Proteomics. 2012;11(12):1724-40.
. Phosphotyrosine signaling analysis of site-specific mutations on EGFRvIII identifies determinants governing glioblastoma cell growth. Mol Biosyst. 2010;6(7):1227-37.
. 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 signaling networks across differentially embedded tumors highlights interpatient heterogeneity in human glioblastoma. J Proteome Res. 2014;13(11):4581-93.
. Simultaneous reconstruction of multiple signaling pathways via the prize-collecting steiner forest problem. J Comput Biol. 2013;20(2):124-36.
. Uncovering therapeutic targets for glioblastoma: a systems biology approach. Cell Cycle. 2007;6(22):2750-4.
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