Publications
AATF/Che-1 acts as a phosphorylation-dependent molecular modulator to repress p53-driven apoptosis. EMBO J. 2012;31(20):3961-75.
. Combined experimental and computational analysis of DNA damage signaling reveals context-dependent roles for Erk in apoptosis and G1/S arrest after genotoxic stress. Mol Syst Biol. 2012;8:568.
. 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.
. Sequential application of anticancer drugs enhances cell death by rewiring apoptotic signaling networks. Cell. 2012;149(4):780-94.
. 14-3-3 proteins as signaling integration points for cell cycle control and apoptosis. Semin Cell Dev Biol. 2011;22(7):688-95.
. Bcl-2 family genetic profiling reveals microenvironment-specific determinants of chemotherapeutic response. Cancer Res. 2011;71(17):5850-8.
. Engineered bivalent ligands to bias ErbB receptor-mediated signaling and phenotypes. J Biol Chem. 2011;286(31):27729-40.
. In vivo systems analysis identifies spatial and temporal aspects of the modulation of TNF-α-induced apoptosis and proliferation by MAPKs. Sci Signal. 2011;4(165):ra16.
. Serendipitous alkylation of a Plk1 ligand uncovers a new binding channel. Nat Chem Biol. 2011;7(9):595-601.
. The combined status of ATM and p53 link tumor development with therapeutic response. Genes Dev. 2009;23(16):1895-909.
. Non-genetic origins of cell-to-cell variability in TRAIL-induced apoptosis. Nature. 2009;459(7245):428-32.
. 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.
. Three-kinase inhibitor combination recreates multipathway effects of a geldanamycin analogue on hepatocellular carcinoma cell death. Mol Cancer Ther. 2009;8(8):2183-92.
. Cytokine-induced signaling networks prioritize dynamic range over signal strength. Cell. 2008;135(2):343-54.
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