Publications
Data-driven modelling of signal-transduction networks. Nat Rev Mol Cell Biol. 2006;7(11):820-8.
. . p53-deficient cells rely on ATM- and ATR-mediated checkpoint signaling through the p38MAPK/MK2 pathway for survival after DNA damage. Cancer Cell. 2007;11(2):175-89.
. Systematic discovery of in vivo phosphorylation networks. Cell. 2007;129(7):1415-26.
. Cytokine-induced signaling networks prioritize dynamic range over signal strength. Cell. 2008;135(2):343-54.
. Linear motif atlas for phosphorylation-dependent signaling. Sci Signal. 2008;1(35):ra2.
. NetworKIN: a resource for exploring cellular phosphorylation networks. Nucleic Acids Res. 2008;36(Database issue):D695-9.
. Polo-like kinase-1 is activated by aurora A to promote checkpoint recovery. Nature. 2008;455(7209):119-23.
. 14-3-3 proteins, FHA domains and BRCT domains in the DNA damage response. DNA Repair (Amst). 2009;8(9):1009-17.
. The combined status of ATM and p53 link tumor development with therapeutic response. Genes Dev. 2009;23(16):1895-909.
. Distinct mechanisms act in concert to mediate cell cycle arrest. Proc Natl Acad Sci U S A. 2009;106(3):785-90.
. Exploiting synthetic lethal interactions for targeted cancer therapy. Cell Cycle. 2009;8(19):3112-9.
. Functional dynamics of Polo-like kinase 1 at the centrosome. Mol Cell Biol. 2009;29(11):3134-50.
. 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.
. Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2. Curr Opin Cell Biol. 2009;21(2):245-55.
. DNA damage activates a spatially distinct late cytoplasmic cell-cycle checkpoint network controlled by MK2-mediated RNA stabilization. Mol Cell. 2010;40(1):34-49.
. Impaired SHP2-mediated extracellular signal-regulated kinase activation contributes to gefitinib sensitivity of lung cancer cells with epidermal growth factor receptor-activating mutations. Cancer Res. 2010;70(9):3843-50.
. A mitotic phosphorylation feedback network connects Cdk1, Plk1, 53BP1, and Chk2 to inactivate the G(2)/M DNA damage checkpoint. PLoS Biol. 2010;8(1):e1000287.
. PTMScout, a Web resource for analysis of high throughput post-translational proteomics studies. Mol Cell Proteomics. 2010;9(11):2558-70.
. 14-3-3 proteins as signaling integration points for cell cycle control and apoptosis. Semin Cell Dev Biol. 2011;22(7):688-95.
. MCAM: multiple clustering analysis methodology for deriving hypotheses and insights from high-throughput proteomic datasets. PLoS Comput Biol. 2011;7(7):e1002119.
. The mTOR-regulated phosphoproteome reveals a mechanism of mTORC1-mediated inhibition of growth factor signaling. Science. 2011;332(6035):1317-22.
. Is post-transcriptional stabilization, splicing and translation of selective mRNAs a key to the DNA damage response?. Cell Cycle. 2011;10(1):23-7.
. Quantitative phospho-proteomics to investigate the polo-like kinase 1-dependent phospho-proteome. Mol Cell Proteomics. 2011;10(11):M111.008540.
. Serendipitous alkylation of a Plk1 ligand uncovers a new binding channel. Nat Chem Biol. 2011;7(9):595-601.
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