Publications
Phospho-Ser/Thr-binding domains: navigating the cell cycle and DNA damage response. Nat Rev Mol Cell Biol. 2013;14(9):563-80.
. 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.
. A rapid survival assay to measure drug-induced cytotoxicity and cell cycle effects. DNA Repair (Amst). 2012;11(1):92-8.
. 14-3-3 proteins as signaling integration points for cell cycle control and apoptosis. Semin Cell Dev Biol. 2011;22(7):688-95.
. A dynamical systems model for combinatorial cancer therapy enhances oncolytic adenovirus efficacy by MEK-inhibition. PLoS Comput Biol. 2011;7(2):e1001085.
. A hybrid model of mammalian cell cycle regulation. PLoS Comput Biol. 2011;7(2):e1001077.
. Quantitative phospho-proteomics to investigate the polo-like kinase 1-dependent phospho-proteome. Mol Cell Proteomics. 2011;10(11):M111.008540.
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14-3-3 proteins, FHA domains and BRCT domains in the DNA damage response. DNA Repair (Amst). 2009;8(9):1009-17.
. Distinct mechanisms act in concert to mediate cell cycle arrest. Proc Natl Acad Sci U S A. 2009;106(3):785-90.
. Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2. Curr Opin Cell Biol. 2009;21(2):245-55.
. Polo-like kinase-1 is activated by aurora A to promote checkpoint recovery. Nature. 2008;455(7209):119-23.
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