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The integrity of our genome relies on our ability to detect damaged DNA and to trigger phosphorylation-mediated signaling events that coordinate processes such as DNA repair and cell cycle progression. Not surprisingly, kinases that signal DNA damage are believed to function as barriers to oncogenesis. Over the last decade, works from several laboratories, including ours, have shown that DNA damage signaling is not a simple and linear pathway, but instead, operates through an extensive network of hundreds of kinase substrates. To study the complex action of DNA damage signaling kinases our laboratory employs a combination of mass spectrometry-based proteomic techniques with genetics and biochemistry in yeast and mammalian systems. I will be presenting our most recent studies of the DNA damage signaling network that revealed new mechanisms for the modulation of kinase action during genotoxic stress and, unexpectedly, during normal DNA replication.

Department:  Biology

Contact: Maria Magana-Lopez | 650-723-2413 | mmagana@stanford.edu

Presenter(s):

• Marcus Smolka Cornell University

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