Cell cycle control in mammalian cells and its deregulation in cancer. Role of cyclins, cyclin dependent kinases (CDKs), Ser/Thr protein phosphatases and tumor suppressor genes.

Research in my laboratory focuses on the molecular mechanisms that govern the cell cycle of normal and malignant eukaryotic cells, with a particular interest in the molecular signaling that controls cell cycle specific gene expression. Our major focus is on the mechanisms that govern cell cycle entry and exit, which operate in the G1 phase of the cell cycle. When higher eukaryotic cells exit the cell cycle they have three different fates, terminal differentiation, senescence or quiescence. While the first two fates are typically irreversible, quiescent cells can reenter the cell cycle when the environment is appropriate. Eukaryotic cells have evolved to respond to a large array of growth promoting and inhibiting signals, which are eventually integrated by a conserved protein engine consisting of distinct cyclin/CDK (Cyclin Dependent Kinase) holoenzymes. CDKs are activated at specific stages of the cell cycle and their activities are required for progression through S phase and mitosis (reviewed by Graña and Reddy, 1995; Graña et al., 1998, Sotillo and Graña, 2010). I am interested in how these regulatory pathways are disrupted in cancer cells as well as in cells transformed by small DNA viruses or infected by HIV (Graña et al., 1998, Garriga and Graña, 2004, Sotillo and Graña, 2010).

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