"A model of calcium transport in Jurkat cells showcasing two competing signaling mechanisms."
: Jurkat cells are an immortalized line of human T lymphocytes that are commonly used to study leukemia, HIV, and Calcium (Ca2+) signaling. Stimulation of Jurkat cells leads to the depletion of the cells internal storage of Ca2+, the Endoplasmic Reticulum (ER), which in turn causes Ca2+ to enter the cell via a mechanism of Store Operated Calcium Entry (SOCE). The combination of these mechanisms causes oscillations in the Ca2+ concentration of the cell. New data obtained last year, however, suggests that Jurkat cells, in addition to presenting SOCE-based oscillations, are also capable of producing ER-based oscillations when the external entry mechanism is genetically eliminated. With this in mind, I construct a model of ordinary differential equations that incorporates both oscillatory mechanisms and can produce both ER and SOCE based oscillations. ER-based oscillations have been studied before in other cell types, but the interplay between the two oscillatory mechanisms is not well understood. In my poster I present the construction of the model, as well as the defining characteristics of each oscillation; finally, I present a hypothesis for how the interaction between the oscillatory mechanisms results in a dominating signal being exhibited under different conditions.
Additional authors: James Sneyd, The University of Auckland; Vivien Kirk, The University of Auckland; Mohammed Trebak, University of Pittsburgh; Cory Benson, University of Pittsburgh