A model of calcium transport in Jurkat cells showcasing two competing signaling mechanisms.

Paco Castaneda

The University of Auckland

"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

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