Oies Hussein

Date of Award


Degree Type


Degree Name

Master of Science


Physiology and Pharmacology


Dr. John MacDonald

Second Advisor

Dr. Michael Jackson


The interaction of Ca2+-calmodulin is known to promote Ca2+-dependent negative feedback on the activity of various Ca permeable channels through Ca -dependent inactivation. Our laboratory has previously observed a progressive, time-dependent inactivation of TRPM2 (melastatin-related transient receptor potential channel 2). Currents were evoked from HEK 293T cells stably expressing TRPM2, through-the intracellular application of ADPR. TRPM2-mediated currents developed rapidly, reaching a peak and decaying to a steady state in the continued presence of extracellular Ca2+. Full recovery of TRPM2 channels from inactivation was dependent on ADPR concentration. Inactivation was reduced at more depolarized membrane potentials, consistent with a reduced driving force and influx of Ca2+. The extent of inactivation was dependent on extra- and intracellular Ca2+. Exogenous application of calmodulin results in a slower recovery of TRPM2 channels, in addition to increased inactivation. In conclusion, I have shown that TRPM2 channels are susceptible to Ca2+-dependent inactivation involving calmodulin.



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