Duke Institute for Brain Sciences

The ultimate signal in excitable cells is a change in intracellular Ca2+, which mediates the effect of cellular electricity. Thus, it is not surprising that internal calcium imparts complex feedback regulation on multiple signaling steps, including direct modulation of various ion channels. The Pitt lab focuses on understanding the integrated Ca2+ signals, particularly how Ca2+ controls ion channel function and the resultant diseases when these regulatory mechanisms are perturbed. Our current areas of interest include mechanisms of channel function and dysfunction in epilepsy and in synaptic plasticity.

M.D. & Ph.D., Johns Hopkins University, 1993

B.A., Yale University, 1984

Seu, L. & Pitt, G.S. Dose-dependent and Isoform-specific Modulation of Ca2+ Channels by RGK GTPases. J. Gen. Physiol. 128, 605-613 (2006).

Wang, H.-G., George, M.S., Kim, J., Wang, C. & Pitt, G.S. Ca2+/Calmodulin Regulates Trafficking of CaV1.2 Ca2+ Channels in Cultured Hippocampal Neurons. J Neuroscience 27, 9086-9093 (2007).

Wang, C., Wang, H.-G., Xie, H. & Pitt, G.S. Ca2+/CaM Controls Ca2+-Dependent Inactivation of NMDA Receptors by Dimerizing the NR1 C Termini. J Neuroscience 28, 1865-1870 (2008).

Miloushev, V. Z., Levine, J. A., Arbing, M. A., Hunt, J. F., Pitt, G. S., Palmer, A. G. III. Solution Structure of the NaV1.2 C-terminal EF-hand Domain J. Biol. Chem. 284, 6446-6454 (2009)

Thomsen MB, Wang C, Özgen N, Wang H-G, Rosen MR and Pitt GS. The Accessory Subunit KChIP2 Modulates the Cardiac L-Type Calcium Current. Circ Res 104, 1382-1389 (2009).