Geoffrey Stuart Pitt, MD

Adjunct Professor in the Department of Medicine
Faculty Network Member of the Duke Institute for Brain Sciences
Campus mail 515 E. 79th Street, Pha, New York, NY 10075
Phone (919) 257-1589
Email address geoffrey.pitt@duke.edu

Our research focuses on how intracellular Ca2+, the ultimate signal of membrane excitability, regulates membrane excitability and the consequent function of excitable cells. We have discovered and described multiple mechanisms that control Ca2+ influx through voltage-gated Ca2+ channels and feedback mechanisms by which internal calcium regulates other channels that influence Ca2+ channel function. The work has entailed structure-function analyses of ion channels and their regulatory subunits and studies of mutations that lead to inherited channelopathies such as cardiac arrhythmias and epilepsy.

Education and Training

  • Fellow in Cardiovascular Medicine, Medicine, Stanford University, 1995 - 1999
  • Medical Resident, Medicine, Stanford University, 1993 - 1995
  • M.D., Johns Hopkins University, 1993

Publications

Chen-Izu, Ye, Robin M. Shaw, Geoffrey S. Pitt, Vladimir Yarov-Yarovoy, Jon T. Sack, Hugues Abriel, Richard W. Aldrich, et al. “Na+ channel function, regulation, structure, trafficking and sequestration.” J Physiol 593, no. 6 (March 15, 2015): 1347–60. https://doi.org/10.1113/jphysiol.2014.281428.

PMID
25772290
Full Text

Andersen, Nicholas D., Kapil V. Ramachandran, Michelle M. Bao, Margaret L. Kirby, Geoffrey S. Pitt, and Mary R. Hutson. “Calcium signaling regulates ventricular hypertrophy during development independent of contraction or blood flow.” J Mol Cell Cardiol 80 (March 2015): 1–9. https://doi.org/10.1016/j.yjmcc.2014.12.016.

PMID
25536179
Full Text

Yang, Lin, Alexander Katchman, Richard L. Weinberg, Jeffrey Abrams, Tahmina Samad, Elaine Wan, Geoffrey S. Pitt, and Steven O. Marx. “The PDZ motif of the α1C subunit is not required for surface trafficking and adrenergic modulation of CaV1.2 channel in the heart.” J Biol Chem 290, no. 4 (January 23, 2015): 2166–74. https://doi.org/10.1074/jbc.M114.602508.

PMID
25505241
Full Text

Yan, Haidun, Juan L. Pablo, Chaojian Wang, and Geoffrey S. Pitt. “FGF14 modulates resurgent sodium current in mouse cerebellar Purkinje neurons.” Elife 3 (September 30, 2014): e04193. https://doi.org/10.7554/eLife.04193.

PMID
25269146
Full Text

Wang, Chaojian, Ben C. Chung, Haidun Yan, Hong-Gang Wang, Seok-Yong Lee, and Geoffrey S. Pitt. “Structural analyses of Ca²⁺/CaM interaction with NaV channel C-termini reveal mechanisms of calcium-dependent regulation.” Nat Commun 5 (September 18, 2014): 4896. https://doi.org/10.1038/ncomms5896.

PMID
25232683
Full Text

Hennessey, Jessica A., Nicole J. Boczek, Yong-Hui Jiang, Joelle D. Miller, William Patrick, Ryan Pfeiffer, Brittan S. Sutphin, et al. “A CACNA1C variant associated with reduced voltage-dependent inactivation, increased CaV1.2 channel window current, and arrhythmogenesis.” Plos One 9, no. 9 (2014): e106982. https://doi.org/10.1371/journal.pone.0106982.

PMID
25184293
Full Text

Hennessey, Jessica A., Cherisse A. Marcou, Chuan Wang, Eric Q. Wei, Chaojian Wang, David J. Tester, Margherita Torchio, et al. “FGF12 is a candidate Brugada syndrome locus.” Heart Rhythm 10, no. 12 (December 2013): 1886–94. https://doi.org/10.1016/j.hrthm.2013.09.064.

PMID
24096171
Full Text

Hennessey, Jessica A., Cherisse A. Marcou, Chuan Wang, Eric Q. Wei, Chaojian Wang, Lia Crotti, Peter Schwartz, Michael J. Ackerman, and Geoffrey S. Pitt. “FGF12 is a Novel Brugada Syndrome Locus.” In Circulation, Vol. 128. LIPPINCOTT WILLIAMS & WILKINS, 2013.

Scholars@Duke

Pages