Geoffrey Stuart Pitt

Geoffrey Stuart Pitt

Adjunct Professor in the Department of Medicine

External Address: 
515 E. 79th Street, Pha, New York, NY 10075
Internal Office Address: 
Duke Box 103030, Durham, NC 27710


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 & Training

  • Fellow in Cardiovascular Medicine, Medicine, Stanford University 1995 - 1999

  • Medical Resident, Medicine, Stanford University 1993 - 1995

  • M.D., Johns Hopkins University 1993

Selected Grants

Basic predoctoral training in neuroscience awarded by National Institutes of Health (Training Faculty). 1992 to 2018

Fibroblast Growth Factor Homologous Factor Modulation and Effect on Cardiac Ion Channel Trafficking awarded by National Institutes of Health (Principal Investigator). 2016 to 2018

Identifying the mechanosensitive domains of the Piezo1 ion channel by application of localized force awarded by National Institutes of Health (Co-Sponsor). 2015 to 2017

Bone-targeted calcium channel agonists for osteoporosis awarded by UH Harrington Discovery Institute (Principal Investigator). 2015 to 2017

Calcium regulation and dysregulation of cardiac ion channels awarded by National Institutes of Health (Principal Investigator). 2008 to 2017

Calmodulin regulation of Na+ channels in neurons and cardiomyocytes awarded by National Institutes of Health (Principal Investigator). 2014 to 2016

Structural studies of NaV1.5 and functional implications awarded by National Institutes of Health (Principal Investigator). 2013 to 2016

Investigation of calcium channel modulation in cardiomyocytes by novel methods awarded by Columbia University (Principal Investigator). 2013 to 2016

Training in Fundamental &Translational Neuroscience awarded by National Institutes of Health (Training Faculty). 2005 to 2016

The role of STIM1 in cardiac and skeletal muscle function awarded by National Institutes of Health (Co Investigator). 2009 to 2014

Pitt, G. S. Ion Channels in Health and Disease. 2016, pp. 1–378. Scopus, doi:10.1016/C2014-0-01711-X. Full Text

Pitt, G. S. Preface. 2016, pp. xiii–xiv. Scopus, doi:10.1016/B978-0-12-802002-9.05001-9. Full Text

Pitt, G. S. “Fibroblast Growth Factor Homologous Factors Modulate Cardiac Sodium and Calcium Channels.” Cardiac Electrophysiology: From Cell to Bedside: Seventh Edition, 2018, pp. 177–79. Scopus, doi:10.1016/B978-0-323-44733-1.00019-5. Full Text

Pitt, G. S., and S. O. Marx. “Calmodulin and CaMKII as Ca2+ Switches for Cardiac Ion Channels.” Cardiac Electrophysiology: From Cell to Bedside: Sixth Edition, 2013, pp. 189–95. Scopus, doi:10.1016/B978-1-4557-2856-5.00019-4. Full Text

Gade, Aravind R., et al. “An interaction between the III-IV linker and CTD in NaV1.5 confers regulation of inactivation by CaM and FHF.J Gen Physiol, vol. 152, no. 2, Feb. 2020. Pubmed, doi:10.1085/jgp.201912434. Full Text

Pitt, Geoffrey S., and Seok-Yong Lee. “Ca2+/CaM interaction with voltage-gated Na+ channels.Proc Natl Acad Sci U S A, Dec. 2019. Pubmed, doi:10.1073/pnas.1909835116. Full Text

Sinden, Daniel S., et al. “Knockout of the X-linked Fgf13 in the hypothalamic paraventricular nucleus impairs sympathetic output to brown fat and causes obesity.Faseb J, vol. 33, no. 10, Oct. 2019, pp. 11579–94. Pubmed, doi:10.1096/fj.201901178R. Full Text

Cao, Chike, et al. “The CaV1.2 L-type calcium channel regulates bone homeostasis in the middle and inner ear.Bone, vol. 125, Aug. 2019, pp. 160–68. Pubmed, doi:10.1016/j.bone.2019.05.024. Full Text

Yang, Lin, et al. “Cardiac CaV1.2 channels require β subunits for β-adrenergic-mediated modulation but not trafficking.J Clin Invest, vol. 129, no. 2, Feb. 2019, pp. 647–58. Pubmed, doi:10.1172/JCI123878. Full Text

Abraham, Dennis M., et al. “The two-pore domain potassium channel TREK-1 mediates cardiac fibrosis and diastolic dysfunction.J Clin Invest, vol. 128, no. 11, Nov. 2018, pp. 4843–55. Pubmed, doi:10.1172/JCI95945. Full Text

Pitt, Geoffrey S. “An update on the journey towards precision medicine in cardiology.Eur Heart J, vol. 39, no. 40, Oct. 2018, pp. 3627–28. Pubmed, doi:10.1093/eurheartj/ehy637. Full Text

Sanders, Stephan J., et al. “Progress in Understanding and Treating SCN2A-Mediated Disorders.Trends Neurosci, vol. 41, no. 7, July 2018, pp. 442–56. Pubmed, doi:10.1016/j.tins.2018.03.011. Full Text

Cao, Chike, et al. “Increased Ca2+ signaling through CaV1.2 promotes bone formation and prevents estrogen deficiency-induced bone loss.Jci Insight, vol. 2, no. 22, Nov. 2017. Pubmed, doi:10.1172/jci.insight.95512. Full Text

Katchman, Alexander, et al. “Proteolytic cleavage and PKA phosphorylation of α1C subunit are not required for adrenergic regulation of CaV1.2 in the heart.Proceedings of the National Academy of Sciences of the United States of America, vol. 114, no. 34, Aug. 2017, pp. 9194–99. Epmc, doi:10.1073/pnas.1706054114. Full Text


Zhang, Hengtao, et al. “STIM1-Ca2+ signaling modulates automaticity of the mouse sinoatrial node.Proc Natl Acad Sci U S A, vol. 112, no. 41, 2015, pp. E5618–27. Pubmed, doi:10.1073/pnas.1503847112. Full Text

Hennessey, Jessica A., et al. “FGF12 is a Novel Brugada Syndrome Locus.” Circulation, vol. 128, no. 22, LIPPINCOTT WILLIAMS & WILKINS, 2013.

Pupillo, M., et al. “cAMP receptor and G-protein interactions control development in Dictyostelium.Cold Spring Harb Symp Quant Biol, vol. 53 Pt 2, 1988, pp. 657–65. Pubmed, doi:10.1101/sqb.1988.053.01.075. Full Text

Kumagai, A., et al. “A molecular analysis of G proteins and control of early gene expression by the cell-surface cAMP receptor in Dictyostelium.Cold Spring Harb Symp Quant Biol, vol. 53 Pt 2, 1988, pp. 675–85. Pubmed, doi:10.1101/sqb.1988.053.01.077. Full Text