Ivy E. Dick, PhD

Limpitikul W. B., Dick, I. E., Ben-Johny M., and Yue D. T. (2016) An autism-associated mutation in Ca_V1.3 channels has opposing effects on voltage- and Ca²⁺- dependent regulation. Scientific Reports 6, 27235.   *corresponding author.  PMCID: PMC4891671

Bazzazi H, Sang L, Dick I. E., Joshi-Mukherjee R, Yang W, and Yue D. T. (2015) Novel fluorescence resonance energy transfer-based reporter reveals differential calcineurin activation in neonatal and adult cardiomyocytes. The Journal of physiology 593:3865-3884.  PMCID: PMC4575574

Dick I. E., Limpitikul W. B., Niu J, Banerjee R, Issa J. B., Ben-Johny M, Adams P. J., Kang P. W., Lee S. R., Sang L, Yang W, Babich J, Zhang M, Bazazzi H, Yue N. C., and Tomaselli G. F. (2015) A rendezvous with the queen of ion channels: Three decades of ion channel research by david t. Yue and his calcium signals laboratory. Channels 10(1):20-32.  PMCID: PMC4802785

Ben-Johny M., Dick I. E., Sang L., Limpitikul W. B., Kang P. W., Niu J., Banerjee R., Yang W., Babich J.S., Issa J. B., Lee S. R., Namkung H., Li J., Zhang M., Yang P. S., Bazzazi H., Adams P. J., Joshi-Mukherjee R., Yue D. N., and Yue D. T. (2015) Towards a unified theory of calmodulin regulation (calmodulation) of voltage-gated calcium and sodium channels. Current molecular pharmacology 8(2):188-205.  PMCID: PMC4960983

Limpitikul, W. B., Dick, I. E., Joshi-Mukherjee, R., Overgaard, M. T., George, A. L., Jr., and Yue, D. T. (2014) Calmodulin mutations associated with long QT syndrome prevent inactivation of cardiac L-type Ca currents and promote proarrhythmic behavior in ventricular myocytes, Journal of molecular and cellular cardiology 74C, 115-124.  PMCID: PMC4262253

Joshi-Mukherjee, R., Dick, I. E., Liu, T., O'Rourke, B., Yue, D. T., and Tung, L. (2013) Structural and functional plasticity in long-term cultures of adult ventricular myocytes, Journal of molecular and cellular cardiology 65, 76-87.  PMCID: PMC4219275

Tay, L. H., Dick, I. E., Yang, W., Mank, M., Griesbeck, O., and Yue, D. T. (2012) Nanodomain Ca²⁺  of Ca²⁺  channels detected by a tethered genetically encoded Ca²⁺  sensor, Nature communications 3, 778.  PMCID: PMC3615648

Tadross, M. R., Dick, I. E., and Yue, D. T. (2008) Mechanism of local and global Ca²⁺  sensing by calmodulin in complex with a Ca²⁺  channel, Cell 133, 1228-1240. (Cover Article) (Faculty of 1000: Biology: http://f1000biology.com/article/id/1119808/evaluation).  

Dick, I. E., Brochu, R. M., Purohit, Y., Kaczorowski, G. J., Martin, W. J., and Priest, B. T. (2007) Sodium channel blockade may contribute to the analgesic efficacy of antidepressants, J Pain 8, 315-324.

Liu, C. J., Priest, B. T., Bugianesi, R. M., Dulski, P. M., Felix, J. P., Dick, I. E., Brochu, R. M., Knaus, H. G., Middleton, R. E., Kaczorowski, G. J., Slaughter, R. S., Garcia, M. L., and Kohler, M. G. (2006) A high-capacity membrane potential FRET-based assay for NaV1.8 channels, Assay Drug Dev Technol 4, 37-48.

Brochu, R. M., Dick, I. E., Tarpley, J. W., McGowan, E., Gunner, D., Herrington, J., Shao, P. P., Ok, D., Li, C., Parsons, W. H., Stump, G. L., Regan, C. P., Lynch, J. J., Jr., Lyons, K. A., McManus, O. B., Clark, S., Ali, Z., Kaczorowski, G. J., Martin, W. J., and Priest, B. T. (2006) Block of peripheral nerve sodium channels selectively inhibits features of neuropathic pain in rats, Mol Pharmacol 69, 823-832.

Liang, J., Brochu, R. M., Cohen, C. J., Dick, I. E., Felix, J. P., Fisher, M. H., Garcia, M. L., Kaczorowski, G. J., Lyons, K. A., Meinke, P. T., Priest, B. T., Schmalhofer, W. A., Smith, M. M., Tarpley, J. W., Williams, B. S., Martin, W. J., and Parsons, W. H. (2005) Discovery of potent and use-dependent sodium channel blockers for treatment of chronic pain, Bioorg Med Chem Lett 15, 2943-2947.

Herrington, J., Sanchez, M., Wunderler, D., Yan, L., Bugianesi, R. M., Dick, I. E., Clark, S. A., Brochu, R. M., Priest, B. T., Kohler, M. G., and McManus, O. B. (2005) Biophysical and pharmacological properties of the voltage-gated potassium current of human pancreatic beta-cells, J Physiol 567, 159-175.

Priest, B. T., Garcia, M. L., Middleton, R. E., Brochu, R. M., Clark, S., Dai, G., Dick, I. E., Felix, J. P., Liu, C. J., Reiseter, B. S., Schmalhofer, W. A., Shao, P. P., Tang, Y. S., Chou, M. Z., Kohler, M. G., Smith, M. M., Warren, V. A., Williams, B. S., Cohen, C. J., Martin, W. J., Meinke, P. T., Parsons, W. H., Wafford, K. A., and Kaczorowski, G. J. (2004) A disubstituted succinamide is a potent sodium channel blocker with efficacy in a rat pain model, Biochemistry 43, 9866-9876.

Felix, J. P., Williams, B. S., Priest, B. T., Brochu, R. M., Dick, I. E., Warren, V. A., Yan, L., Slaughter, R. S., Kaczorowski, G. J., Smith, M. M., and Garcia, M. L. (2004) Functional assay of voltage-gated sodium channels using membrane potential-sensitive dyes, Assay Drug Dev Technol 2, 260-268.

Smith, H. A., Church, J., Fournier, J., Lisle, J., Gay, P., Kolenberg, K., Carney, B. W., Dick, I., Peterson, R., and Hakes, B. (2003) The Blazhko Effect of RR Lyrae in 1996, Publ. Astron. Soc. Pacific 115, 43-48.

Voltage-gated calcium channels (CaV) are critical conduits for Ca2+ entry into the heart, smooth muscle and brain. Ca2+ entry through these channels must be precisely controlled, thus these channels employ two major forms of feedback regulation: voltage dependent inactivation (VDI) and Ca2+ dependent inactivation (CDI). Disruption of these important regulatory processes results in severe clinical phenotypes including autism, ataxia and long QT syndrome. My research has focused on gaining mechanistic understanding of these regulatory processes, and applying those findings to gain new insight into the pathogenesis and treatment options for Ca2+ channelopathies and related diseases. Recent work has focused on unraveling the mechanisms leading to cardiac arrhythmias in calcium channelopathies such as Timothy Syndrome (TS). By examining the inactivation defects underlying two different L-type channel TS mutations, we uncovered a remarkable divergence in the mechanisms leading to deficits in CDI. These findings promise new insight into customized treatment for TS, and illustrate how in depth biophysical understanding can inform on therapeutic interventions in patients. Overall, my lab studies the mechanisms underlying the regulation of voltage-gated calcium channels, how these mechanisms are disrupted by genetic mutations, and how new therapeutic strategies can address these disruptions.

2016 - Appointed Assistant Professor in Physiology and named the inaugural John C. Hemmeter Scholar for 3 years.

2017 - Maryland Stem Cell Research Fund Discovery award

• Electrophysiology: whole cell and single channel patch clamp
• Molecular biology
• Calcium and FRET imaging
• Tissue culture and utilization of induced pluripotent stem cells (iPSCs)