Associate Director, Medical Scientist Training Program
A graduate of the University of Notre Dame, Timothy Kamp attended medical school at the University of Chicago, receiving his doctorate in pharmacological and physiological sciences in 1987 and a medical degree in 1989. While at the University of Chicago, Kamp received the Medical Alumni Association prize for most outstanding research presentation and the Harry Ginsburg Memorial prize for outstanding students in physiology. He completed his Internal Medicine residency and fellowship in Cardiovascular Medicine at Johns Hopkins Hospital in 1996, receiving an American Heart Association research fellowship and the Howard Hughes post-doctoral fellowship for physicians.
Kamp joined the faculty of the University of Wisconsin Cardiovascular Medicine Division in 1996 and is currently an Associate Professor of Medicine with an affiliate appointment in Physiology. He has served as Associate Director for the Medical Scientist Training program at UW since 1999. His teaching activities focus on cardiac physiology and pharmacology. Kamp trains graduate students in several cross-departmental programs, including medical scientists (MD/PhD), molecular and cellular pharmacology, and cellular and molecular biology. Board certified in Internal Medicine and Cardiovascular Disease, Kamp's clinical activities include general cardiology with an emphasis on noninvasive cardiac electrophysiology and heart failure. He is a Fellow of the American College of Cardiology and a Fellow of the American Heart Association.
His research focuses on ion channel proteins in the heart, the coupling of cardiac electrical activity to mechanical contraction, and the molecular mechanisms underlying heart failure. In addition, more recent efforts have focused on applications of stem cells in cardiovascular research and therapy. A variety of research approaches are employed including cellular electrophysiology, cell culture, molecular biology, pharmacology, biochemistry, transgenic animal models, and animal models of heart failure.
Kamp directs an active basic science laboratory working closely with two research scientists, post-doctoral fellows, graduate students, research technicians, and undergraduate students. He enjoys collaborations with investigators in the Anatomy, Pharmacology, Physiology and Surgery departments. His research is funded by National Institutes of Health grants and other private grants. He also participates in translational research and is co-recipient of a UW Cardiovascular Research Center Collaborative/Translational research grant with James Thomson (Dept. of Anatomy). He has been an investigator in several clinical trials of antiarrhythmic drug treatment for atrial fibrillation.
Kamp participates widely in peer-review activities, including being on the editorial board for Circulation Research and being a regular reviewer for multiple cardiovascular-related journals. Kamp has served on multiple peer review panels including the American Heart Association National Committee on Cellular Cardiovascular Physiology and Pharmacology and multiple ad hoc National Institutes of Health study sections.
Search for Timothy Kamp's literature abstracts on PubMed
He, J.-Q., Ma, Y, Lee,Y., Thomson, J.A. and Kamp, T.J. (2003). Human Embryonic Stem Cells Develop into Multiple Types of Cardiac Myocytes: Action Potential Characterization. Circ. Res. 93:32-9.
Delisle B.P., Anderson C.L., Balijepalli R.C,. Anson B.D., Kamp T.J., January C.T. (2003). Thapsigargin selectively rescues the trafficking-defective LQT2 channels G601S and F805C. J. Biol Chem. 278:35749-54.
Robu V.G., Pfeiffer E.S., Robia S.L., Balijepalli R.C., Pi Y., Kamp T.J., Walker JW. (2003). Localization of functional endothelin receptor signaling complexes in cardiac transverse tubules. J. Biol. Chem. 278:48154-6.
Foell J.D., Balijepalli R.C., Delisle B.P., Yunker A.M.R., Robia S.L., Walker J.W., McEnery M.W., January C.T., and Kamp T.J. (2004). Molecular heterogeneity of calcium channel ƒÒ subunits in canine and human heart: Evidence for differential subcellular localization. Physiol. Genomics 17: 183-200.
Kumar D., Hacker T.A., Buck J., Whitesell L.S., Kaji E.H. Douglas P.S., Kamp, T.J. (2005). Distinct mouse coronary anatomy and myocardial infarction consequent to ligation. Coron. Artery Dis. 16:41-4.
Kamp TJ and January CT (2004). Inherited and acquired long QT syndromes: new insights and evolving technology. Drug Discovery Today: Disease Mechanisms 1:45-51.
Kamp TJ and Odorico J. (2005). Clinical applications for human ES cells (Chapter 14). In, Human Embryonic Stem Cells, J. Odorico, S.-C. Zhang and R. Pedersen, Eds. Abingdon, UK, Garland Science/BIOS Scientific Publishers, 257-280.
Valdivia C.R., Chu W.W., Pu J., Foell J.D., Haworth R.A., Wolff M.R., Kamp T.J., Makielski, J.C. (2005). Increased late sodium current in myocytes from a canine heart failure model and from failing human heart. J. Mol. Cell. Cardiol. 38:475-483.
Lokuta A.J., Maertz N.A., Meethal S.V., Potter K.T., Kamp T.J., Valdivia H.H. Haworth R.A. (2005). Increased nitration of the sarcoplasmic reticulum Ca2+ ATPase in human heart failure. Circulation 111:988-995.
Cohen R.M., Foell, J.D., Balijepalli, R.C., Shah, V., Hell, J.W., Kamp, T.J. (2005). Unique modulation of L-type Ca2+ channels by short auxiliary ƒÒ1d subunit present in cardiac muscle. Am. J. Physiol. 288(5):H2363-74.
Delisle B.P., Slind J.K., Kilby J.A., Anderson C.L., Anson B.D., Balijepalli R.C., Tester D.J., Ackerman M.J., Kamp T.J., January C.T. (2005). Intragenic suppression of trafficking-Defective KCNH2 channels associated with long QT syndrome. Mol. Pharmocol. 68:233-40.
He, J.-Q., Balijepalli, R.C, Haworth, R.A., and Kamp T.J. (2005). Crosstalk of ƒÒ-adrenergic receptor subtypes through Gi blunts ƒÒ-adrenergic stimulation of L-type Ca2+ channels in Canine Heart Failure. Circ. Res. 97:566-73.
Singla D., Hacker T.A., Ma L., Douglas P., Sullivan R., Lyons G.E., and Kamp T.J. (2006). Embryonic Stem Cells Repair Infarcted Mouse Heart: Formation of Multiple Cell Types. J. Molec. Cell. Cardiol. 40:195-200.
Rajamani, S., Anderson C.L., Valdivia C.R., Eckhardt L.L., Foell J.D., Robertson G.A., Kamp T.J., Makielski J.C., Anson B.D., January C.T. (2006). Specific serine proteases selectively damage KCNH2 (hERG1) potassium channels and IKr. Am. J. Physiol. 290(3):H1278-88.