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Photo of Ravi Balijepalli
Ravi Balijepalli, PhD



MADISON, WI 53705-2275

(608) 263-4066


Dr. Balijepalli graduated with a PhD from the Dept. of Biophysics, National Institute of Mental Health and Neuroscience, India. He then moved to UW Madison as a post-doctoral fellow in Dr. Timothy Kamp's lab in 2000. He is currently an Assistant Professor in the Department of Medicine. Dr. Balijepalli's research focuses on trafficking and regulation of voltage-activated cardiac ion channels to specialized microdomains in the plasma membrane called caveolae. Caveolae are defined as invaginations of the surface membrane with distinct lipid composition, being highly enriched in cholesterol and sphingolipids, with caveolins as signature proteins. Caveolin-3 (Cav-3) is specifically expressed in muscle cells including the cardiomyocytes. A number of cardiac ion channels have been proposed to reside in caveolae in cardiomyocytes including Cav1.2, HCN4, Kv1.5 channels, Kir6.2/Sur2a channels, and Nav1.5. The subcellular localization of ion channels to caveolae allows the integration of these channels into specific macromolecular signaling complexes in a distinct lipid microenvironment. The newly identified Cav-3 mutations are associated with an inherited arrhythmia syndrome, the congenital long QT syndrome type 9 (LQT9). Dysfunction of caveolar ion channels or their regulation has been implicated in the genesis of inherited arrhythmias such as LQT3 and LQT9 and potentially in acquired arrhythmias in conditions such as heart failure. Dr. Balijepalli's recent work has demonstrated that a subpopulation of L-type Ca2+ channels are localized to caveolae in association with Cav-3 and proteins of ß2-adrenergic receptor signaling cascade in ventricular myocytes. One or more of the auxiliary Ca2+ channel ß subunits (Cavß) may be involved in targeting of the Cav1.2 channels to caveolar microdomains, which is necessary for ß2-adrenergic receptor (AR) regulation of ICa,L. The overall goal of Dr. Balijepalli's research is to understand the functional role(s) of caveolae in the heart as well as their contribution to cardiac pathology such as arrhythmia syndromes, cardiac hypertrophy and heart failure. The lab research strategy employs conditional Cav-3 knockout mouse model and mouse models of cardiac hypertrophy and a variety of research techniques including fluorescence confocal imaging, electron microscopy, FRET, electrophysiological (patch clamp) techniques and proteomic approaches.


  1. Ravi C Balijepalli and Timothy J Kamp. (2009) Caveolae, Ion Channels and Cardiac Arrhythmias. Progress in Biophysics and Molecular Biology. In Press (doi:10.1016/j.pbiomolbio.2009.01.012)
  2. Bin Ye, Ravi C. Balijepalli, Jason D. Foell, Stacie Kroboth, Qi Ye, Yu-Hong Luo, and Nian-Qing Shi (2008). Caveolin-3 associates with and affects function of the Hyperpolarization-activated Cyclic Nucleotide-gated channel 4. Biochemistry. 47 (47), 12312-12318.
  3. Balijepalli RC, Delisle BP, Balijepalli SY, Foell JD, Slind JK, Kamp TJ, January CT. (2007). Delayed rectifier voltage-gated K+ channels localize into distinct cholesterol and sphingolipid enriched membrane microdomains in canine and mouse ventricular myocytes. Channels. 1(4):263-272.
  4. Balijepalli RC, Foell JD., Hall DD, Hell JW, and Kamp TJ. (2006) Cardiac L-type Ca2+ channels are part of a caveolar macromolecular signaling complex required for ß2-AR regulation of ICa,L. Proc. Natl. Acad. Sci. USA. 103(19):7500-5
  5. He J-Q, Balijepalli RC, Haworth RA, and Kamp TJ. (2005). Crosstalk of ß-adrenergic receptor subtypes through Gi blunts ß-adrenergic stimulation of L-type Ca2+ channels in canine heart failure. Circulation Res. 97:566-573.
  6. Balijepalli RC, Foell JD, and Kamp TJ. Blocking the L-type Ca2+ channel with aGGem: A paradigm for a more specific Ca2+ channel blocker. (2004) Editorial. Circulation Res. 95:337-339.
  7. Foell JD, Balijepalli RC, Robia SL, Yunker AM, McEnery MW, Walker JW, and Kamp TJ. (2004). Molecular heterogeneity of calcium channel ß subunits in canine and human heart: evidence for differential subcellular localization. Physiological Genomics 17(2):183-200.
  8. Balijepalli RC, Foell JD, and Kamp TJ. Blocking the L-type Ca2+ channel with aGGem: A paradigm for a more specific Ca2+ channel blocker. (2004) Editorial. Circulation Res. 95:337-339.
  9. Balijepalli RC, Lokuta AJ, Maertz NA, Buck JM, Haworth RA, Valdivia HH, and Kamp TJ. (2003) Depletion of T-tubules and specific subcellular changes in sarcolemmal proteins in tachycardia-induced heart failure. Cardiovasc. Res. (59):67-77.

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