Research Interests

The overall area of interest in my laboratory is to understand the factors that modulate neuronal excitability in disease, from the study of ion channel function and dysfunction. Our lab is currently focused on trying to understand the molecular basis of dysfunction of voltage-gated
calcium channels in two main areas of research.  In the first area or research, we study the functional changes in calcium channels in calcium channelopathies, or mutations in ion channel proteins that lead to neurological diseases, such as Spinocereberallar ataxia type 6 (SCA6).

We are currently studying the function of the actin-binding protein Kelch-like 1 or KLHL1, as it relates to calcium channel function modulation. This novel protein is located in the Spinocereberallar ataxia type 8 (SCA8) gene locus, which suggests KLHL1 is implicated in this movement disorder.  With the aid of NSF-funded grants, our lab has pioneered the investigation of this protein function and is currently elucidating its mechanisms of modulation of calcium channels.

Our second current project involves the study of abnormal function of neuronal calcium channels in metabolic disease (diabetes), specifically in diabetic neuropathy; our goal is to understand the molecular mechanisms of up-regulation of voltage-gated calcium channels during hyperglycemia. Our experimental approaches include electrophysiology , and cellular and biochemical techniques such as immunocytochemistry, biochemistry and confocal microscopy.

Publications

Selected Publications

• Aromolaran, K.A., Benzow, K. A., Cribbs, L.L., Koob, M.D. and E. S. Piedras-Rentería. Elimination of the actin-binding domain in Kelch-like 1 protein induces T-type calcium channel modulation only in the presence of action potential waveforms. Journal of Signal Transduction, submitted.
• Shankarappa, S.A., Piedras-Renterίa, E.S. and E.B. Stubbs, Jr. 2011. Forced exercise delays neuropathic pain in experimental diabetes: effects on voltage-activated calcium channels. J. Neurochem. 118 (2), 224-236.
• Aromolaran, K.A., Benzow, K. A., Cribbs, L.L., Koob, M.D. and E. S. Piedras-Rentería. T-type current modulation by the actin-binding protein Kelch-like 1 (KLHL1). American Journal of Physiology, Cell Physiology, 298: C1353-C1362, 2010.
• Aromolaran, K.A., Benzow, K. A., Cribbs, L.L., Koob, M.D. and E. S. Piedras-Rentería. 2009. Kelch-like 1 protein up-regulates T-type currents by an actin-F dependent increase in 1H channels via the recycling endosome. Channels, 3:6, 1-11, 2009.
• Aromolaran, K.A. Benzow, K. A., Koob, M.D. and E. S. Piedras-Rentería. The Kelch-like protein 1 modulates P/Q-type current density. Neuroscience, 145 (3): 841-850, 2007.
• Chen, H. and E.S. Piedras-Rentería. Calcium-dependent facilitation, inactivation and interactions with beta subunits in SCA6 P/Q-type calcium channels. Am. J. Physiol. Cell Physiol. Mar 2007; 292: C1078 - C1086.

Book Chapter

Piedras-Rentería, Erika S., Barrett, Curtis F., Cao, Yu-qing and Richard W. Tsien. Voltage-gated Calcium Channels, Calcium Signaling and Channelopathies. In: Calcium a matter of life or death, Joachim Krebs & Marek Michalak Eds., New Comprehensive Biochemistry Series no. 41, Series Editor G. Bernardi, Elsevier, Amsterdam, Netherlands. Pp 127-166, 2007.

Other Publications