Coeli Lopes, Ph.D.

Lopes Lab Page

Coeli Lopes , Ph.D. Assistant Professor Coeli_Lopes@urmc.rochester.edu Primary Appointment: Department of Medicine in the Aab Cardiovascular Research Institute University of Rochester School of Medicine and Dentistry 601 Elmwood Ave, Box 679 MRBX - Rm. 2-9634 Rochester, New York 14642 Phone: (585) 273-5661 (585) 276-1914

The major focus of Dr. Lopes current work involves the regulation of the slow delayed rectifier-like current (IKs) in the heart and the pathogenesis of the Long QT (LQT1) syndrome. KCNQ1 is co-assembled with the KCNE1 gene product in the heart to produce IKs, which is one of the main currents responsible for myocyte repolarization. The most commonly inherited cardiac arrhythmia, long-QT1 (LQT1), is due to mutations in the KCNQ1 potassium channel. Stress and exercise are triggers known to precipitate arrhythmias, in particular for LQT1 patients. Dr. Lopes research focus on the understanding of the regulation of IKs channels, their importance for heart function and the molecular mechanism by which their down-regulation leads to the LQT1 syndrome. In addition, Dr. Lopes is interested in phospholipid regulation of ion channels. Phosphatidylinositol 4,5-bisphosphate (PIP2) is an important membrane-delimited second messenger. It has been shown to be crucial for the activity of a number of transporters and ion channels. Several PIP2-sensitive channels have also been show to be regulated by physiological changes in PIP2 levels in the plasma membrane. Dr. Lopes is interested in the study of the crosstalk of PIP2 modulation with other common regulatory mechanisms of different ion channel families such as mechanosensitivity, voltage-gating and phosphorylation.

Recent Publications

1. PIP2 underlies agonist-induced inhibition and controls voltage-gating of 2-P domain K+ channels. C.M.B. Lopes, T. Rohacs, G. Czirjak, T. Balla, P. Enyedi and D.E. Logothetis (in press).
2. Characteristic Interactions with PIP2 determine regulation of Kir channels by diverse modulators, X. Du, H. Zhang, C.M.B. Lopes, T. Mirshari, T. Rohacs, D.E. Logothetis, J. Biol. Chem. (2004) May 20.
3. Sorcin mediates calcium-dependent inactivation of cardiac L-type calcium channels., Meyers M. B., Y. Sun, C.M.B. Lopes, T. Rohacs, and Fishman G. J. Biol. Chem. (2003) 278: 28865-28871.
4. PIP2 activates KCNQ channels: Tracking down the mysterious diffusible second messenger that underlies M current inhibition., Zhang H.,L. Cracium,T. Mirshahi, T. Rohacs, C.M.B. Lopes, T. Jin, D.E. Logothetis, Neuron (2003) 37: 963-975.
5. C and N Terminal Determinants of the Specificity of Interaction of Inwardly Rectifying K+ channels with PIP2, . Roh CS, C.M.B. Lopes, T. Jin, D. E Logothetis;
   Proc Natl Acad Sci (2003) 100:745-50.
6. Alterations in Conserved Interactions PIP2 and Kir Channels Underlie Channelopathies, C.M.B. Lopes, H. Zhang, T. Rohacs, T. Jin, J. Yang and D.E. Logothetis Neuron (2002) 34: 933-944.
7. Assaying phosphatidylinositol bisphosphate regulation of potassium channels
   T. Rohacs, C. Lopes, T. Mirshahi, T. Jin, H. Zhang, D.E. Logothetis G protein pathways: effector mechanisms, Meth. Enz. (2002) 345: 71-92.
8. Block of Kcnk3 by protons: evidence that 2-P-domain potassium channel subunits function as homodimers, C.M.B. Lopes, N.Zimmenberg, S.A.N. Goldstein
   J. Biol. Chem. (2001) 276, 24449-52.
9. Proton block and voltage gating are potassium-dependent in the cardiac leak channel kcnk3., C.M.B. Lopes, Gallagher P.G., Buck M.E., Butler M.H. and Goldstein S.A., J. Biol. Chem. (2000) 275, 16969-78.