Skip to main content
Explore URMC

Lopes Lab

Coeli Lopes, Ph.D.

Research Associate Professor, Department of Medicine, Aab Cardiovascular Research Institute
1997 | PhD | Biophysics | Imperial College | UK
1992 | MS | Physics | Brazil-Pontificia Universidade Catolica
1989 | BS | Physics | Brazil-Pontificia Universidade Catolica

Research Overview

We study the regulation of ion channels by diverse G-protein signaling pathways in normal and pathological states.


Lopes Lab Image

One major focus of our current work is the changes in function and regulation of cardiac ion channels that cause the most common form of inherited cardiac arrhythmia, Long QT syndrome. Our work translates channel dysfunction and dysregulation at the cellular level to clinical phenotype and patient’s response to treatment.

A second focus of our current research is the study of pathological remodeling of the slow delayed rectifier-like current (IKs) in heart failure. Our current research focus on stress signals caused by chronic stimulation of kinase signaling pathways, and their consequence for ion channel function and membrane trafficking. We explore novel antiarrhythmic treatments to reverse IKs pathological remodeling during heart failure.

Recent Publications

  1. Isoform-specific dynamic translocation of PKC by α1-adrenoceptor stimulation in live cells.
    O-Uchi J, Sorenson J, Jhun BS, Mishra J, Hurst S, Williams K, Sheu SS, Lopes CM.
    Biochem Biophys Res Commun. 2015 Aug 12. pii: S0006-291X(15)30430-7
  2. Impaired IKs channel activation by Ca(2+)-dependent PKC shows correlation with emotion/arousal-triggered events in LQT1.
    O-Uchi J, Rice JJ, Ruwald MH, Parks XX, Ronzier E, Moss AJ, Zareba W, Lopes CM.
    J Mol Cell Cardiol. 2015 Feb;79:203-11
  3. Risk of life-threatening cardiac events among patients with long QT syndrome and multiple mutations. Heart Rhythm., Mullally J, Goldenberg I, Moss AJ, Lopes CM, et al., 2013;10(3):378-382.
  4. Prognostic implications of mutation-specific QTc standard deviation in congenital long QT syndrome., Mathias A, Moss AJ, Lopes CM, et al., Heart Rhythm. 2013;10(5):720-725.
  5. Adrenergic signaling controls RGK-dependent trafficking of cardiac voltage-gated L-type Ca2+ channels through PKD1., Jhun BS, O-Uchi J, Wang W, Ha CH, Zhao J, Kim JY, Wong C, Dirksen RT, Lopes CM, Jin ZG.., Circ Res. 2012;110(1):59-70.
  6. In silico cardiac risk assessment in patients with long QT syndrome: type 1: clinical predictability of cardiac models., Hoefen R, Reumann M, Goldenberg I, et al., J Am Coll Cardiol. 2012;60(21):2182-2191.
  7. Trigger-specific ion-channel mechanisms, risk factors, and response to therapy in type 1 long QT syndrome., Goldenberg I, Thottathil P, Lopes CM, et al., Heart Rhythm. 2012;9(1):49-56.
  8. Genotype- and Sex-Specific QT-RR Relationship in the Type-1 Long-QT Syndrome., Couderc JP, Xia X, Denjoy I, Extramiana F, Maison-Blanche P, Moss AJ, Zareba W, Lopes CM.., J Am Heart Assoc. 2012;1(2):e000570.

More papers:PubMed