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From the Institute of Molecular Cardiology (H.Y., J.W., J.Z., Z.P., H.W., W.S., M.R.E.-M., W.B., J.D., D.M., I.S.C.), Department of Physiology & Biophysics (H.Y., J.W., I.P., J.Z., H.W., W.S., M.R.E.-L., W.B., J.D., I.S.C.), and Department of Neurobiology & Behavior (Z.P., D.M.), SUNY at Stony Brook, Stony Brook, NY; Department of Biology (R.W., R.T.W., B.H.), University of Tulsa, Tulsa, Okla; and Department of Pharmacology (R.B.R.), Columbia University, New York, NY. Current address for H.Y. is Department of Physiology, New York Institute of Technology, Old Westbury, NY.
Correspondence to Dr Ira S. Cohen, Department of Physiology & Biophysics, 8661 SUNY, Stony Brook, NY 11794-8661. E-mail icohen{at}physiology.pnb.sunysb.edu
Abstract
AbstractThe HCN family of ion channel subunits underlies the currents If in heart and Ih and Iq in the nervous system. In the present study, we demonstrate that minK-related peptide 1 (MiRP1) is a ß subunit for the HCN family. As such, it enhances protein and current expression as well as accelerating the kinetics of activation. Because MiRP1 also functions as a ß subunit for the cardiac delayed rectifier IKr, these results suggest that this peptide may have the unique role of regulating both the inward and outward channels that underlie cardiac pacemaker activity. The full text of this article is available at http://www.circresaha.org.
Key Words: HCN family MiRP1 KCNE family ß subunit
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J. Qu, Y. Kryukova, I. A. Potapova, S. V. Doronin, M. Larsen, G. Krishnamurthy, I. S. Cohen, and R. B. Robinson MiRP1 Modulates HCN2 Channel Expression and Gating in Cardiac Myocytes J. Biol. Chem., October 15, 2004; 279(42): 43497 - 43502. [Abstract] [Full Text] [PDF] |
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