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D. Pillers (1999)
Dystrophin and the retina.Molecular genetics and metabolism, 68 2
J. Jurevičius, R. Fischmeister (1996)
cAMP compartmentation is responsible for a local activation of cardiac Ca2+ channels by beta-adrenergic agonists.Proceedings of the National Academy of Sciences of the United States of America, 93 1
A. Beggs, T. Byers, J. Knoll, F. Boyce, G. Bruns, Louis Kunkels
Cloning and Characterization of Two Human Skeletal Muscle 0-actinin Genes Located on Chromosomes 1 and 11*
Barry Johnson, Jeffrey Brousal, Blaise Peterson, Peter Gallombardo, G. Hockerman, Y. Lai, T. Scheuer, W. Catterall (1997)
Modulation of the Cloned Skeletal Muscle L-Type Ca2+Channel by Anchored cAMP-Dependent Protein KinaseThe Journal of Neuroscience, 17
W. Tomlinson, A. Stea, E. Bourinet, P. Charnet, J. Nargeot, T. Snutch (1993)
Functional properties of a neuronal class C L-type calcium channelNeuropharmacology, 32
X. Wei, E. Perez-Reyes, A. Lacerda, G. Schuster, A. Brown, L. Birnbaumer (1991)
Heterologous regulation of the cardiac Ca2+ channel alpha 1 subunit by skeletal muscle beta and gamma subunits. Implications for the structure of cardiac L-type Ca2+ channels.The Journal of biological chemistry, 266 32
J. Hell, R. Westenbroek, C. Warner, M. Ahlijanian, W. Prystay, M. Gilbert, T. Snutch, W. Catterall (1993)
Identification and differential subcellular localization of the neuronal class C and class D L-type calcium channel alpha 1 subunitsThe Journal of Cell Biology, 123
B. Hille (2001)
Ionic channels of excitable membranes
Edward Perez-Reyes, Antonio Castellano, Haeyoung Kim, P. Bertrand, E. Baggstrom, Antonio Lacerda, Xiangyang Wei, L. Birnbaumer (1992)
Cloning and expression of a cardiac/brain beta subunit of the L-type calcium channel.The Journal of biological chemistry, 267 3
K. Ishikawa, C. Shirato, M. Yotsukura, T. Ishihara, T. Tamura, M. Inoue (1982)
Sequential changes in high frequency notches on QRS complexes in progressive muscular dystrophy of the Duchenne type--a 3-year follow-up study.Journal of electrocardiology, 15 1
K. Furukawa, Weiming Fu, Ying Li, W. Witke, D. Kwiatkowski, M. Mattson (1997)
The Actin-Severing Protein Gelsolin Modulates Calcium Channel and NMDA Receptor Activities and Vulnerability to Excitotoxicity in Hippocampal NeuronsThe Journal of Neuroscience, 17
Gabriele Lück, W. Hoch, C. Hopf, D. Blottner (2000)
Nitric Oxide Synthase (NOS-1) Coclustered With Agrin-Induced AChR-Specializations on Cultured Skeletal MyotubesMolecular and Cellular Neuroscience, 16
J. Krupp, B. Vissel, C. Thomas, S. Heinemann, G. Westbrook (1999)
Interactions of Calmodulin and α-Actinin with the NR1 Subunit Modulate Ca2+-Dependent Inactivation of NMDA ReceptorsThe Journal of Neuroscience, 19
Mariko Nakamura, M. Sunagawa, T. Kosugi, Nicholas Sperelakis (2000)
Actin filament disruption inhibits L-type Ca(2+) channel current in cultured vascular smooth muscle cells.American journal of physiology. Cell physiology, 279 2
T. Gao, T. Puri, B. Gerhardstein, A. Chien, R. Green, M. Hosey (1997)
Identification and Subcellular Localization of the Subunits of L-type Calcium Channels and Adenylyl Cyclase in Cardiac Myocytes*The Journal of Biological Chemistry, 272
A. Dunah, M. Wyszynski, Deborah Martin, Morgan Sheng, D. Standaert (2000)
alpha-actinin-2 in rat striatum: localization and interaction with NMDA glutamate receptor subunits.Brain research. Molecular brain research, 79 1-2
G. Porter, G. Dmytrenko, John Winkelmann, Robert Bloch (1992)
Dystrophin colocalizes with beta-spectrin in distinct subsarcolemmal domains in mammalian skeletal muscleThe Journal of Cell Biology, 117
D. Blake, S. Kröger (2000)
The neurobiology of Duchenne muscular dystrophy: learning lessons from muscle?Trends in Neurosciences, 23
S. Bhattacharya, A. Crawford, J. Pate (1987)
Electrocardiographic, biochemical, and morphologic abnormalities in dystrophic hamsters with cardiomyopathyMuscle & Nerve, 10
M. Yotsukura, Akira Yamamoto, T. Kajiwara, T. Nishimura, K. Sakata, T. Ishihara, K. Ishikawa (1999)
QT dispersion in patients with Duchenne-type progressive muscular dystrophy.American heart journal, 137 4 Pt 1
S. Gee, R. Madhavan, S. Levinson, J. Caldwell, R. Sealock, S. Froehner (1998)
Interaction of Muscle and Brain Sodium Channels with Multiple Members of the Syntrophin Family of Dystrophin-Associated ProteinsThe Journal of Neuroscience, 18
G. Waites, I. Graham, P. Jackson, D. Millake, B. Patel, A. Blanchard, P. Weller, I. Eperon, David CritchleyS (1992)
Mutually exclusive splicing of calcium-binding domain exons in chick alpha-actinin.The Journal of biological chemistry, 267 9
D. Cukovic, Grace Lu, B. Wible, D. Steele, D. Fedida (2001)
A discrete amino terminal domain of Kv1.5 and Kv1.4 potassium channels interacts with the spectrin repeats of α‐actinin‐2FEBS Letters, 498
Y. Chan, C. Bönnemann, H. Lidov, L. Kunkel (1998)
Molecular Organization of Sarcoglycan Complex in Mouse Myotubes in CultureThe Journal of Cell Biology, 143
R. Bies, D. Friedman, R. Roberts, M. Perryman, C. Caskey (1992)
Expression and Localization of Dystrophin in Human Cardiac Purkinje FibersCirculation, 86
Johnson Bd (1999)
The company they keep: ion channels and their intracellular regulatory partners.Advances in second messenger and phosphoprotein research, 33
R. Grady, H. Teng, Mia Nichol, J. Cunningham, R. Wilkinson, J. Sanes (1997)
Skeletal and Cardiac Myopathies in Mice Lacking Utrophin and Dystrophin: A Model for Duchenne Muscular DystrophyCell, 90
M. Wyszynski, Jerry Lin, A. Rao, E. Nigh, A. Beggs, A. Craig, M. Sheng (1997)
Competitive binding of α-actinin and calmodulin to the NMDA receptorNature, 385
Neil Maruoka, D. Steele, Billie Au, P. Dan, Xue Zhang, E. Moore, D. Fedida (2000)
α‐Actinin‐2 couples to cardiac Kv1.5 channels, regulating current density and channel localization in HEK cellsFEBS Letters, 473
T. Mcdonald, S. Pelzer, W. Trautwein, D. Pelzer (1994)
Regulation and modulation of calcium channels in cardiac, skeletal, and smooth muscle cells.Physiological reviews, 74 2
G. Mitchell, A. Jeron, G. Koren (1998)
Measurement of heart rate and Q-T interval in the conscious mouse.American journal of physiology. Heart and circulatory physiology, 274 3
A. Lader, D. Kwiatkowski, H. Cantiello (1999)
Role of gelsolin in the actin filament regulation of cardiac L-type calcium channels.American journal of physiology. Cell physiology, 277 6
Abstract The actin-binding proteins dystrophin and α-actinin are members of a family of actin-binding proteins that may link the cytoskeleton to membrane proteins such as ion channels. Previous work demonstrated that the activity of Ca 2+ channels can be regulated by agents that disrupt or stabilize the cytoskeleton. In the present study, we employed immunohistochemical and electrophysiological techniques to investigate the potential regulation of cardiac L-type Ca 2+ channel activity by dystrophin and α-actinin in cardiac myocytes and in heterologous cells. Both actin-binding proteins were found to colocalize with the Ca 2+ channel in mouse cardiac myocytes and to modulate channel function. Inactivation of the Ca 2+ channel in cardiac myocytes from mice lacking dystrophin ( mdx mice) was reduced compared with that in wild-type myocytes, voltage dependence of activation was shifted by 5 mV to more positive potentials, and stimulation by the β-adrenergic pathway and the dihydropyridine agonist BAY K 8644 was increased. Furthermore, heterologous coexpression of the Ca 2+ channel with muscle, but not nonmuscle, forms of α-actinin was also found to reduce inactivation. As might be predicted from a reduction of Ca 2+ channel inactivation, a prolonging of the mouse electrocardiogram QT was observed in mdx mice. These results suggest a combined role for dystrophin and α-actinin in regulating the activity of the cardiac L-type Ca 2+ channel and a potential mechanism for cardiac dysfunction in Duchenne and Becker muscular dystrophies. muscular dystrophy intracellular regulation Footnotes This work was supported by an American Heart Association Scientist Development Grant (B. D. Johnson) and by start-up funds from the University of Connecticut Research Foundation. Address for reprint requests and other correspondence: B. D. Johnson, Dept. of Pharmacology and Therapeutics, Univ. of British Columbia, 3650 Wesbrook Mall, Vancouver, Canada BC V6S 2L2 (E-mail: barrydjohnson@telus.net ). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. First published February 13, 2002;10.1152/ajpcell.00435.2001 Copyright © 2002 the American Physiological Society
AJP - Cell Physiology – The American Physiological Society
Published: Jun 1, 2002
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