Sep. 28, 2010 The heart beat, nerve cell communication, and skeletal muscle function are all controlled by channels in the cell membrane that regulate the movement of sodium ions (Na+). Mutations in these so called voltage-gated Na+ channels result in forms of epilepsy and heart conditions such as long QT syndrome that are characterized by an irregular heart beat.
New research, conducted by a team of investigators led by Peter Mohler and Thomas Hund, at the University of Iowa Carver College of Medicine, Iowa City, has now identified a multifunctional regulatory platform for voltage-gated Na+ channels in mice.
In the study, the structural protein beta-IV-spectrin was found to be part of the multi-protein complex containing the predominant voltage-gated Na+ channel in heart muscle cells in mice. Further, beta-IV-spectrin recruited to the multi-protein complex the protein CaMKII, which in turn modified the voltage-gated Na+ channel, modulating its function. In the presence of mutant forms of beta-IV-spectrin, the function of the voltage-gated Na+ channel in the heart was impaired and the mice exhibited an abnormal heart beat. As discussed by Robert Kass and Kevin Sampson, at Columbia University, New York, in an accompanying commentary, these data provide new insight into the control of the heart beat and might provide new therapeutic targets.
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- Thomas J. Hund, Olha M. Koval, Jingdong Li, Patrick J. Wright, Lan Qian, Jedidiah S. Snyder, Hjalti Gudmundsson, Crystal F. Kline, Nathan P. Davidson, Natalia Cardona, Matthew N. Rasband, Mark E. Anderson, Peter J. Mohler. A βIV-spectrin/CaMKII signaling complex is essential for membrane excitability in mice. Journal of Clinical Investigation, 2010; DOI: 10.1172/JCI43621
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