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Molecular Interventions 3:131-136 (2003)
© 2003 American Society of Pharmacology and Experimental Therapeutics

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LQT4 Gene: The "Missing" Ankyrin

Sandro Yong, Xiaoli Tian and Qing Wang

Center for Molecular Genetics, Department of Molecular Cardiology, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, OH, 44195; Center for Cardiovascular Genetics, The Cleveland Clinic Foundation, Cleveland, OH, 44195

SUMMARY

Mutations in ion channels have been implicated in the formation of long QT syndrome (LQTS). However, Mohler et al. have recently uncovered a role for ankyrin-B, a non-ion channel protein, in type IV LQTS. Calcium signalling is altered, and the functions of several channels and pumps that normally interact with wild-type ankyrin-B are impaired in the presence of mutant ankyrin-B. The authors suggest that by disrupting the functions of these channels, a new mechanism has been uncovered that can lead to cardiac myopathy.




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Copyright © 2003 by the American Society for Pharmacology and Experimental Therapeutics.