Journal
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
Volume 22, Issue 2, Pages 166-170Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcdb.2010.09.013
Keywords
Ankyrin; Nav1.5; Intercalated disc; Transverse-tubule; Arrhythmia; Sodium channel; Targeting
Categories
Funding
- NIH [HL084583, HL083422, HL092232]
- Pew Scholars Trust
- Fondation LeDucq Award (Alliance for Calmodulin Kinase Signaling in Heart Disease)
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The coordinate activities of ion channels and transporters regulate myocyte membrane excitability and normal cardiac function. Dysfunction in cardiac ion channel and transporter function may result in cardiac arrhythmias and sudden cardiac death. While the past fifteen years have linked defects in ion channel biophysical properties with human disease, more recent findings illustrate that ion channel and transporter localization within cardiomyocytes is equally critical for normal membrane excitability and tissue function. Ankyrins are a family of multifunctional adapter proteins required for the expression, membrane localization, and regulation of select cardiac ion channels and transporters. Notably, loss of ankyrin expression in mice, and ankyrin loss-of-function in humans is now associated with defects in myocyte excitability and cardiac physiology. Here, we provide an overview of the roles of ankyrin polypeptides in cardiac physiology, as well as review other recently identified pathways required for the membrane expression and regulation of key cardiac ion channels and transporters. (C) 2010 Elsevier Ltd. All rights reserved.
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