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Sci. Signal., 24 June 2008 PERSPECTIVESDoes Contractile Ca2+ Control Calcineurin-NFAT Signaling and Pathological Hypertrophy in Cardiac Myocytes?Steven R. Houser1* and Jeffery D. Molkentin2*
1Department of Physiology, Temple University School of Medicine, 3400 North Broad Street, Philadelphia, PA 19140, USA. Abstract: In noncontractile cells, a sustained increase in total cytoplasmic Ca2+ concentration is typically needed to activate the intracellular protein phosphatase calcineurin, leading to dephosphorylation of the transcription factor nuclear factor of activated T cells (NFAT), its nuclear translocation, and induction of gene expression. It remains a mystery exactly how Ca2+-dependent signaling pathways, such as that mediated by calcineurin-NFAT, are regulated in contracting cardiac myocytes given the highly specialized manner in which Ca2+ concentration rhythmically cycles in excitation-contraction coupling. Here, we critically review evidence that supports the hypothesis that calcineurin-NFAT signaling is regulated by contractile Ca2+ transients in cardiac myocytes. *Corresponding authors. E-mail, srhouser{at}temple.edu (S.R.H.); jeff.molkentin{at}cchmc.org (J.D.M.)
Citation: S. R. Houser, J. D. Molkentin, Does Contractile Ca2+ Control Calcineurin-NFAT Signaling and Pathological Hypertrophy in Cardiac Myocytes? Sci. Signal. 1, pe31 (2008). The editors suggest the following Related Resources on Science sites:In Science Signaling
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