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Cardiovascular Research 2007 73(4):629-630; doi:10.1016/j.cardiores.2007.01.005
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Copyright © 2007, European Society of Cardiology

Calmodulin and Ca2+/calmodulin kinases in the heart – Physiology and pathophysiology

Lars S. Maiera,*, Donald M. Bersb and Joan Heller Brownc

aDepartment of Cardiology and Pneumology, Georg-August-University Göttingen, Robert-Koch-Str. 40, 37075 Göttingen, Germany
bDepartment of Physiology, Loyola University Chicago, IL, USA
cDepartment of Pharmacology, UCSD, CA, USA

* Corresponding author. Tel.: +49 551 39 9481 or 8921; fax: +49 551 39 8941 or 14370. Email address: lmaier@med.uni-goettingen.de

Received 5 January 2007; accepted 8 January 2007

The first 10% of the full text of this article appears below.

See reviews in this series by Maier and Bers [5] (pages 631–640), Pitt [6] (pages 641–647), Mattiazzi et al. [7] (pages 648–656), Anderson [8] (pages 657–666), and McKinsey [9] (pages 667–677) in this issue.

Original articles in the series are by Yurukova et al. [10] (pages 678–688) and Vila-Petroff et al. [11] (pages 689–698), also in this issue.

Over the last decade our view of calmodulin and Ca2+/calmodulin kinase (CaMK) in the heart has progressed extensively. This includes improved understanding of the fundamental CaMKII . . . [Full Text of this Article]


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