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J Physiol Volume 586, Number 7, 1785-1789, April 1, 2008 DOI: 10.1113/jphysiol.2007.148254
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SYMPOSIUM REPORT

Kv7.1 (KCNQ1) properties and channelopathies

 David Peroz1,2,3, Nicolas Rodriguez1,2,3, Frank Choveau1,2,3, Isabelle Baró1,2,3, Jean Mérot1,2,3 and Gildas Loussouarn1,2,3

1 INSERM, U915, Nantes, F-44000, France
2 Université de Nantes, Faculté de Médecine, Nantes, F-44000, France
3 CNRS, ERL-3147, F-44000, France

KCNQ1 is the pore-forming subunit of a channel complex whose expression and function have been rather well characterized in the heart. Almost 300 mutations of KCNQ1 have been identified in patients and a vast majority of the described mutations are linked to the long QT syndrome. Only a few mutations are linked to other pathologies such as atrial fibrillation and the short QT syndrome. However, a considerable amount of work remains to be done to get a clear picture of the molecular mechanisms responsible for the pathogenesis related to each mutation. The present review gives three examples of recent studies towards this goal and illustrates the diversity of the molecular mechanisms involved.

(Received 15 November 2007; accepted after revision 14 December 2007; first published online 20 December 2007)
Corresponding author G. Loussouarn: INSERM, U533, Nantes, F-44000, France. Email: gildas.loussouarn{at}nantes.inserm.fr

This report was presented at a symposium on Kv7 (KCNQ) potassium channels that are mutated in human diseases, held at a joint meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies in Bratislava, Slovakia on 14 September 2007. It was commissioned by the Editorial Board and reflects the views of the authors.




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