Long QT syndrome (LQTS) involves delayed repolarisation of the heart, causing heart problems or sudden death. It can be congenital (usually due to mutations in genes encoding cardiac ion channels, such as KCNH2) or acquired, and is also a side effect of many drugs, but there are limited treatment options. Among model organisms, the zebrafish offers many advantages for analysing LQTS. Peal et al. carried out an in vivo functional screen using the zebrafish breakdance mutant, which displays many features of human LQTS owing to a mutation in kcnh2, and identified two drugs that correct the cardiac phenotype. These results and future in vivo screens will contribute to the development of novel targeted therapeutics for LQTS patients.
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RESEARCH HIGHLIGHT| 01 January 2011
In vivo screen for suppressors of long QT syndrome
Online Issn: 1754-8411
Print Issn: 1754-8403
© 2011. Published by The Company of Biologists Ltd
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.
Dis Model Mech (2011) 4 (1): 2.
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In vivo screen for suppressors of long QT syndrome. Dis Model Mech 1 January 2011; 4 (1): 2. doi:
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