Congenital heart disease is a common inherited birth defect. Much is known about electrical conduction and Ca2+ handling in the adult heart, but not about how these characteristics are established during embryogenesis. Wythe et al. use a zebrafish embryo screen to identify a highly conserved gene encoding heart adaptor protein 1 (HADP1), a membrane-bound factor that interacts with phosphatidylinositol (PI) derivatives. Pharmacological experiments implicate PI4-kinase (PI4K) as an upstream regulator of HADP1 function, indicating that interaction between PI4K and Ca2+ signalling might regulate heart morphogenesis, function and disease. Page 607
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IN THIS ISSUE| 01 September 2011
HADP1: new regulator of cardiac contractility
Online ISSN: 1754-8411
Print ISSN: 1754-8403
Written by editorial staff. © 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 (5): 557.
HADP1: new regulator of cardiac contractility. Dis Model Mech 1 September 2011; 4 (5): 557. doi:
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