It has been proposed that disruption of the microtubule (MT) cytoskeleton can contribute to heart disease. Dees et al. now provide genetic evidence to support this hypothesis by characterising mice with cardiomyocyte-specific knockout of CENP-F, a multifunctional MT-binding protein whose decreased expression was recently linked to end-stage dilated cardiomyopathy in humans. Mutant mice have smaller hearts with multiple defects including thinner ventricular walls, reduced myocyte proliferation and fewer intercalated discs (myocyte-specific junctional complexes responsible for electrical and force transduction). Mutant mice also develop progressive dilated cardiomyopathy, arrhythmias and cardiac fibrosis. These results reveal a new disease mechanism and suggest that mutations in other MT-associated proteins could also contribute to heart disease. Page 468
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IN THIS ISSUE| 01 July 2012
Heart-specific deletion of CENP-F causes dilated cardiomyopathy
Online Issn: 1754-8411
Print Issn: 1754-8403
Written by editorial staff. © 2012. 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 (2012) 5 (4): 414.
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Heart-specific deletion of CENP-F causes dilated cardiomyopathy. Dis Model Mech 1 July 2012; 5 (4): 414. doi:
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