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Citations to this article

Nkx2-5 mutation causes anatomic hypoplasia of the cardiac conduction system
Patrick Y. Jay, … , Charles I. Berul, Seigo Izumo
Patrick Y. Jay, … , Charles I. Berul, Seigo Izumo
Published April 15, 2004
Citation Information: J Clin Invest. 2004;113(8):1130-1137. https://doi.org/10.1172/JCI19846.
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Article Cardiology

Nkx2-5 mutation causes anatomic hypoplasia of the cardiac conduction system

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Abstract

Heterozygous mutations of the cardiac transcription factor Nkx2-5 cause atrioventricular conduction defects in humans by unknown mechanisms. We show in KO mice that the number of cells in the cardiac conduction system is directly related to Nkx2-5 gene dosage. Null mutant embryos appear to lack the primordium of the atrioventricular node. In Nkx2-5 haploinsufficiency, the conduction system has half the normal number of cells. In addition, an entire population of connexin40–/connexin45+ cells is missing in the atrioventricular node of Nkx2-5 heterozygous KO mice. Specific functional defects associated with Nkx2-5 loss of function can be attributed to hypoplastic development of the relevant structures in the conduction system. Surprisingly, the cellular expression of connexin40, the major gap junction isoform of Purkinje fibers and a putative Nkx2-5 target, is unaffected, consistent with normal conduction times through the His-Purkinje system measured in vivo. Postnatal conduction defects in Nkx2-5 mutation may result at least in part from a defect in the genetic program that governs the recruitment or retention of embryonic cardiac myocytes in the conduction system.

Authors

Patrick Y. Jay, Brett S. Harris, Colin T. Maguire, Antje Buerger, Hiroko Wakimoto, Makoto Tanaka, Sabina Kupershmidt, Dan M. Roden, Thomas M. Schultheiss, Terrence X. O’Brien, Robert G. Gourdie, Charles I. Berul, Seigo Izumo

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Total citations by year

Year: 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 2006 2005 Total
Citations: 7 4 3 5 4 7 9 5 5 8 6 2 8 8 3 6 3 7 4 1 105
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