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肌球蛋白重链6突变导致房间隔缺损。

Mutation in myosin heavy chain 6 causes atrial septal defect.

作者信息

Ching Yung-Hao, Ghosh Tushar K, Cross Steve J, Packham Elizabeth A, Honeyman Louise, Loughna Siobhan, Robinson Thelma E, Dearlove Andrew M, Ribas Gloria, Bonser Andrew J, Thomas Neil R, Scotter Andrew J, Caves Leo S D, Tyrrell Graham P, Newbury-Ecob Ruth A, Munnich Arnold, Bonnet Damien, Brook J David

机构信息

Institute of Genetics, University of Nottingham, Queen's Medical Centre, Nottingham NG7 2UH, UK.

出版信息

Nat Genet. 2005 Apr;37(4):423-8. doi: 10.1038/ng1526. Epub 2005 Feb 27.

Abstract

Atrial septal defect is one of the most common forms of congenital heart malformation. We identified a new locus linked with atrial septal defect on chromosome 14q12 in a large family with dominantly inherited atrial septal defect. The underlying mutation is a missense substitution, I820N, in alpha-myosin heavy chain (MYH6), a structural protein expressed at high levels in the developing atria, which affects the binding of the heavy chain to its regulatory light chain. The cardiac transcription factor TBX5 strongly regulates expression of MYH6, but mutant forms of TBX5, which cause Holt-Oram syndrome, do not. Morpholino knock-down of expression of the chick MYH6 homolog eliminates the formation of the atrial septum without overtly affecting atrial chamber formation. These data provide evidence for a link between a transcription factor, a structural protein and congenital heart disease.

摘要

房间隔缺损是先天性心脏畸形最常见的形式之一。我们在一个显性遗传房间隔缺损的大家族中,确定了一个与14号染色体q12区域相连的新基因座,该区域与房间隔缺损有关。潜在的突变是α-肌球蛋白重链(MYH6)中的错义替换I820N,MYH6是一种在发育中的心房中高水平表达的结构蛋白,它影响重链与其调节轻链的结合。心脏转录因子TBX5强烈调节MYH6的表达,但导致 Holt-Oram 综合征的TBX5突变形式则不然。鸡MYH6同源物表达的吗啉代敲低消除了房间隔的形成,而没有明显影响心房腔的形成。这些数据为转录因子、结构蛋白与先天性心脏病之间的联系提供了证据。

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