期刊
JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY
卷 34, 期 3-4, 页码 239-246出版社
SPRINGER
DOI: 10.1007/s10974-013-9348-7
关键词
Tropomyosin; Phosphorylation; Transgenic mice; Heart
类别
资金
- NIH [HO1 HL-081680, T32 HL-07382]
The focus of this review is on the very recent work we have conducted that addresses the molecular, morphological, and physiological significance of cardiac tropomyosin phosphorylation in the heart. We employ transgenic mice to address questions of how cardiomyocytes and the whole heart respond when the tropomyosin phosphorylation site (Ser283) is converted to a non-phosphorylatable amino acid (Ala). We address the phenotype of these mice during normal development and in response to acute cardiac stress (transaortic coarctation). In addition, we also examined how transgenic mice encoding the altered tropomyosin phosphorylation site (Ser283Ala) would respond to chronic cardiac stress through an encoded hypertrophic cardiomyopathy mutation (Glu180Gly). These studies are the first to address the in vivo significance of tropomyosin phosphorylation in the heart. In this review manuscript, we report the recent findings of these investigations.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据