Article
Lack of S100A1 in mice confers a gender-dependent hypertensive phenotype and increased mortality after myocardial infarction.
American journal of physiology. Heart and circulatory physiology - 1 May 2009
Desjardins Jean-Francois, Pourdjabbar Ali, Quan Adrian, Leong-Poi Howard, Teichert-Kuliszewska Krystyna, Verma Subodh, Parker Thomas G
Abstract excerpt
S100A1 is a small Ca(2+)-binding protein expressed in the myocardium and blood vessels that is downregulated in the diseased heart and plays a role in the regulation of cardiac muscle Ca(2+) homeostasis and contractility. To understand its physiological role under basal conditions and after myocardial infarction (MI), we used a mouse strain with targeted deletion of the S100A1 gene [S100A1 knockout (KO) mice]. We...
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