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完整动物体内的牛磺酸耗竭会刺激大鼠心脏线粒体部分中一种约44 kDa蛋白质的体外磷酸化。

Taurine depletion in the intact animal stimulates in vitro phosphorylation of an approximately 44-kDa protein present in the mitochondrial fraction of the rat heart.

作者信息

Lombardini J B

机构信息

Department of Pharmacology, Texas Tech University Health Sciences Center, Lubbock 79430, USA.

出版信息

J Mol Cell Cardiol. 1996 Sep;28(9):1957-61. doi: 10.1006/jmcc.1996.0188.

Abstract

Sprague-Dawley rats were treated with 1.5% guanidinoethanesulfonic (GES) acid in their water in order to deplete the taurine levels partially in cardiac tissue. After 6 weeks of GES treatment, in vitro phosphorylation of a approximately 44 kDa protein present in the mitochondrial fraction of the rat heart was increased by 85%. The increase in the in vitro phosphorylation of the specific approximately 44 kDa protein after GES treatment was reversed when the animals were subsequently given 1.5% taurine in their drinking water for an additional 6 weeks. Taurine (1.5%) alone for a period of 6 weeks had no effect on the phosphorylation of the approximately 44 kDa protein. These results suggest that taurine has a regulatory role in the phosphorylation of a specific protein in cardiac tissue.

摘要

将Sprague-Dawley大鼠饲养于含1.5%胍基乙磺酸(GES)的饮水中,以部分耗尽心脏组织中的牛磺酸水平。GES处理6周后,大鼠心脏线粒体部分中一种约44 kDa蛋白质的体外磷酸化增加了85%。当随后给这些动物饮用含1.5%牛磺酸的饮水6周时,GES处理后特定约44 kDa蛋白质的体外磷酸化增加得以逆转。单独给予1.5%牛磺酸6周对约44 kDa蛋白质的磷酸化没有影响。这些结果表明,牛磺酸在心脏组织中特定蛋白质的磷酸化过程中具有调节作用。

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