Thorburn A
Dept. of Human Genetics, Eccles Institute of Human Genetics, University of Utah, Salt Lake City 84112.
Biochem Biophys Res Commun. 1994 Dec 15;205(2):1417-22. doi: 10.1006/bbrc.1994.2823.
The mitogen-activated protein (MAP) kinases are a family of kinases whose activity is implicated in a number of growth and differentiation responses. Recently, we and others have shown that these kinases are activated by agonists which induce cardiac muscle cell hypertrophy. Inhibition of MAP kinase activation prevents some of the phenotypes associated with phenylephrine-induced cardiac cell hypertrophy, indicating that this activation is of functional significance. In this communication, we show that active Ras can induce MAP kinase activation in cardiac muscle cells. In addition, phenylephrine-induced activation of the MAP kinases requires Ras activity since a dominant negative Ras mutant (Ala15Ras) and a Ras-blocking, Raf mutant (C4B Raf) prevent activation of the MAP kinase Erk2 by phenylephrine. These data indicate that phenylephrine signaling to the MAP kinases is mediated through Ras.
丝裂原活化蛋白（MAP）激酶是一类激酶家族，其活性与多种生长和分化反应有关。最近，我们和其他人已经表明，这些激酶被诱导心肌细胞肥大的激动剂激活。抑制MAP激酶激活可预防一些与去氧肾上腺素诱导的心肌细胞肥大相关的表型，表明这种激活具有功能意义。在本通讯中，我们表明活性Ras可诱导心肌细胞中MAP激酶激活。此外，去氧肾上腺素诱导的MAP激酶激活需要Ras活性，因为显性负性Ras突变体（Ala15Ras）和Ras阻断性Raf突变体（C4B Raf）可阻止去氧肾上腺素激活MAP激酶Erk2。这些数据表明，去氧肾上腺素向MAP激酶的信号传导是通过Ras介导的。
