ENDOTHELIN-1, PHORBOL ESTERS AND PHENYLEPHRINE STIMULATE MAP KINASE-ACTIVITIES IN VENTRICULAR CARDIOMYOCYTES
ENDOTHELIN-1, PHORBOL ESTERS AND PHENYLEPHRINE STIMULATE MAP KINASE-ACTIVITIES IN VENTRICULAR CARDIOMYOCYTES
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DOI：
10.1016/0014-5793(93)81291-7
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发表时间：
1993-02-15
期刊：
影响因子：
3.5
通讯作者：
SUGDEN, PH
中科院分区：
文献类型：
--
作者：
BOGOYEVITCH, MA;GLENNON, PE;SUGDEN, PH
ET-1刺激培养心肌细胞MBP激酶活性。最大活化（3.5倍）为5 min。EC 50为0.2 nM。PMA或PE也增加MBP激酶（分别为4或2.5倍）。PMA预处理可下调ET-1或PMA的后续反应。在Mono Q上通过FPLC将ET-1或PMA刺激的MBP激酶拆分为2个主峰（峰II和IV）和2个次峰。峰II和IV被LAR或PP 2A灭活。在含有MBP的凝胶中SDS-PAGE和免疫印迹分析后，复性的MBP激酶活性显示峰II是p42 MAP激酶，峰IV是p44 MAP激酶。
ET-1 stimulated MBP kinase activity in cultured cardiomyocytes. Maximal activation (3.5-fold) was at 5 min. EC50 was 0.2 nM. PMA or PE also increased MBP kinase (4- or 2.5-fold, respectively). Pre-treatment with PMA down-regulated the subsequent response to ET-1 or PMA. ET-1- or PMA-stimulated MBP kinase was resolved into 2 major (peaks II and IV) and 2 minor peaks by FPLC on Mono Q. Peaks II and IV were inactivated by either LAR or PP2A. Renatured MBP kinase activities following SDS-PAGE in MBP-containing gels and immunoblot analysis showed that peak II was a p42 MAP kinase and peak IV was a p44 MAP kinase.