Alexandrov A, Keffel S, Goepel M, Michel M C
Departments of Medicine and Urology, University of Essen, Essen, Germany.
Biochem Biophys Res Commun. 1999 Aug 2;261(2):372-6. doi: 10.1006/bbrc.1999.1015.
We have investigated the alpha(1A)-adrenoceptor-mediated activation of 46 and 54 kDa isoforms of c-jun N-terminal kinase (JNK) and of p38 mitogen-activated protein kinase. The alpha(1)-adrenoceptor agonist phenylephrine activated all three kinases but with different time courses and maximal effects. Activation of all three kinases was insensitive to the phosphatidylinositol-3-kinase inhibitor wortmannin but was enhanced by the protein kinase C inhibitor bisindolylmaleimide I; a protein kinase C-activating phorbol ester inhibited JNK but not p38 activation. Activation of 54 kDa JNK, but not of the other two kinases, was inhibited by pertussis toxin and the phospholipase C inhibitor U 73,122. We conclude that alpha(1)-adrenoceptor stimulation activates 46 kDa JNK, 54 kDa JNK and p38 but uses at least partly different pathways to do so.
我们研究了α(1A)-肾上腺素能受体介导的c-jun氨基末端激酶（JNK）46 kDa和54 kDa亚型以及p38丝裂原活化蛋白激酶的激活情况。α(1)-肾上腺素能受体激动剂去氧肾上腺素激活了所有这三种激酶，但具有不同的时间进程和最大效应。所有这三种激酶的激活对磷脂酰肌醇-3-激酶抑制剂渥曼青霉素不敏感，但被蛋白激酶C抑制剂双吲哚马来酰胺I增强；一种激活蛋白激酶C的佛波酯抑制JNK的激活，但不抑制p38的激活。百日咳毒素和磷脂酶C抑制剂U 73,122抑制54 kDa JNK的激活，但不抑制其他两种激酶的激活。我们得出结论，α(1)-肾上腺素能受体刺激激活46 kDa JNK、54 kDa JNK和p38，但至少部分通过不同的途径来实现。
