Hernández-Sotomayor S M, García-Sáinz J A
Instituto de Fisiología Celular, U.N.A.M., México, D.F.
Biochim Biophys Acta. 1988 Jan 18;968(1):138-41. doi: 10.1016/0167-4889(88)90053-5.
Vasopressin, angiotensin II, epinephrine (alpha 1-adrenergic action) and phorbol 12-myristate 13-acetate (PMA) induce increases in membrane-associated protein kinase C activity concomitant with decreases in the cytosolic activity. The data indicate that the calcium-mobilizing hormones and the active phorbol ester induce translocation from the cytosol to the plasma membrane of this protein kinase. The protein kinase C inhibitor, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine, blocked the translocation to the membrane of this protein kinase induced by PMA and vasopressin.
血管加压素、血管紧张素 II、肾上腺素（α1-肾上腺素能作用）和佛波酯 12-肉豆蔻酸酯 13-乙酸酯（PMA）可诱导膜相关蛋白激酶 C 活性增加，同时胞质活性降低。数据表明，钙动员激素和活性佛波酯可诱导该蛋白激酶从胞质转移至质膜。蛋白激酶 C 抑制剂 1-(5-异喹啉磺酰基)-2-甲基哌嗪可阻断由 PMA 和血管加压素诱导的该蛋白激酶向膜的转移。
