Sassa T, Richter W W, Uda N, Suganuma M, Suguri H, Yoshizawa S, Hirota M, Fujiki H
Cancer Prevention Division, National Cancer Center Research Institute, Tokyo, Japan.
Biochem Biophys Res Commun. 1989 Mar 31;159(3):939-44. doi: 10.1016/0006-291x(89)92199-2.
A cytosolic fraction of mouse brain gave two peaks of protein kinase activity on DEAE-cellulose column chromatography. The first peak of protein kinase corresponded to protein kinase C. The second peak contained protein kinases that were "activated" dose-dependently by the okadaic acid class tumor promoters, okadaic acid and dinophysistoxin-1. This "activation" was not achieved by other tumor promoters, such as 12-0-tetradecanoyl-phorbol-13-acetate, teleocidin, aplysiatoxin, or palytoxin. In addition, the second peak contained phosphatases. The phosphate liberation from phosphorylated histone type III-S by incubation with the second peak was inhibited by okadaic acid or dinophysistoxin-1, dose-dependently. The resulting apparent "activation" of protein kinases by okadaic acid is indicated and would imply a new pathway of tumor promotion on mouse skin.
小鼠脑的胞质部分在二乙氨基乙基纤维素柱层析上产生了两个蛋白激酶活性峰。第一个蛋白激酶峰对应蛋白激酶C。第二个峰包含的蛋白激酶被冈田酸类肿瘤启动子(冈田酸和鳍藻毒素-1)剂量依赖性地“激活”。其他肿瘤启动子,如12-0-十四烷酰佛波醇-13-乙酸酯、远霉素、海兔毒素或岩沙海葵毒素,无法实现这种“激活”。此外,第二个峰还含有磷酸酶。与第二个峰一起孵育时,冈田酸或鳍藻毒素-1剂量依赖性地抑制了从磷酸化组蛋白III-S释放的磷酸盐。文中指出了冈田酸对蛋白激酶产生的明显“激活”作用,这可能意味着小鼠皮肤肿瘤促进的新途径。