Yatsunami J, Fujiki H, Suganuma M, Yoshizawa S, Eriksson J E, Olson M O, Goldman R D
Cancer Prevention Division, National Cancer Center Research Institute, Tokyo, Japan.
Biochem Biophys Res Commun. 1991 Jun 28;177(3):1165-70. doi: 10.1016/0006-291x(91)90662-q.
Okadaic acid and dinophysistoxin-1 (35-methylokadaic acid) induced hyperphosphorylation of a 58 kDa protein in primary human fibroblasts, due to inhibition of protein phosphatase 1 and 2A activities. The protein was present in the nuclear and cytosolic fractions. Its pI was 5.3. The hyperphosphorylated protein reacted with monoclonal and polyclonal anti-vimentin antibodies, but not with anti-nucleolin antibody. Phosphorylation of vimentin was stimulated in vitro by dinophysistoxin-1 dose-dependently in the presence of protein phosphatase 2A and protein kinases.
冈田酸和鳍藻毒素-1（35-甲基冈田酸）可抑制原代人成纤维细胞中蛋白磷酸酶1和2A的活性，从而诱导一种58 kDa蛋白发生过度磷酸化。该蛋白存在于细胞核和细胞溶质组分中。其等电点为5.3。过度磷酸化的蛋白与抗波形蛋白单克隆抗体和多克隆抗体发生反应，但不与抗核仁素抗体反应。在蛋白磷酸酶2A和蛋白激酶存在的情况下，鳍藻毒素-1可在体外剂量依赖性地刺激波形蛋白的磷酸化。
