Suzuki K, Kizaki H, Tadakuma T, Ishimura Y
Department of Biochemistry, School of Medicine, Keio University, Tokyo, Japan.
Biochem Biophys Res Commun. 1990 Sep 14;171(2):827-31. doi: 10.1016/0006-291x(90)91220-m.
12-O-Tetradecanoylphorbol 13-acetate (TPA) potentiated the action of cAMP in DNA cleavage in thymocytes induced by a low concentration of adenosine receptor-site agonists such as adenosine, 2-chloroadenosine and forskolin. The enhancement of DNA cleavage by TPA was also observed in dibutyryl cAMP-treated thymocytes. On the other hand, TPA suppressed accumulation of cAMP by the adenosine receptor-site agonists. These results suggest that activation of protein kinase C inhibits cAMP production, but stimulates cAMP-triggered process to induce DNA cleavage and death of thymocytes.
12 - 十四酰佛波醇 - 13 - 乙酸酯（TPA）增强了低浓度腺苷受体位点激动剂（如腺苷、2 - 氯腺苷和福司可林）诱导胸腺细胞DNA裂解过程中cAMP的作用。在二丁酰cAMP处理的胸腺细胞中也观察到TPA增强了DNA裂解。另一方面，TPA抑制了腺苷受体位点激动剂引起的cAMP积累。这些结果表明，蛋白激酶C的激活抑制了cAMP的产生，但刺激了cAMP触发的过程，从而诱导胸腺细胞的DNA裂解和死亡。
