Martin-Pérez J, Siegmann M, Thomas G
Cell. 1984 Feb;36(2):287-94. doi: 10.1016/0092-8674(84)90222-8.
Epidermal growth factor (10(-9)M), prostaglandin (8.5 X 10(-7)M), F2 alpha, and insulin (10(-9)M), each of which only leads to a partial phosphorylation of 40S ribosomal protein S6, generate the same first eight phosphopeptides induced by 10% serum, suggesting all three activate a common regulatory pathway for the phosphorylation of S6. Added together, they induce almost maximal S6 phosphorylation and a phosphopeptide pattern nearly equivalent to that of serum. Unlike the agents above, 8-Br-cAMP or PGE1 has no significant effect on protein synthesis, but does induce a small increase in S6 phosphorylation. Surprisingly, the three peptides that become phosphorylated are identical with insulin-induced phosphopeptides 10b, 11, and 9, based on either comigration, limited acid hydrolysis, or V8 protease digestion. Incubation of 40S subunits with cAMP-dependent protein kinase induces the phosphorylation of these same three phosphopeptides. The in vitro and in vivo studies described here raise the possibility that cAMP could, in part, be responsible for mediating the phosphorylation of S6 during the mitogenic response.
表皮生长因子(10⁻⁹M)、前列腺素(8.5×10⁻⁷M)、F2α和胰岛素(10⁻⁹M),每一种仅能导致40S核糖体蛋白S6发生部分磷酸化,它们产生与10%血清诱导的相同的前8种磷酸肽,这表明这三种物质均激活了一条共同的S6磷酸化调节途径。将它们相加,可诱导几乎最大程度的S6磷酸化以及一种几乎等同于血清诱导的磷酸肽图谱。与上述物质不同,8-溴-cAMP或前列腺素E1对蛋白质合成无显著影响,但确实可诱导S6磷酸化出现小幅增加。令人惊讶的是,基于共迁移、有限酸水解或V8蛋白酶消化,发生磷酸化的三种肽与胰岛素诱导的磷酸肽10b、11和9相同。用依赖cAMP的蛋白激酶孵育40S亚基可诱导相同的这三种磷酸肽发生磷酸化。本文所述的体外和体内研究提出了一种可能性,即cAMP可能在一定程度上负责在有丝分裂反应过程中介导S6的磷酸化。