Chou I N, Black P H, Roblin R O
Proc Natl Acad Sci U S A. 1974 May;71(5):1748-52. doi: 10.1073/pnas.71.5.1748.
The protease inhibitors N-tosyl-L-phenylalanylchloromethyl ketone (TPCK) and N-tosyl-L-lysylchloromethyl ketone (TLCK) have previously been shown to selectively inhibit growth of simian virus 40-transformed cells, suggesting that proteolytic enzymes play a role in loss of cellular growth control following viral transformation. In contrast, this study shows that TPCK-mediated growth inhibition is non-selective, since the growth of both simian virus 40-transformed and untransformed 3T3 cells is similarly reduced by TPCK treatment. Under certain conditions, TPCK treatment of simian virus 40-transformed cells yields a reversible "growth plateau" condition which mimics, but is not equivalent to, contact inhibition of growth. The growth inhibitory effects of TPCK are due to inhibition of protein synthesis, since TPCK treatment resulted in a diminution of protein synthesis and since the "growth plateau" effect was also observed in cultures treated with cycloheximide.
蛋白酶抑制剂N-对甲苯磺酰-L-苯丙氨酰氯甲基酮（TPCK）和N-对甲苯磺酰-L-赖氨酰氯甲基酮（TLCK）此前已被证明可选择性抑制猿猴病毒40转化细胞的生长，这表明蛋白水解酶在病毒转化后细胞生长控制丧失中发挥作用。相比之下，本研究表明TPCK介导的生长抑制是非选择性的，因为TPCK处理同样降低了猿猴病毒40转化和未转化的3T3细胞的生长。在某些条件下，用TPCK处理猿猴病毒40转化细胞会产生一种可逆的“生长平台期”状态，这种状态模拟但不等同于生长的接触抑制。TPCK的生长抑制作用是由于蛋白质合成受到抑制，因为TPCK处理导致蛋白质合成减少，并且在用环己酰亚胺处理的培养物中也观察到了“生长平台期”效应。
