Lacal J C, Fleming T P, Warren B S, Blumberg P M, Aaronson S A
Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892.
Mol Cell Biol. 1987 Nov;7(11):4146-9. doi: 10.1128/mcb.7.11.4146-4149.1987.
Microinjection of purified protein kinase C (PKC) into Swiss 3T3 fibroblasts pretreated with the phorbol ester phorbol-12,13-dibutyrate restores the mitogenic response of the cells to phorbol-12,13-dibutyrate (G. Pasti, J.C. Lacal, B.S. Warren, S.A. Aaronson, and P.M. Blumberg, Nature [London] 324:375-377, 1986). Our present studies demonstrate that the mitogenic activity of the H-ras oncogene in H-ras p21-microinjected quiescent cells is markedly reduced under conditions in which PKC is downregulated by chronic phorbol ester treatment. The ability to reconstitute the mitogenic response upon microinjection of both H-ras p21 and PKC implies involvement of functional PKC in the mitogenic activity of the H-ras oncogene product.
将纯化的蛋白激酶C(PKC)显微注射到用佛波酯佛波醇-12,13-二丁酸预处理过的瑞士3T3成纤维细胞中,可恢复细胞对佛波醇-12,13-二丁酸的促有丝分裂反应(G. 帕斯蒂、J.C. 拉卡尔、B.S. 沃伦、S.A. 阿伦森和P.M. 布隆伯格,《自然》[伦敦] 324:375 - 377,1986年)。我们目前的研究表明,在通过长期佛波酯处理使PKC下调的条件下,显微注射H-ras p21的静止细胞中H-ras癌基因的促有丝分裂活性显著降低。显微注射H-ras p21和PKC后重建促有丝分裂反应的能力意味着功能性PKC参与了H-ras癌基因产物的促有丝分裂活性。