Mukaida N, Yagisawa H, Kawai T, Kasahara T
Department of Clinical Pathology, Jichi Medical School, Tochigi-ken, Japan.
Biochem Biophys Res Commun. 1988 Jul 15;154(1):187-93. doi: 10.1016/0006-291x(88)90668-7.
Role of protein kinase C (PKC) in interleukin (IL) 2-induced proliferation was investigated by utilizing two murine IL 2-dependent cell lines, CT6 and CTLL-2 cell lines. CT6 cells showed a marked proliferative response to phorbol 12-myristate 13-acetate (PMA), while CTLL-2 did not. PMA induced PKC translocation from cytosol to membrane only in a PMA-responsive cell line. IL 2 failed to stimulate PKC translocation in both cell lines. H-7, a potent and specific PKC inhibitor, however, inhibited the proliferation of both cell lines induced by IL 2. Taken collectively, IL 2 may induce PKC activation without its translocation.
通过利用两种小鼠白细胞介素2（IL-2）依赖细胞系CT6和CTLL-2细胞系，研究了蛋白激酶C（PKC）在IL-2诱导的增殖中的作用。CT6细胞对佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）表现出明显的增殖反应，而CTLL-2细胞则没有。PMA仅在PMA反应性细胞系中诱导PKC从胞质溶胶转位到细胞膜。IL-2未能刺激这两种细胞系中的PKC转位。然而，强效特异性PKC抑制剂H-7抑制了IL-2诱导的这两种细胞系的增殖。总体而言，IL-2可能在不发生转位的情况下诱导PKC活化。
