Nishikawa M, Uemura Y, Hidaka H, Shirakawa S
Life Sci. 1986 Sep 22;39(12):1101-7. doi: 10.1016/0024-3205(86)90202-x.
Treatment of the human promyelocytic leukemia cell line HL-60, with 12-o-tetradecanoylphorbol acetate (TPA) results in the differentiation into macrophage-like cell. A potent inhibitor of protein kinase C, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine(H-7), suppressed the proliferation of HL-60 cells and also inhibited TPA-induced cell differentiation of these cells. N-(2-guanidinoethyl)-5-isoquinolinesulfonamide(HA-1004), a weaker analog of H-7, failed to inhibit this TPA-induced cell differentiation. H-7 also inhibited TPA-induced protein phosphorylation in these cells. Thus, protein kinase C-mediated phosphorylation may be involved in the process of TPA-induced HL-60 cell differentiation.
用12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯（TPA）处理人早幼粒细胞白血病细胞系HL - 60会导致其分化为巨噬细胞样细胞。蛋白激酶C的强效抑制剂1 -（5 - 异喹啉磺酰基）- 2 - 甲基哌嗪（H - 7）抑制了HL - 60细胞的增殖，并且也抑制了这些细胞中TPA诱导的细胞分化。H - 7的较弱类似物N -（2 - 胍基乙基）- 5 - 异喹啉磺酰胺（HA - 1004）未能抑制这种TPA诱导的细胞分化。H - 7还抑制了这些细胞中TPA诱导的蛋白质磷酸化。因此，蛋白激酶C介导的磷酸化可能参与了TPA诱导的HL - 60细胞分化过程。
