Koizumi T, Nakao Y, Matsui T, Katakami Y, Mihara K, Takahashi R, Maeda S, Sugiyama T, Fujita T
Department of Medicine and Pathology, Kobe University School of Medicine, Japan.
Immunology. 1988 May;64(1):93-6.
In order to analyse the molecular mechanism of lymphocyte activation defect in MRL/MP-lpr (MRL/1) mice, c-myc proto-oncogene expression was examined in MRL/1 lymph node cells stimulated by various agents. Since a transient increase of c-myc RNA in early hours is required for lymphocyte activation, detection of c-myc messenger RNA is useful to determine whether or not an appropriate signal is transduced to the nucleus. Stimulation by concanavalin A (Con A) plus 12-O-tetradecanoyl phorbol 13-acetate (TPA) or A23187 plus TPA markedly increased c-myc mRNA expression and cell proliferation, whereas stimulation by Con A alone failed to do so. These results suggest that an abnormality exists in the early signal transduction process, and that it could be bypassed by calcium influx and direct activation of protein kinase C.
为了分析MRL/MP-lpr(MRL/1)小鼠淋巴细胞激活缺陷的分子机制,我们检测了用各种试剂刺激的MRL/1淋巴结细胞中c-myc原癌基因的表达。由于淋巴细胞激活需要在早期数小时内c-myc RNA短暂增加,因此检测c-myc信使RNA有助于确定是否有适当的信号转导至细胞核。用刀豆球蛋白A(Con A)加12-O-十四酰佛波醇-13-乙酸酯(TPA)或A23187加TPA刺激可显著增加c-myc mRNA表达和细胞增殖,而单独用Con A刺激则无此效果。这些结果表明,早期信号转导过程存在异常,并且钙内流和蛋白激酶C的直接激活可以绕过这一异常。