Deguchi Y, Negoro S, Hosokawa T, Kishimoto S
Third Department of Internal Medicine, Osaka University School of Medicine, Japan.
Clin Exp Immunol. 1989 Aug;77(2):157-62.
We characterized the nuclear proteins with specific binding ability against c-myc gene by gel-shift assay in cell extracts of peripheral blood mononuclear cells (PBMC) from SLE patients and SLE-prone mice with use of distinct c-myc fragments. With the fragment named Fmyc in our experiments, two kinds of complexes which we call C1 and C2 respectively were found in PBMC from SLE patients and SLE-prone mice. The C1 was shown to be inducible in PBMC from healthy persons without nascent protein synthesis after lectin binding to the cell and found to be elevated in the SLE patients and in all of the established cell lines we examined. The C2 seemed to be peculiar to SLE subjects. The binding site of the C1 factor (C1F) and C2 factor (C2F) which forms C1 and C2 respectively with Fmyc appeared to be common and were found to reside at 51 kbp sequence (from XhoI to Sau3A) of exon I of c-myc gene. Interestingly, XhoI site of the binding site was highly demethylated in PBMC of SLE patients as compared with healthy persons. The roles of these binding factors for the pathogenesis of SLE are discussed.
我们利用不同的c-myc片段，通过凝胶迁移试验对外周血单个核细胞（PBMC）来自系统性红斑狼疮（SLE）患者和SLE易感小鼠的细胞提取物中具有针对c-myc基因特异性结合能力的核蛋白进行了表征。在我们的实验中，使用名为Fmyc的片段，在SLE患者和SLE易感小鼠的PBMC中发现了两种复合物，我们分别称之为C1和C2。C1在凝集素与细胞结合后，在无新生蛋白质合成的健康人的PBMC中可诱导产生，且在SLE患者以及我们检测的所有已建立的细胞系中均升高。C2似乎是SLE患者所特有的。分别与Fmyc形成C1和C2的C1因子（C1F）和C2因子（C2F）的结合位点似乎是相同的，且发现位于c-myc基因外显子I的51kbp序列（从XhoI到Sau3A）处。有趣的是，与健康人相比，SLE患者PBMC中结合位点的XhoI位点高度去甲基化。讨论了这些结合因子在SLE发病机制中的作用。
