Classon M, Wennborg A, Henriksson M, Klein G
Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.
Gene. 1993 Nov 15;133(2):153-61. doi: 10.1016/0378-1119(93)90633-e.
We have demonstrated previously that overproduction of c-Myc, N-Myc and, to a lesser extent, L-Myc facilitates the replication of simian virus 40 (SV40)-based vectors in human lymphoid cells. Using a series of c-myc deletion mutants, we investigated which c-Myc regions are important in stimulating SV40 replication. The ability of c-Myc to promote SV40 replication was significantly reduced by deletions in the second exon domain, formerly shown to be crucial for c-Myc's transforming capacity. The c-myc mutants with a disrupted basic region (b) or leucine zipper (Zip) motif were also unable to stimulate SV40 replication. These regions are implicated in protein-DNA and protein-protein interactions, respectively, suggesting that the c-Myc protein might be associated with the DNA-protein replication complex. We present data obtained from gel mobility shift assays and from an immunocomplex-binding assay substantiating this hypothesis.
我们之前已经证明，c-Myc、N-Myc的过量表达以及程度较轻的L-Myc的过量表达，有助于基于猿猴病毒40（SV40）的载体在人淋巴细胞中复制。我们使用一系列c-myc缺失突变体，研究了c-Myc的哪些区域在刺激SV40复制中起重要作用。c-Myc促进SV40复制的能力在第二个外显子结构域缺失后显著降低，该结构域先前已被证明对c-Myc的转化能力至关重要。具有破坏的碱性区域（b）或亮氨酸拉链（Zip）基序的c-myc突变体也无法刺激SV40复制。这些区域分别与蛋白质-DNA和蛋白质-蛋白质相互作用有关，这表明c-Myc蛋白可能与DNA-蛋白质复制复合物相关。我们展示了从凝胶迁移率变动分析和免疫复合物结合分析中获得的数据，证实了这一假设。
