Nikiforov M A, Kotenko I, Petrenko O, Beavis A, Valenick L, Lemischka I, Cole M D
Department of Molecular Biology, Princeton University, New Jersey 08544-1014, USA.
Oncogene. 2000 Oct 5;19(42):4828-31. doi: 10.1038/sj.onc.1203880.
The targeted knockout of the c-myc gene from rat fibroblasts leads to a stable defect in cell proliferation. We used complex cDNA libraries expressed from retroviral vectors and an efficient sorting procedure to rapidly select for cDNAs that can restore the growth rate of c-myc deficient cells. All of the biologically active cDNAs contained either c-myc or N-myc, suggesting that no other cellular genes can effectively bypass the requirement for c-myc in fibroblast proliferation. This approach provides a powerful screening method for cell cycle changes in genetically defined systems.
从大鼠成纤维细胞中靶向敲除c-myc基因会导致细胞增殖出现稳定缺陷。我们使用从逆转录病毒载体表达的复杂cDNA文库和高效分选程序,快速筛选出能够恢复c-myc缺陷细胞生长速率的cDNA。所有具有生物活性的cDNA都包含c-myc或N-myc,这表明没有其他细胞基因能够有效绕过成纤维细胞增殖中对c-myc的需求。这种方法为在基因定义系统中研究细胞周期变化提供了一种强大的筛选方法。