Beecham E J, Mushinski J F, Shacter E, Potter M, Bohr V A
Laboratory of Molecular Pharmacology, National Cancer Institute, NIH, Bethesda, MD 20892.
Curr Top Microbiol Immunol. 1990;166:285-91. doi: 10.1007/978-3-642-75889-8_35.
We have studied DNA repair after UV damage in the murine c-myc locus. It appears that a region in B cells upstream of the murine c-myc gene is repaired with a different efficiency in plasmacytoma-resistant DBA/2N mice than in plasmacytoma-susceptible BALB/cAn mice. The region just upstream of c-myc is inefficiently repaired in B lymphoblasts derived from BALB/cAn mice. In contrast, this same region of c-myc is efficiently repaired in B lymphoblasts derived from DBA/2N mice. DNA fragments located in the coding region of c-myc and in another gene, dihydrofolate reductase (DHFR), are repaired with equal efficiency in cells from these two strains of mice. It is possible that repair efficiency of the 5' flank of c-myc may be involved in tumor susceptibility of the mouse strain.
我们研究了小鼠c-myc基因座紫外线损伤后的DNA修复情况。结果显示,在抗浆细胞瘤的DBA/2N小鼠中,与易患浆细胞瘤的BALB/cAn小鼠相比,小鼠c-myc基因上游B细胞中的一个区域修复效率不同。c-myc基因上游紧邻区域在源自BALB/cAn小鼠的B淋巴母细胞中修复效率低下。相反,在源自DBA/2N小鼠的B淋巴母细胞中,c-myc基因的同一区域能高效修复。位于c-myc编码区以及另一个基因二氢叶酸还原酶(DHFR)中的DNA片段,在这两种品系小鼠的细胞中修复效率相同。c-myc基因5'侧翼的修复效率可能与小鼠品系的肿瘤易感性有关。