Dunn W C, Foote R S, Hand R E, Mitra S
Carcinogenesis. 1986 May;7(5):807-12. doi: 10.1093/carcin/7.5.807.
O6-methylguanine-DNA methyltransferase (MGMT) was measured in partially synchronized cultures of C3H/10T1/2 mouse embryo cells as a function of cell cycle. The degree of synchrony and progression of the cell cycle were monitored by flow cytometry. The MGMT level was significantly reduced prior to the onset of S-phase. This reduction was concomitant with the inhibition of in vivo repair of O6-methylguanine in DNA of S-phase cells as observed earlier. The recovery of the MGMT level paralleled the progression of synchronized cells into G2. S-phase cells purified by cell sorting contained approximately 15% of the MGMT present in G0 or early G1 cells. A comparison of the in vivo repair of O6-methylguanine and MGMT levels suggests that the lack of repair of O6-methylguanine in DNA of the mouse embryo cells is due only in part to a temporal loss of MGMT.
在C3H/10T1/2小鼠胚胎细胞的部分同步培养物中，检测了O6-甲基鸟嘌呤-DNA甲基转移酶（MGMT）作为细胞周期的函数。通过流式细胞术监测细胞周期的同步程度和进程。在S期开始之前，MGMT水平显著降低。如先前观察到的，这种降低与S期细胞DNA中O6-甲基鸟嘌呤的体内修复抑制同时发生。MGMT水平的恢复与同步细胞进入G2期的进程平行。通过细胞分选纯化的S期细胞所含MGMT约为G0期或早期G1期细胞的15%。对O6-甲基鸟嘌呤的体内修复和MGMT水平的比较表明，小鼠胚胎细胞DNA中O6-甲基鸟嘌呤缺乏修复仅部分归因于MGMT的暂时缺失。
