Yu Y N, Fang M, Dai Y F, Chen X R
Proc Chin Acad Med Sci Peking Union Med Coll. 1989;4(3):157-61.
The cell cycle dependent fluctuation of adenosine diphosphoribosyl transferase (ADPRT) activity was demonstrated by both nicotinamide adenine dinucleotide (3H-NAD+) incorporation into the acid insoluble fraction of permeabilized cells and changes in the cellular content of NAD, the only substrate of ADPRT, in intact FL cells. The ADPRT activity was lowest in the G1 phase and highest in the S/G2-G2 phase. Aphidicolin, a specific inhibitor of DNA polymerase a, abolished the fluctuation of ADPRT activity. Meanwhile, in 5-fluorodeoxy-uridine (FUdR) exposed cells whose DNA synthesis was interfered with by the inhibition of thymidylate synthetase and the rate of ligation of short replicative intermediates, the ADPRT activity remained at a higher level than in controls. However, 3-aminobenzamide (3AB), a potent ADPRT inhibitor, showed down DNA synthesis in the S phase and also extended the S phase. These results indicate that ADP-ribosylation may be involved in DNA replication and cell cycle progression, and suggest that ADPRT activity may be stimulated by transient short fragments of newly replicated DNA, exerting its effects at the later stages of DNA replication, most probably at the ligation step of DNA synthesis.
通过将烟酰胺腺嘌呤二核苷酸（3H-NAD+）掺入通透细胞的酸不溶性部分以及完整FL细胞中ADPRT唯一底物NAD的细胞含量变化，证实了腺苷二磷酸核糖基转移酶（ADPRT）活性的细胞周期依赖性波动。ADPRT活性在G1期最低，在S/G2-G2期最高。阿非迪霉素，一种DNA聚合酶α的特异性抑制剂，消除了ADPRT活性的波动。同时，在5-氟脱氧尿苷（FUdR）处理的细胞中，其DNA合成因胸苷酸合成酶的抑制和短复制中间体的连接速率而受到干扰，ADPRT活性仍高于对照组。然而，3-氨基苯甲酰胺（3AB），一种有效的ADPRT抑制剂，在S期显示DNA合成下降，并且还延长了S期。这些结果表明，ADP-核糖基化可能参与DNA复制和细胞周期进程，并表明ADPRT活性可能受到新复制DNA的瞬时短片段刺激，在DNA复制的后期发挥作用，最有可能在DNA合成的连接步骤。
