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阿非科林对腺病毒DNA合成和细胞DNA合成的差异作用。

Differential effect of aphidicolin on adenovirus DNA synthesis and cellular DNA synthesis.

作者信息

Kwant M M, van der Vliet P C

出版信息

Nucleic Acids Res. 1980 Sep 11;8(17):3993-4007. doi: 10.1093/nar/8.17.3993.

Abstract

There is strong evidence for a participation of DNA polymerase gamma in the replication of adenovirus (Ad) DNA. To study a possible additional role of DNA polymerase alpha we measured the effect of aphidicolin on viral DNA replication. In intact cells, aphidicolin inhibits Ad DNA synthesis weakly. The drug concentration required for 50% inhibition of Ad DNA replication was 300-400 fold higher than for a similar effect on cellular DNA synthesis. Such a differential inhibition was also observed in AGMK cells doubly infected with SV40 and the simian adenovirus SA7. No evidence was found for modification of aphidicolin in infected cells or for a change in aphidicolin sensitivity of DNA polymerase alpha after infection. The extent of inhibition of purified DNA polymerase alpha was dependent upon the dCTP concentration. The same situation was observed when DNA synthesis was studied in isolated nuclei from uninfected cells. However, in nuclei from Ad infected cells no effect of dCTP on aphidicolin sensitivity was found. These results were taken as evidence that DNA polymerase alpha does not participate in the replication of adenovirus DNA.

摘要

有充分证据表明DNA聚合酶γ参与腺病毒(Ad)DNA的复制。为了研究DNA聚合酶α可能的其他作用,我们测定了阿非科林对病毒DNA复制的影响。在完整细胞中,阿非科林对Ad DNA合成的抑制作用较弱。抑制50%的Ad DNA复制所需的药物浓度比抑制细胞DNA合成的类似作用所需浓度高300 - 400倍。在同时感染SV40和猴腺病毒SA7的AGMK细胞中也观察到了这种差异抑制。未发现感染细胞中阿非科林有修饰,也未发现感染后DNA聚合酶α对阿非科林的敏感性发生变化。纯化的DNA聚合酶α的抑制程度取决于dCTP浓度。在未感染细胞分离的细胞核中研究DNA合成时也观察到了同样的情况。然而,在Ad感染细胞的细胞核中,未发现dCTP对阿非科林敏感性有影响。这些结果被视为DNA聚合酶α不参与腺病毒DNA复制的证据。

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The effect of aphidicolin on adenovirus DNA synthesis.阿非科林对腺病毒DNA合成的影响。
Nucleic Acids Res. 1979 Jul 25;6(10):3369-86. doi: 10.1093/nar/6.10.3369.

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The mechanism of adenovirus-DNA synthesis in isolated nuclei.分离细胞核中腺病毒DNA合成的机制。
Eur J Biochem. 1972 Nov 7;30(3):584-92. doi: 10.1111/j.1432-1033.1972.tb02130.x.

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