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[甲基亚硝基胍对人和动物细胞DNA合成的影响。对异步和同步培养细胞中DNA合成的抑制作用]

[The effect of methylnitronitrosoguanidine on DNA synthesis in human and animal cells. Inhibition of DNA synthesis in asynchronous and synchronous cultured cells].

作者信息

Dulatova Sh N, Liapunova N A

出版信息

Mol Gen Mikrobiol Virusol. 1985 Sep(9):23-7.

PMID:3916233
Abstract

Methylnitronitrosoguanidine (MNNG) is reported to inhibit DNA synthesis in intact human cells, in the cells from patients with ataxia telangiectasia (AT) or the cells from two rodent species. DNA synthesis in different cell lines exhibits varying sensitivity to MNNG inhibitory effect. 4-5-fold higher concentrations of MNNG are required for 50% inhibition of DNA synthesis in AT cells or in field vole cells as compared with the concentration required for human cells or Chinese hamster. The different compactness of two chromatin fractions might possibly result in lower sensitivity of DNA synthesis in heterochromatin to MNNG-induced inhibition as compared with the sensitivity of euchromatin. The genetic expression of AT defect on the cellular level is supposed to be connected with changes in supramolecular packaging of chromatin in interphase nuclei.

摘要

据报道,甲基硝基亚硝基胍(MNNG)可抑制完整人类细胞、共济失调毛细血管扩张症(AT)患者的细胞或两种啮齿动物的细胞中的DNA合成。不同细胞系中的DNA合成对MNNG的抑制作用表现出不同的敏感性。与人类细胞或中国仓鼠相比,AT细胞或田鼠细胞中50%抑制DNA合成所需的MNNG浓度要高4-5倍。两种染色质组分的不同紧密程度可能导致异染色质中DNA合成对MNNG诱导抑制的敏感性低于常染色质。AT缺陷在细胞水平上的基因表达被认为与间期核中染色质超分子包装的变化有关。

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