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嘌呤霉素氨基核苷对细胞从G1静止期向G1复制前期转变的抑制作用。

Inhibition of cellular transition from G1-resting to G1-prereplicative phase by aminonucleoside of puromycin.

作者信息

Cholon J J, Knopf R G, Pine R M

出版信息

In Vitro. 1979 Sep;15(9):736-42. doi: 10.1007/BF02618254.

Abstract

Human embryonic lung fibroblasts (IMR-90 and WI-38) were arrested in the G1 phase of the cell cycle by serum deprivation and high population density. Within 1 hr after the addition of medium containing fresh serum, these cells showed an increase in rRNA synthesis. The inclusion of 100 micrograms per ml aminonucleoside of puromycin (AMS) in the fresh medium eliminated the serum stimulation of rRNA synthesis and prevented the cells from making the G1-resting phase to G1-prereplicative phase transition. AMS also prevented the synthesis of HnRNA normally found within 10 hr after serum stimulation. Serum-stimulated RNA synthesis in starved, SV-40 transformed fibroblasts (WI-38-VA-13 cells) was inhibited, but not completely prevented, by AMS indicating that transformed cells may produce specific RNA's that are not AMS-sensitive and that may be responsible for the failure of transformed cells to be arrested in G1.

摘要

人胚肺成纤维细胞(IMR - 90和WI - 38)通过血清剥夺和高细胞密度被阻滞在细胞周期的G1期。在添加含新鲜血清的培养基后1小时内,这些细胞的rRNA合成增加。在新鲜培养基中加入每毫升100微克的嘌呤霉素氨基核苷(AMS)消除了血清对rRNA合成的刺激,并阻止细胞从G1静止期向G1复制前期转变。AMS还阻止了通常在血清刺激后10小时内出现的HnRNA的合成。在饥饿的、SV - 40转化的成纤维细胞(WI - 38 - VA - 13细胞)中,血清刺激的RNA合成受到AMS抑制,但未被完全阻止,这表明转化细胞可能产生对AMS不敏感的特定RNA,这可能是转化细胞不能被阻滞在G1期的原因。

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