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胰岛素在血清饥饿的胶质瘤细胞中引发的瞬时凋亡涉及Fas/Fas-L和Bcl-2。

Transient apoptosis elicited by insulin in serum-starved glioma cells involves Fas/Fas-L and Bcl-2.

作者信息

Yang B C, Wang Y S, Wang C H, Lin H H, Tang M J, Yang T L

机构信息

Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, Republic of China.

出版信息

Cell Biol Int. 1999;23(8):533-40. doi: 10.1006/cbir.1999.0408.

Abstract

The expression of fas gene in glioma cells varies with growth stage. When insulin-elicited transient apoptosis of glioma cells was in progress, the expression of fas gene increased at both transcriptional and translational levels. In contrast, the expression of fas-L gene in glioma cells remained constant. Apoptosis occurred in the cells having high level of surface Fas protein. When the expression of Fas-L in U-373MG cells was suppressed by ribozyme, the insulin-elicited transient apoptosis vanished. Overexpression of Bcl-2 in U-373MG cells did not alter significantly the cell cycle progression and the expression of fas gene. However, these cells were resistant to insulin-trigged death. Therefore, insulin-elicited apoptosis involved Fas-related death signal, and which could be prevented by the protective effect of Bcl-2.

摘要

fas基因在胶质瘤细胞中的表达随生长阶段而变化。当胰岛素诱导胶质瘤细胞发生短暂凋亡时,fas基因在转录和翻译水平上的表达均增加。相比之下,胶质瘤细胞中fas-L基因的表达保持恒定。凋亡发生在表面Fas蛋白水平较高的细胞中。当U-373MG细胞中Fas-L的表达被核酶抑制时,胰岛素诱导的短暂凋亡消失。U-373MG细胞中Bcl-2的过表达并未显著改变细胞周期进程和fas基因的表达。然而,这些细胞对胰岛素触发的死亡具有抗性。因此,胰岛素诱导的凋亡涉及Fas相关死亡信号,并且可被Bcl-2的保护作用所阻止。

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