BCL-2 INHIBITION OF NEURAL DEATH - DECREASED GENERATION OF REACTIVE OXYGEN SPECIES
BCL-2 INHIBITION OF NEURAL DEATH - DECREASED GENERATION OF REACTIVE OXYGEN SPECIES
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DOI：
10.1126/science.8235659
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发表时间：
1993-11-19
期刊：
影响因子：
56.9
通讯作者：
BREDESEN, DE
中科院分区：
文献类型：
--
作者：
KANE, DJ;SARAFIAN, TA;BREDESEN, DE
原癌基因bcl-2抑制凋亡和坏死神经细胞死亡。Bcl-2在GT1-7神经细胞系中的表达可防止谷胱甘肽耗竭导致的死亡。在缺乏谷胱甘肽的对照细胞中，细胞内活性氧和脂质过氧化物迅速增加，而表达Bcl-2的细胞则表现出迟钝的增加和完全存活。活性氧增加的调节影响细胞死亡的程度。酵母超氧化物歧化酶无效的突变体通过Bcl-2的表达部分获救。因此，Bcl-2通过减少活性氧的净细胞生成来防止细胞死亡。
The proto-oncogene bcl-2 inhibits apoptotic and necrotic neural cell death. Expression of Bcl-2 in the GT1-7 neural cell line prevented death as a result of glutathione depletion. Intracellular reactive oxygen species and lipid peroxides rose rapidly in control cells depleted of glutathione, whereas cells expressing Bcl-2 displayed a blunted increase and complete survival. Modulation of the increase in reactive oxygen species influenced the degree of cell death. Yeast mutants null for superoxide dismutase were partially rescued by expression of Bcl-2. Thus, Bcl-2 prevents cell death by decreasing the net cellular generation of reactive oxygen species.