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NSE-bcl-2转基因小鼠,一种用于研究神经元死亡和存活的模型系统。

NSE-bcl-2 transgenic mice, a model system for studying neuronal death and survival.

作者信息

Bernard R, Farlie P, Bernard O

机构信息

Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Parkville, Vic., Australia.

出版信息

Dev Neurosci. 1997;19(1):79-85. doi: 10.1159/000111188.

Abstract

Bcl-2 is a crucial regulator of cell survival and death. We have recently demonstrated that transgenic mice overexpressing the human Bcl-2 protein specifically in their neurons have an increased number of neuronal cells which can survive in tissue culture in the absence of neurotrophic factors. In order to understand why only some neurons can be rescued from developmental and neurotrophic factor deprivation-induced death, we have studied the expression pattern of the transgene during embryonic development an in adulthood. We have demonstrated that transgene expression starts in embryos at E12.5 and that only half of the sensory neurons of the dorsal root ganglia expressed detectable levels of the human Bcl-2. These results may explain why only 40% of the sensory neurons survived in tissue culture in the absence of neurotrophic factors.

摘要

Bcl-2是细胞存活与死亡的关键调节因子。我们最近证明,在其神经元中特异性过表达人类Bcl-2蛋白的转基因小鼠,在没有神经营养因子的情况下,其神经元细胞在组织培养中存活的数量有所增加。为了理解为什么只有一些神经元能够从发育和神经营养因子剥夺诱导的死亡中被挽救,我们研究了胚胎发育期间及成年期转基因的表达模式。我们已经证明,转基因表达在胚胎期E12.5开始,并且背根神经节中只有一半的感觉神经元表达可检测水平的人类Bcl-2。这些结果可能解释了为什么在没有神经营养因子的情况下,只有40%的感觉神经元在组织培养中存活。

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