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truncations相关的网络例句

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与 truncations 相关的网络例句 [注:此内容来源于网络,仅供参考]

The junction sequences between T-DNA borders and the rice genome were determined for the left borders of 233 T-DNA insertions and the right borders of 190 T-DNA insertions. The results showed that truncations of T-DNA borders, insertions of filler DNA and the formation of inverted and direct repeat occurred during T-DNA integration.

分析了233个T-DNA左边界和190个'l&-DNA /ti 边界与水稻基因组交接位点的序列,结果表明T-DNA在整合过程中不仅伴随着左右边界序列的缺失及&filler DNA的插入,而且还以单拷贝或多拷贝的形式插入在基因组中的同一个位点。

To investigate the function of Nogo-A in neurons, human embryonic kidney cell line 293FT was used as a model, along with the pathway profiling reporter system to check the involvement of Nogo-A in regulating the intracellular signaling pathway. It was found that over-expression of Nogo-A could activate NF-κB signaling specifically, then followed by using different Nogo-A alternative splicing isoforms and a serial of truncations, it was confirmed that the activation of NF-κB by Nogo-A relied on its N-terminal proline rich domain. Furthermore, by co-expressing the dominant negative mutants of some NF-κB pathway associated proteins, it revealed that the IκBα,TRAF6, Rac/Cdc42 were involved in Nogo-A inducing activation of NF-κB.

为探讨神经元内Nogo-A的功能,以HEK293FT细胞为模型,利用信号途径报告基因系统筛选过表达Nogo-A对多种信号途径的调控作用,发现过表达Nogo-A能特异激活NF-κB信号,利用不同的Nogo-A剪接体和截断体形式研究,证明Nogo-A激活NF-κB信号依赖于其氨基端的proline rich结构域,进一步使用NF-κB信号途径相关分子显性突变体揭示IκBα、TRAF6、 Rac/Cdc42 参与Nogo-A激活NF-κB信号。

Since antibodies are frequently available from related biochemical studies, they can often be applied more readily than molecular biology (point mutants, truncations, molecular engineering). However, it seems MOBO gets faster and easier with each passing year.

由于单链抗体相对容易获得,它比一般通过分子生物学改造蛋白,比如截短、点突变等更加方便。

To investigate the function of Nogo-A in neurons, human embryonic kidney cell line 293FT was used as a model, along with the pathway profiling reporter system to check the involvement of Nogo-A in regulating the intracellular signaling pathway. It was found that over-expression of Nogo-A could activate NF-KB signaling specifically, then followed by using different Nogo-A alternative splicing isoforms and a serial of truncations, it was confirmed that the activation of NF-kB by Nogo-A relied on its N-terminal proline rich domain. Furthermore, by co-expressing the dominant negative mutants of some NF-kB pathway associated proteins, it revealed that the IkBα,TRAF6, Rac/Cdc42 were involved in Nogo-A inducing activation of NF-kB.

为探讨神经元内Nogo-A的功能,以HEK293FT细胞为模型,利用信号途径报告基因系统筛选过表达Nogo-A对多种信号途径的调控作用,发现过表达Nogo-A能特异激活NF-kB信号,利用不同的Nogo-A剪接体和截断体形式研究,证明Nogo-A激活NF-kB信号依赖于其氨基端的proline rich结构域,进一步使用NF-KB信号途径相关分子显性突变体揭示IkBα、TRAF6、Rac/Cdc42参与Nogo-A激活NF-kB信号。

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