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Transposons find a small RIP in NFkB pathway

机译:转座子在NFkB途径中发现一个小的RIP

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摘要

Hyperactivation of NFkB is common in a variety of human diseases. Although numerous transient regulators have been found, it is still unclear which ones can permanently sustain the abnormal status of NFkB in circumvention of several feedback mechanisms and without the associated toxicity. Activation of NFkB could be used to build readouts for genetic screening, and this phenotype has been interrogated using various forward genetics techniques. Mutants with altered activity of NFkB have been obtained using chemical mutagenesis or selected from libraries of full-length cDNAs, genetic suppressor elements or small interfering RNAs. More recently, reversible insertional mutagenesis using retroviral vectors has been tried in this system as well. The authors of the latter report used insertion of a strong promoter to generate dominant mutants, which could be distinguished from the spontaneous mutants by their dependence on the promoter function#
机译:NFkB的过度激活在多种人类疾病中很常见。尽管已经发现了许多瞬态调节器,但仍不清楚哪些能永久维持NFkB的异常状态,从而规避了几种反馈机制并且没有相关的毒性。 NFkB的激活可用于建立用于基因筛选的读数,并且已使用各种正向遗传学技术对该表型进行了询问。 NFkB活性改变的突变体已通过化学诱变获得,或选自全长cDNA,遗传抑制元件或小干扰RNA的文库。最近,在该系统中也尝试了使用逆转录病毒载体的可逆插入诱变。后者报告的作者使用了强启动子的插入来生成显性突变体,可以通过依赖于启动子功能将其与自发突变体区分开来。

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