Adenovirus-mediated overexpression of novel mutated IκBα inhibits nuclear factor κB activation in endothelial cells  

作　　者：ZHOU Lin-fu YIN Kai-sheng ZHU Zi-lu ZHU Yi YAO Xin MAO Hui XIE Wei-ping HUANG Mao 

机构地区：[1]Department of Respiratory Medicine, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China [2]Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing 210029, China

出　　处：《Chinese Medical Journal》2005年第17期1422-1428,共7页中华医学杂志（英文版）

基　　金：This study was supported by grants from the National Youth NaturalScience Foundation of China(No.30400191)and the Key Subjectof’135’Project of Jiangsu Province(No.20013102).

摘　　要：Nuclear factor κB （NF-κB） overactivation, requiring phosphorylation and degradation of its inhibitor IκBα, is the basis for chronicity of airway inflammation in asthma. Based on our previous plasmid pShuttle-IκBα, carrying an IκBα gene from human placenta, we optimized a novel IκBα mutant （IκBα） gene, constructed and characterized its replication-deficient recombinant adenovirus （AdIκBαM）, and tested whether AdIκBαM-mediated overexpression of IκBαM could inhibit the NF-κB activation in endothelial cells.Nuclear factor κB （NF-κB） overactivation, requiring phosphorylation and degradation of its inhibitor IκBα, is the basis for chronicity of airway inflammation in asthma. Based on our previous plasmid pShuttle-IκBα, carrying an IκBα gene from human placenta, we optimized a novel IκBα mutant （IκBα） gene, constructed and characterized its replication-deficient recombinant adenovirus （AdIκBαM）, and tested whether AdIκBαM-mediated overexpression of IκBαM could inhibit the NF-κB activation in endothelial cells.

关 键 词：IκBα mutant nuclear factor κB recombinant adenovirus gene therapy asthma 

分 类 号：R373[医药卫生—病原生物学]