Role of atypical IκB protein IκBζ in HCC formation (A06)

A06项目（Schulze-Osthoff/Hailfinger；非典型IκB蛋白IκBζ在HCC形成中的作用）表明，一类新的非典型核IκB蛋白不仅增加了tnf诱导的信号传导的复杂性，而且通过调节一组选定的靶基因的表达来影响肝癌的发生，包括编码关键调节细胞因子的基因，如IL-6、IL-10和CCL2。i - κ b ζ缺乏使小鼠对HCC产生抗性，因此该项目旨在确定非典型i - κ b蛋白致癌功能背后的机制。

Project A06 (Schulze-Osthoff/Hailfinger; Role of atypical IκB protein IκBζ in HCC formation) has shown that a new class of atypical nuclear IκB proteins not only adds complexity to TNF-induced signaling but influences liver carcinogenesis via modulating the expression of a selected set of target genes including those encoding key regulatory cytokines, such as IL-6, IL-10, and CCL2. IκBζ deficiency renders mice resistant to HCC development and therefore the project aims at identifying the mechanism behind the oncogenic function of atypical IκB proteins.