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

点击翻译按钮获取中文摘要

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.