Reduction of REDD1 expression by IL-6
This project focuses on the analysis of a new interaction between inflammatory and metabolic cellular signalling pathways.
The kinase mTOR is a central mediator of cellular growth and metabolism. Activation of mTOR occurs through growth-promoting metabolic signals and after stimulation with cytokines. Cellular stress caused by ionising radiation, metabolic messengers such as insulin, but also drugs such as chemotherapeutic agents or glucocorticoids inhibit mTOR. This inhibition is mediated by the induction of the regulatory protein REDD1 (DDIT4). In contrast, IL-6 reduces the expression of REDD1 in a STAT3-dependent manner. The reduction of REDD1 expression is independent of STAT3 function as an activating transcription factor.
In this project, we investigate the molecular mechanisms of this so far unknown non-canonical function of STAT3 and the molecular mechanisms of the interaction of inflammatory and metabolic signalling pathways.
