Regulation of SAMHD1: impact on inflammation, viral replication and malignant diseases
SAMHD1, a known antiviral factor, has been attributed many novel functions and is frequently mutated in a variety of cancer types. It is hypothesised that downregulated or mutated SAMHD1 might trigger a type I interferon-mediated response that contributes to a pro-tumor microenvironment. In the last funding period, we identified the phosphatase PP2A-B55α acting on SAMHD1 as a main regulator to turn on the antiviral activity. A key to understand the role of SAMHD1 in chronic viral infections and cancer will be to characterize the further impact of (phospho)-regulation and the impact of cancer-associated mutations on the diverse functions of SAMHD1, the IFN environment and tumorigenicity.
Principal Investigator:
Dr. Renate König
(Photo: PEI, Langen)