In our work we address the fundamental question how alternative splicing regulates cellular function and identity. Our main model systems are body temperature-controlled alternative splicing, e.g. in a circadian setting or during fever, and immune cell activation. In addition to splicing functionality, we investigate mechanisms behind signal-induced and temperature-controlled alternative splicing, with a focus on the CLK family of kinases, as their activity reacts extremely sensitive to changes in the physiologically relevant temperature range. In another mechanistic project focused on the core spliceosome we have recently started to investigate NAGNAG alternative splicing. We employ a variety of techniques ranging from bioinformatics to RNA-protein interaction assays, in vitro splicing, minigenes, cell culture and mouse models.

See here for a newspaper article describing our work connecting body
temperature with viral infections (in German):   Tagesspiegel_Viren_und_Koerpertemperatur