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Michael Kracht: The role of CDK - NF-κB crosstalk in shaping de novo protein synthesis, shedding and secretion of inflammatory mediators

Michael Kracht plans to characterize the mechanisms by which CDK family members affect the NF-κB-driven de novo protein synthesis and the release of immunomodulatory regulatory mediators with a specific focus on the less well-characterized members of the CDK family. He will also analyze the role of the CDK-NF-kB crosstalk for the expression of checkpoint inhibitors such as PD-L1/2. He will track the source of secreted factors and identify the responding cells within co-culture systems or more complex models such as precision-cut tumor slices provided by the consortium.

Fig. 4 The different NF-κB signaling pathways (canonical IκBa, IKKa/b; non-canonical characterized by p100 processing; atypical NF-κB associated with ATM phosphorylation) are analyzed in tumor cells to unravel their impact on the secretome and its biological function. The role of the interaction of NF-κB signaling with CDKs for shaping de novo protein synthesis, shedding and secretion of inflammatory mediators and their impact on plasticity and function of tumor-associated immune cells will be investigated.