Boosting autophagy and career- Konstantin Sparrer awarded with Young Investigator Fund

Together with the Schering Stiftung, the Fritz Thyssen Foundation offers start-up grants to realize promising research ideas by young scientists. Dr. Konstantin Sparrer, a Marie Skłodowska-Curie fellow at the Institute of Molecular Virology is granted a Young Investigator Fund starting in January 2019 to support his projects.

The program specifically targets highly motivated young investigators who want to start their independent research career. Konstantin explores the complex interplay between viruses and cellular anti-viral autophagy1,2. His aim is to modulate this cellular degradation pathway to promote anti-viral host responses. Konstantin specifies: “We want to use human-derived peptides for the development of highly specific anti-viral drugs, which boost our own anti-viral defenses.”

Thus, his project is closely associated with CRC1279 (see also article from 20.09.2018: Young researchers realizing innovative ideas). Together with Carina Conzelmann, a PhD student at the Institute of Molecular Virology, he recently initiated a “screening group”. This initiative will help to optimize and simplify the interaction between the different groups working with peptide libraries within CRC1279. With his great expertise in innate immunity and virology as well as his innovative ideas and methodologies, Konstantin Sparrer productively contributes to and complements our CRC. The grant will be used for technical assistance and consumables and is an excellent starting basis for Konstantin to establish his independent junior research group and apply for a subsequent multiannual third-party funding.

For more information about the grant see:

“Boost Your Research – Young Investigator Fund for Innovative Research Ideas”

1Sparrer, Konstantin MJ, and Michaela U. Gack. "TRIM proteins: New players in virus-induced autophagy." PLoS pathogens 14.2 (2018): e1006787.  

2Sparrer, Konstantin MJ, et al. "TRIM23 mediates virus-induced autophagy via activation of TBK1." Nature microbiology 2.11 (2017): 1543.