Postdoc Group Gekara bei Universitätsklinikum Freiburg

Research focus:

The immune system that mediates pathogen clearance and tissue healing, and the DNA repair system that protects our genome are the primary defence system against external and internal threats. Dysregulations in these systems lay at the core of many health afflictions, including infections, autoimmune/inflammatory diseases, neurodegeneration, cancer and many age-associated health afflictions. Current research efforts are focused on the crosstalk between these defence systems, the regulatory components involved and how to target these components in disease management. Diseases of current interest include infections, inflammatory diseases and cancer. We apply multidisciplinary approaches combining cutting-edge microscopy, in vivo (in mice) imaging techniques for monitoring infections, tumors and inflammatory processes, as well as molecular/cell biology and biochemical approaches for studying protein-protein interactions and post-translational modifications. Our goal is understand fundamental biological processes with the view that some of our discoveries will benefit human health.

The advertised position is initially for three years with the possibility of renewal. The position will become available as soon as can be arranged. The job tasks include coordination of existing and initiation of independent projects within the areas of interest of the laboratory. The successful applicant will participate in the supervision of other researchers (postdocs, graduate and Master students), grant application and preparation of manuscripts. The salary will be determined in accordance with TV-L.

Please include a letter of motivation, a brief description of research accomplishments/experience (max. 3 pages), CV with publication list and 3+ contact details for referees.

Relevant publications:

• Erttmann SF, Swacha P, Aung KM, Brindefalk B, Jiang H, Härtlova A, Uhlin BE, Wai SN, Gekara NO. (2022). The gut microbiota prime systemic antiviral immunity via the cGAS-STING-IFN-I axis. Immunity. 55(5):847-861. PMID: PMID: 35545033
• Jiang H, Swacha P, Gekara NO. (2021). Nuclear AIM2-Like Receptors Drive Genotoxic Tissue Injury by Inhibiting DNA Repair. Advanced Science. 8(22). PMID: 34658166
• Jiang H, Xue X, Panda S, Kawale A, Hooy RM, Liang F, Sohn J, Sung P, Gekara NO. (2021). Chromatin-bound cGAS is an inhibitor of DNA repair and hence accelerates genome destabilization and cell death. EMBO J. 2019 Sep 23:e102718. PMID: 31544964
• Erttmann SF, Gekara NO. (2019). Hydrogen peroxide release by bacteria suppresses inflammasome-dependent innate immunity. Nat Commun. 2019 Aug 2;10(1):3493. PMID: 31375698
• Panda S, Gekara NO. (2018). The deubiquitinase MYSM1 dampens NOD2-mediated inflammation and tissue damage by inactivating the RIP2 complex. Nat Commun. 2018 Nov 7;9(1):4654. PMID: 30405132
• Erttmann SF, Härtlova A, Sloniecka M, Raffi FA, Hosseinzadeh A, Edgren T, Rofougaran R, Resch U, Fällman M, Ek T, Gekara NO. (2016). Loss of the DNA Damage Repair Kinase ATM Impairs Inflammasome-Dependent Anti-Bacterial Innate Immunity. Immunity. 2016 Jul 19;45(1):106-18. PMID: 27421701
• Panda S, Nilsson JA and Gekara NO. (2015). Deubiquitinase MYSM1 regulates innate immunity through inactivation of TRAF3 and TRAF6 complexes. Immunity. 2015 Oct 13;43(4). PMID: 26474655
• Härtlova A, Erttmann SF, Raffi FA, Schmalz AM, Resch U, Anugula S, Lienenklaus S, Nilsson LM, Kröger A, Nilsson JA, Ek T, Weiss S, Gekara NO. (2015). DNA damage primes the type I interferon system via the cytosolic DNA sensor STING to promote anti-microbi