Contact information
Flow Cytometry Core
Mecical Faculty
University of Cologne
Robert-Koch-Straße 21
50931 Cologne
CV
Academic education
| 2013 - 2018 | PhD programm in Genetics, IIMMIH, University Hospital Cologne, Germany |
| 2011 - 2013 | MSc, Biological Sciences, University of Cologne, Germany |
Scientific degrees
| 2018 | PhD, in Genetics, supervisor: Prof. H. Kashkar, Institute of Medical Microbiology, Immunology and Hygiene (IMMIH), University Hospital Cologne, Germany |
Scientific career
| 2024 - present | Head of Flow Cytometry Core, Medical Faculty, University of Cologne, Germany |
| 2020 - 2024 | Postdoctoral Fellow, Center for Biochemistry, H. Walczak Lab, University Hospital Cologne, Germany |
| 2018 - 2020 | Postdoctoral Fellow, IMMIH, H. Kashkar Lab, University Hospital Cologne, Germany |
Honors/ Awards/ Memberships
| 2019 | KFO-286 Advancement of Female Scientists Grant (10.000€), Cologne, Germany |
| 2018 | CECAD Travel Grant (1.000€) for Fusion Conference “The Ubiquitin System: Function, Physiology and its Role in Disease”, Nassau, Bahamas |
Publications
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Caspase-8 is the molecular switch for apoptosis, necroptosis and pyroptosis
Caspase-8 is the initiator caspase of extrinsic apoptosis1,2 and inhibits necroptosis mediated by RIPK3 and MLKL. Accordingly, caspase-8 deficiency in mice causes embryonic lethality3, which can be rescued by deletion of either Ripk3 or Mlkl4,5,6. Here we show that the expression of enzymatically…
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Mitochondrial respiration controls neoangiogenesis during wound healing and tumour growth
The vasculature represents a highly plastic compartment, capable of switching from a quiescent to an active proliferative state during angiogenesis. Metabolic reprogramming in endothelial cells (ECs) thereby is crucial to cover the increasing cellular energy demand under growth conditions. Here we…
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CHIP ubiquitylates NOXA and induces its lysosomal degradation in response to DNA damage
The BH3-only protein NOXA is a regulator of mitochondrial apoptosis by specifically antagonizing the anti-apoptotic protein MCL-1. Here we show that the E3 ubiquitin ligase CHIP controls NOXA stability after DNA damage. Our findings reveal that CHIP and MCL-1 are binding partners of NOXA and…