Karina Reiss

Consolidated Researcher Details:

Department of Dermatology, University of Kiel
Research Area:
Prof. Dr. rer. nat.
Karina Reiss
kreiss [at] dermatology.uni-kiel.de
+49 (0) 431 / 500 - 21 330
Researcher ID: B-3175-2010

Why this profession?

During my biology studies I developed major interests in two fields of cellular biology: one of them was the immune system and the other was the nervous system. To address the first issue I spent one year at the Research Center Borstel analyzing the role of NK cell activation for bladder cancer therapy. Afterwards, I took the opportunity to address my second field of interest at the Institute of Anatomy in Kiel and analyzed the mechanisms of neuronal migration during ontogenesis. Growing interest in neuronal pathology prompted me take a scientific assistant position at the Institute of Biochemistry, Kiel in 2002, where I studied the molecular mechanisms of Alzheimer`s disease. I have a lasting interest in the function and regulation of the proteases involved in the cleavage of the Amyloid-Precursor-Protein, namely the alpha-secretases (ADAMs) and the beta-secretase. In 2006, I took up a junior professorship and extended my studies, since we learned that these enzymes are critically involved in several other physiologic (developmental, homeostatic) processes as well as in pathology (tumour progression, inflammation). Thus, my scientific interest focused on the regulation and dysregulation of transmembrane proteases in inflammatory diseases. In 2008, I was appointed to a W2 professorship in the Cluster of Excellence at the Department of Dermatology at the University of  Kiel. Since then, I am still interested in understanding the molecular mechanisms of protease regulation and the relevance of transmembrane proteases for inflammatory disorders. One new aspect of our analyses that we are now addressing is the role of environmental and epigenetic influence on our favourite enzymes.

Why RTG Genes, Environment and Inflammation?

Our major interest focuses on the regulation of transmembrane proteases such as ADAMs (A Disintegrin and Metalloprotease). Any imbalance of these enzymes can have severe consequences for several diseases (atherosclerosis, inflammatory bowel disease, tumour progression). Too much enzyme activity will propagate inflammatory processes. Too little enzyme activity could have the same effects, because these proteins are required to maintain cellular homeostasis. Thus, it is mandatory that we increase our knowledge about the mechanisms of enzyme regulation. So far, only the modulation of protein localization and maturation has been described, while environmental or genetic influences have not been addressed. The RTG project enables us to interact and cooperate with colleagues who are experts in the field of such analyses. Thus, we can now join forces and hopefully obtain new insights into the complex process of inflammation and the role and regulation of transmembrane proteases in this context.