Vice President Drug Discovery, Director Sealy Institute Drug Discovery
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Sever was born and raised in Zagreb, Croatia. In 1990 she began graduate school in Molecular Biology at the Faculty of Science, University of Zagreb. She came to the United States in 1993 as a visiting graduate student in the Molecular Biophysics and Biochemistry Department at Yale University, joining the laboratory of Professor Dieter Soll. There she studied the molecular mechanisms by which aminoacyl-tRNA synthetases recognize their amino acids. After graduating in 1996 with a PhD in Molecular Biology she joined the laboratory of Professor Sandra Schmidt at the Scripps Research Institute in La Jolla. There where she initiated her studies on the role of dynamin in endocytosis. In 2002, she joined the faculty at Harvard Medical School (HMS) as an assistant professor in the Department of Medicine, and she established her laboratory within the Nephrology Division at Massachusetts General Hospital in Boston. There she initiated her studies on the role of dynamin in kidney-specific cells, podocytes. She was promoted into associate professor of Medicine at Harvard Medical School in 2018. Recently, she has expended her studies on the role of a soluble form of urokinase-type plasminogen activator receptor urokinase activator receptor, suPAR, in kidney diseases. In 2024, she joined the Sealy Institute for Drug Discover (SIDD) at the University of Texas Medical Branch as its Director.
Dr. Sever’s lab has made the following contributions to our understanding of dynamin’s role in endocytosis and the interplay between the immune system and kidney injury:
- identified direct dynamin-actin interactions, and showed that those interactions regulate dynamin oligomerization in the cytoplasm
- shown that dynamin oligomerization induces F-actin polymerization by displacing gelsolin from the barbed ends
- shown that small molecule allosteric activator of actin-dependent dynamin oligomerization ameliorates diverse types of chronic kidney injury
- shown that dynamin oligomers crosslink F-actin into bundles and networks, which underlies cell polarity, and protects kidney-specific cells from acute injury
- shown that proteolytic product of uPAR, D2D3 protein, causes simultaneous injury to two different cell types: kidney podocytes and b-cells of the pancreas
