Gunilla T Westermark
Linköping University, Sweden
E-mail: gunwe@ibk.liu.se
Phone: + 46 13 223906
Overall research program
The research in the amyloid field includes studies on amyloid induction and innate clearance of amyloid. We work with the mouse model for reactive (AA-) amyloidosis, and have established multiple monoclonal antibodies from mice clearing amyloid. We are now in progress in characterization of their capacity and role in amyloid clearance.
Our aim is to clarify the endogenous way for amyloid clearance and especially pinpoint the innate way. Our ultimate goal is to use this knowledge to trigger and stimulate the patients own healing force. In addition, the group works on the pathophysiological mechanisms behind amyloid formation in the islets of Langerhans, particularly with regard to seeding mechanisms and diets. We are in progress of setting up a Drosophila-model for studies of protein interactions.
Five key publications
1. Paulsson JF, Westermark GT: Aberrant processing of human islet amyloid
polypeptide results in increased amyloid formation Diabetes 54, 2117-2125, 2005
2. Tatarek-Nossol M, Yan LM, Schmauder A, Tenidis K, Westermark G, Kapurniotu A:
Inhibition of hIAPP amyloid-fibril formation and apoptotic cell death by a
designed hIAPP amyloid-core-containing hexapeptide Chem Biol 12:797-809, 2005
3. K Lundmark, GT Westermark, A Olsén, P Westermark: Protein fibrils occurring in
nature can induce AA amyloidosis in mice: cross-seeding as a disease
mechanism Proc Natl Acad Sci USA 102, 6098-6102, 2005
4. K Lundmark, GT Westermark, S Nyström, CL Murphy, A Solomon, P Westermark:
Transmissability of systemic amyloidosis by a prion-like mechanism Proc
Natl Acad Sci USA 99, 6979-6984, 2002
5. K Ganowiak Johan, GT Westermark, U Engström, Å Gustavsson, P Hultman, P
Westermark: Acceleration of AA-amyloidosis by amyloid-like synthetic fibrils Proc
Natl Acad Sci USA 95, 2558-2563, 1998