During my undergraduate studies in Chemistry I majored in Biochemistry. I therefore decided to carry out a biochemical PhD project on hyaluronan at the Max-Planck-Institute of Biochemistry in Martinsried/Germany. In 1988, I joined Dr. Rupert Timpl, a world-renowned expert in extracellular matrix proteins, as a post-doc at the Max-Planck-Institute and worked mainly on the structure/function relationship of extracellular matrix/basement membrane proteins. Research to which I have contributed has involved the biochemical study of nidogen, a major component of basement membranes, and the identification of its binding repertoire to collagen type IV, perlecan and laminin. Of special importance was the identification of the nidogen-binding site within the laminin g1 chain, its characterisation as a single epidermal growth factor-like module of 56 amino acids and its structural characterisation. This work had world-wide impact and generated a model how basement membranes are assembled.
In 1992, I moved to the Max-Planck Research Group for extracellular matrix in Erlangen. During that period I initiated in vivo analysis of basement membrane proteins and their cellular receptors using mouse knock-out technology. From 1993-2001, I worked in the Max-Planck-Institute of Biochemistry in Martinsried/Germany as an independent senior scientist in the Department of Protein Chemistry (head: Dr. Rupert Timpl) and established my research group. We were first in demonstrating that mutations in integrin alpha7 lead to a muscular dystrophy and we were amongst the first groups introducing subtle mutations in mice, which allowed us to study a protein-protein interaction in vivo.
In 2000 I joined the Wellcome Trust Centre for Cell-Matrix research at the University of Manchester and finally moved to the School of Biological Sciences at the University of East Anglia in 2006 as Professor of Cell Biology.
I am still deeply connected with the research area I was trained in as a PhD student and Post-doc, but am taking now a broader approach to understand disease mechanisms when cells fail to communicate with their environment, especially in skeletal muscle.
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