Group Leader, Institute of Experimental Genetics, Research Group ‘Functional Genetics’
Dr. Rer. Nat. Gerhard Przemeck
“Insulin is a treatment, but not a cure”, said Nobel laureate Frederick Banting. Today, diabetics usually need daily medication for life. And tomorrow? Cure diabetes with a single treatment – that’s what we work for!
Together with Martin Hrabě de Angelis, Gerhard heads the Functional Genetics group. The group has many years of experience in genetic engineering of mouse models and thorough phenotyping. Their focus in on molecular signaling pathways and pathophysiological events leading to metabolic disorders and diabetes. Recently, they examined the contributions of developmental control genes to metabolic processes and maintenance of the adult pancreas. By transferring their results from basic research, the group is developing novel therapy strategies. In this context, they are piloting gene therapy approaches for various forms for hereditary diabetes.
Fields of Work and Expertise
Mouse models for metabolic diseases Monogenic diabetes Gene therapy ENU mutagenesis Embryogenesis Developmental Biology
Professional Background
Gerhard, a developmental geneticist by training, joined Helmholtz Munich in 1998 at what was then the Institute of Mammalian Genetics, where he investigated the influence of the Delta/Notch signaling pathway on the formation of the left-right body axis. Gerhard received his PhD in genetics form the Ludwig-Maximilians University in Munich, where he studied cell expansion in the plant embryo in the group of Prof. Thomas Berleth. He studied biology at the Ludwig-Maximilians University and received his diploma for his work on the plant transcription factor Monopteros. In 2000, Gerhard moved to the newly founded Institute of Experimental Genetics, where he was involved in setting up the institute’s infrastructure and the German Mouse Clinic I.
Honors and Awards
- PhD Scholarship, Konrad-Adenauer-Foundation 1994-1997
- Paula-and-Richard-von Hertwig-Award for Interdisciplinary Research 2003
Selected Publications
Kandaswamy, S. ; Zobel, L. ; John, B. ; Santhiya, S.T. ; Bogedein, J. ; Przemeck, G.K.H. ; Gailus-Durner, V. ; Fuchs, H. ; Biel, M. ; Hrabě de Angelis, M. ; Graw, J. ; Michalakis, S. ; Amarie, O.V.
Mutations within the cGMP-binding domain of CNGA1 causing autosomal recessive retinitis pigmentosa in human and animal model.Chhabra, N.F. ; Amend, A.-L. ; Bastidas-Ponce, A. ; Sabrautzki, S. ; Tarquis Medina, M. ; Sachs, S. ; Rubey, M. ; Lorenz-Depiereux, B. ; Feuchtinger, A. ; Bakhti, M. ; Lickert, H. ; Przemeck, G.K.H. ; Hrabě de Angelis, M.
A point mutation in the Pdia6 gene results in loss of pancreatic β-cell identity causing overt diabetes.Chhabra, N.F. ; Amarie, O.V. ; Wu, M. ; Amend, A.-L. ; Rubey, M. ; Gradinger, D. ; Irmler, M. ; Beckers, J. ; Rathkolb, B. ; Wolf, E. ; Feuchtinger, A. ; Huypens, P. ; Teperino, R. ; Rozman, J. ; Przemeck, G.K.H. ; Hrabě de Angelis, M.
PAX6 mutation alters circadian rhythm and beta cell function in mice without affecting glucose tolerance.Rubey, M. ; Chhabra, N.F. ; Gradinger, D. ; Sanz-Moreno, A. ; Lickert, H. ; Przemeck, G.K.H. ; Hrabě de Angelis, M.
DLL1- and DLL4-mediated Notch signaling is essential for adult pancreatic islet homeostasis.Yan, X. ; Atorf, J. ; Ramos, D. ; Thiele, F. ; Weber, S. ; Dalke, C. ; Sun, M. ; Puk, O. ; Michel, D. ; Fuchs, H. ; Klaften, M. ; Przemeck, G.K.H. ; Sabrautzki, S. ; Favor, J. ; Ruberte, J. ; Kremers, J. ; Hrabě de Angelis, M. ; Graw, J. ; German Mouse Clinic Consortium
Mutation in Bmpr1b leads to optic disc coloboma and ventral retinal gliosis in mice.Sabrautzki, S. ; Kaiser, G. ; Przemeck, G.K.H. ; Gerst, F. ; Lorza-Gil, E. ; Panse, M. ; Sartorius, T. ; Hoene, M. ; Marschall, S. ; Häring, H.-U. ; Hrabě de Angelis, M. ; Ullrich, S.
Point mutation of Ffar1 abrogates fatty acid-dependent insulin secretion, but protects against HFD-induced glucose intolerance.Tiedemann, H.B. ; Schneltzer, E. ; Beckers, J. ; Przemeck, G.K.H. ; Hrabě de Angelis, M.
Modeling coexistence of oscillation and Delta/Notch-mediated lateral inhibition in pancreas development and neurogenesis.Chhabra, N.F. ; Wu, M. ; Fütterer, M. ; Irmler, M. ; Beckers, J. ; Götz, M. ; Rozman, J. ; Przemeck, G.K.H. ; Hrabě de Angelis, M.
Systemic metabolic effects exerted by a point mutation in the RED subdomain of PAX6.Fütterer, M. ; Chhabra, N.F. ; Irmler, M. ; Beckers, J. ; Przemeck, G.K.H. ; Hrabě de Angelis, M.
Dll1-and Dll4-mediated Notch signalling in adult pancreatic beta cells is essential for the structural integrity of islets and maintenance of glucose homeostasis.
