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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Nadja Herbach

Institute of Veterinary Pathology

Veterinaerstr. 13

80539 Munich



Name/email consistency: high



  • Institute of Veterinary Pathology, Veterinaerstr. 13, 80539 Munich, Germany. 2005 - 2009


  1. Diabetic kidney lesions of GIPRdn transgenic mice: podocyte hypertrophy and thickening of the GBM precede glomerular hypertrophy and glomerulosclerosis. Herbach, N., Schairer, I., Blutke, A., Kautz, S., Siebert, A., Göke, B., Wolf, E., Wanke, R. Am. J. Physiol. Renal Physiol. (2009) [Pubmed]
  2. Diets influence the diabetic phenotype of transgenic mice expressing a dominant negative glucose-dependent insulinotropic polypeptide receptor (GIPRdn). Herbach, N., Göke, B., Wolf, E., Wanke, R. Regul. Pept. (2008) [Pubmed]
  3. Dominant-negative effects of a novel mutated Ins2 allele causes early-onset diabetes and severe beta-cell loss in Munich Ins2C95S mutant mice. Herbach, N., Rathkolb, B., Kemter, E., Pichl, L., Klaften, M., de Angelis, M.H., Halban, P.A., Wolf, E., Aigner, B., Wanke, R. Diabetes (2007) [Pubmed]
  4. Overexpression of a dominant negative GIP receptor in transgenic mice results in disturbed postnatal pancreatic islet and beta-cell development. Herbach, N., Goeke, B., Schneider, M., Hermanns, W., Wolf, E., Wanke, R. Regul. Pept. (2005) [Pubmed]
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