1 results match your criteria: "Switzerland (C.Wolfrum); and German Centre for Cardiovascular Research[Affiliation]"
Adam17 Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling in Mice.
Arterioscler Thromb Vasc Biol
February 2017
From the Institute of Laboratory Medicine (A.N., B.H.N., K.S., A.H., A.K., D.T., L.M.H.) and Institute for Cardiovascular Prevention (Z.Z., C.Weber, S.S.), Ludwig-Maximilians-University Munich, Germany; Institute of Biochemistry, Christian Albrechts University, Kiel, Germany (A.C., S.R.-J.); Institute of Food, Nutrition and Health, ETH Zurich, Schwerzenbach, Switzerland (C.Wolfrum); and German Centre for Cardiovascular Research, partner site Munich Heart Alliance, Germany (C. Weber, S.S.).
Objective: ADAM17 (a disintegrin and metalloproteinase 17) is a sheddase releasing different types of membrane-bound proteins, including adhesion molecules, cytokines, and their receptors as well as inflammatory mediators. Because these substrates modulate important mechanisms of atherosclerosis, we hypothesized that ADAM17 might be involved in the pathogenesis of this frequent disease.
Approach And Results: Because Adam17-knockout mice are not viable, we studied the effect of Adam17 deficiency on atherosclerosis in Adam17 hypomorphic mice (Adam17), which have low residual Adam17 expression.