The loss of Nucleoside Diphosphate Kinase (NDPK) B but not of the similarly abundant isoform NDPK A
blunts VEGF-driven angiogenic responses in animal models (zebrafish, mice) and in cultured
endothelial cells. NDPK B is a not well characterized regulator of major signaling cascades acting either
as a scaffold protein or as a protein histidine kinase on G proteins and KCa3.1 potassium channels. The
project aims to identify the mechanisms by which NDPK B preferentially influences pathological
angiogenesis. We will therefore investigate a) the role of NDPK B and its complex partners in VEGFinduced
opening of endothelial junctions and b) the importance of NDPK B as a constitutive activator of
KCa3.1 during vascular remodeling.