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@ARTICLE{Fantin:120520,
      author       = {A. Fantin and A. Lampropoulou and V. Senatore and J. T.
                      Brash and C. Prahst and C. A. Lange and S. E. Liyanage and
                      C. Raimondi and J. W. Bainbridge and H. G. Augustin$^*$ and
                      C. Ruhrberg},
      title        = {{VEGF}165-induced vascular permeability requires {NRP}1 for
                      {ABL}-mediated {SRC} family kinase activation.},
      journal      = {Journal of experimental medicine},
      volume       = {214},
      number       = {4},
      issn         = {1540-9538},
      address      = {New York, NY},
      publisher    = {Rockefeller Univ. Press},
      reportid     = {DKFZ-2017-00949},
      pages        = {1049 - 1064},
      year         = {2017},
      abstract     = {The vascular endothelial growth factor (VEGF) isoform
                      VEGF165 stimulates vascular growth and hyperpermeability.
                      Whereas blood vessel growth is essential to sustain organ
                      health, chronic hyperpermeability causes damaging tissue
                      edema. By combining in vivo and tissue culture models, we
                      show here that VEGF165-induced vascular leakage requires
                      both VEGFR2 and NRP1, including the VEGF164-binding site of
                      NRP1 and the NRP1 cytoplasmic domain (NCD), but not the
                      known NCD interactor GIPC1. In the VEGF165-bound receptor
                      complex, the NCD promotes ABL kinase activation, which in
                      turn is required to activate VEGFR2-recruited SRC family
                      kinases (SFKs). These results elucidate the receptor complex
                      and signaling hierarchy of downstream kinases that transduce
                      the permeability response to VEGF165. In a mouse model with
                      choroidal neovascularisation akin to age-related macular
                      degeneration, NCD loss attenuated vessel leakage without
                      affecting neovascularisation. These findings raise the
                      possibility that targeting NRP1 or its NCD interactors may
                      be a useful therapeutic strategy in neovascular disease to
                      reduce VEGF165-induced edema without compromising vessel
                      growth.},
      cin          = {A190},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {321 - Basic Concepts (POF3-321)},
      pid          = {G:(DE-HGF)POF3-321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28289053},
      pmc          = {pmc:PMC5379968},
      doi          = {10.1084/jem.20160311},
      url          = {https://inrepo02.dkfz.de/record/120520},
}