% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Feng:119929,
      author       = {Y. Feng and S. Gross and N. M. Wolf and V. M. Butenschön
                      and Y. Qiu and K. Devraj and S. Liebner and J. Kroll$^*$ and
                      E. Y. Skolnik and H.-P. Hammes and T. Wieland},
      title        = {{N}ucleoside diphosphate kinase {B} regulates angiogenesis
                      through modulation of vascular endothelial growth factor
                      receptor type 2 and endothelial adherens junction proteins.},
      journal      = {Arteriosclerosis, thrombosis, and vascular biology},
      volume       = {34},
      number       = {10},
      issn         = {1524-4636},
      address      = {Philadelphia, Pa.},
      publisher    = {Lippincott, Williams $\&$ Wilkins},
      reportid     = {DKFZ-2017-00520},
      pages        = {2292 - 2300},
      year         = {2014},
      abstract     = {Nucleoside diphosphate kinase B (NDPKB) participates in the
                      activation of heterotrimeric and monomeric G proteins, which
                      are pivotal mediators in angiogenic signaling. The role of
                      NDPKB in angiogenesis has to date not been defined.
                      Therefore, we analyzed the contribution of NDPKB to
                      angiogenesis and its underlying mechanisms in
                      well-characterized in vivo and in vitro models.Zebrafish
                      embryos were depleted of NDPKB by morpholino-mediated
                      knockdown. These larvae displayed severe malformations
                      specifically in vessels formed by angiogenesis.
                      NDPKB-deficient (NDPKB(-/-)) mice were subjected to
                      oxygen-induced retinopathy. In this model, the number of
                      preretinal neovascularizations in NDPKB(-/-) mice was
                      strongly reduced in comparison with wild-type littermates.
                      In accordance, a delayed blood flow recovery was detected in
                      the NDPKB(-/-) mice after hindlimb ligation. In in vitro
                      studies, a small interfering RNA-mediated knockdown of NDPKB
                      was performed in human umbilical endothelial cells. NDPKB
                      depletion impaired vascular endothelial growth factor
                      (VEGF)-induced sprouting and hampered the VEGF-induced
                      spatial redistributions of the VEGF receptor type 2 and
                      VE-cadherin at the plasma membrane. Concomitantly, NDPKB
                      depletion increased the permeability of the human umbilical
                      endothelial cell monolayer.This is the first report to show
                      that NDPKB is required for VEGF-induced angiogenesis and
                      contributes to the correct localization of VEGF receptor
                      type 2 and VE-cadherin at the endothelial adherens
                      junctions. Therefore, our data identify NDPKB as a novel
                      molecular target to modulate VEGF-dependent angiogenesis.},
      keywords     = {Antigens, CD (NLM Chemicals) / Cadherins (NLM Chemicals) /
                      NM23 Nucleoside Diphosphate Kinases (NLM Chemicals) /
                      Zebrafish Proteins (NLM Chemicals) / cadherin 5 (NLM
                      Chemicals) / KDR protein, human (NLM Chemicals) / Vascular
                      Endothelial Growth Factor Receptor-2 (NLM Chemicals) / NME2
                      protein, human (NLM Chemicals) / Nme2 protein, mouse (NLM
                      Chemicals)},
      cin          = {A190},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25147336},
      doi          = {10.1161/ATVBAHA.114.304239},
      url          = {https://inrepo02.dkfz.de/record/119929},
}