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@ARTICLE{Savant:127444,
      author       = {S. Savant$^*$ and S. La Porta$^*$ and A. Budnik$^*$ and K.
                      Busch$^*$ and J. Hu$^*$ and N. Tisch and C. Korn$^*$ and A.
                      F. Valls$^*$ and A. V. Benest$^*$ and D. Terhardt$^*$ and X.
                      Qu and R. H. Adams and H. S. Baldwin and C. Ruiz de
                      Almodóvar and H.-R. Rodewald$^*$ and H. Augustin$^*$},
      title        = {{T}he {O}rphan {R}eceptor {T}ie1 {C}ontrols {A}ngiogenesis
                      and {V}ascular {R}emodeling by {D}ifferentially {R}egulating
                      {T}ie2 in {T}ip and {S}talk {C}ells.},
      journal      = {Cell reports},
      volume       = {12},
      number       = {11},
      issn         = {2211-1247},
      address      = {Maryland Heights, MO},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2017-03467},
      pages        = {1761 - 1773},
      year         = {2015},
      abstract     = {Tie1 is a mechanistically poorly characterized endothelial
                      cell (EC)-specific orphan receptor. Yet, Tie1 deletion is
                      embryonic lethal and Tie1 has been implicated in critical
                      vascular pathologies, including atherosclerosis and tumor
                      angiogenesis. Here, we show that Tie1 does not function
                      independently but exerts context-dependent effects on the
                      related receptor Tie2. Tie1 was identified as an EC
                      activation marker that is expressed during angiogenesis by a
                      subset of angiogenic tip and remodeling stalk cells and
                      downregulated in the adult quiescent vasculature.
                      Functionally, Tie1 expression by angiogenic EC contributes
                      to shaping the tip cell phenotype by negatively regulating
                      Tie2 surface presentation. In contrast, Tie1 acts in
                      remodeling stalk cells cooperatively to sustain Tie2
                      signaling. Collectively, our data support an interactive
                      model of Tie1 and Tie2 function, in which dynamically
                      regulated Tie1 versus Tie2 expression determines the net
                      positive or negative effect of Tie1 on Tie2 signaling.},
      keywords     = {Receptor, TIE-1 (NLM Chemicals) / Receptor, TIE-2 (NLM
                      Chemicals)},
      cin          = {A190 / D110 / L101},
      ddc          = {570},
      cid          = {I:(DE-He78)A190-20160331 / I:(DE-He78)D110-20160331 /
                      I:(DE-He78)L101-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26344773},
      doi          = {10.1016/j.celrep.2015.08.024},
      url          = {https://inrepo02.dkfz.de/record/127444},
}