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@ARTICLE{Scholz:130518,
      author       = {B. Scholz$^*$ and C. Korn$^*$ and J. Wojtarowicz$^*$ and C.
                      Mogler$^*$ and I. Augustin$^*$ and M. Boutros$^*$ and C.
                      Niehrs$^*$ and H. Augustin$^*$},
      title        = {{E}ndothelial {RSPO}3 {C}ontrols {V}ascular {S}tability and
                      {P}runing through {N}on-canonical {WNT}/{C}a(2+)/{NFAT}
                      {S}ignaling.},
      journal      = {Developmental cell},
      volume       = {36},
      number       = {1},
      issn         = {1534-5807},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2017-05597},
      pages        = {79 - 93},
      year         = {2016},
      abstract     = {The WNT signaling enhancer R-spondin3 (RSPO3)
                      is prominently expressed in the vasculature.
                      Correspondingly, embryonic lethality of Rspo3-deficient mice
                      is caused by vessel remodeling defects. Yet the mechanisms
                      underlying vascular RSPO3 function remain elusive. Inducible
                      endothelial Rspo3 deletion (Rspo3-iECKO) resulted in
                      perturbed developmental and tumor vascular remodeling.
                      Endothelial cell apoptosis and vascular pruning led to
                      reduced microvessel density in Rspo3-iECKO mice. Rspo3-iECKO
                      mice strikingly phenocopied the non-canonical WNT
                      signaling-induced vascular defects of mice deleted for the
                      WNT secretion factor Evi/Wls. An endothelial screen for
                      RSPO3 and EVI/WLS co-regulated genes identified Rnf213,
                      Usp18, and Trim30α. RNF213 targets filamin A and NFAT1 for
                      proteasomal degradation attenuating
                      non-canonical WNT/Ca(2+) signaling. Likewise, USP18 and
                      TRIM5α inhibited NFAT1 activation. Consequently, NFAT
                      protein levels were decreased in endothelial cells of
                      Rspo3-iECKO mice and pharmacological NFAT inhibition
                      phenocopied Rspo3-iECKO mice. The data identify endothelial
                      RSPO3-driven non-canonical WNT/Ca(2+)/NFAT signaling as a
                      critical maintenance pathway of the remodeling vasculature.},
      keywords     = {NFATC Transcription Factors (NLM Chemicals) / R-spondin3
                      protein, mouse (NLM Chemicals) / Thrombospondins (NLM
                      Chemicals) / Transcription Factors (NLM Chemicals) / Wnt
                      Proteins (NLM Chemicals) / Calcium (NLM Chemicals)},
      cin          = {A190 / B110 / A050 / L101},
      ddc          = {570},
      cid          = {I:(DE-He78)A190-20160331 / I:(DE-He78)B110-20160331 /
                      I:(DE-He78)A050-20160331 / I:(DE-He78)L101-20160331},
      pnm          = {321 - Basic Concepts (POF3-321)},
      pid          = {G:(DE-HGF)POF3-321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26766444},
      doi          = {10.1016/j.devcel.2015.12.015},
      url          = {https://inrepo02.dkfz.de/record/130518},
}