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@ARTICLE{Luck:170294,
      author       = {R. Luck and A. Karakatsani and B. Shah and G. Schermann and
                      H. Adler and J. Kupke and N. Tisch and H.-W. Jeong and M. K.
                      Back and F. Hetsch and A. D'Errico and M. De Palma and E.
                      Wiedtke and D. Grimm and A. Acker-Palmer and J. von
                      Engelhardt and R. H. Adams and H. G. Augustin$^*$ and C.
                      Ruiz de Almodóvar},
      title        = {{T}he angiopoietin-{T}ie2 pathway regulates {P}urkinje cell
                      dendritic morphogenesis in a cell-autonomous manner.},
      journal      = {Cell reports},
      volume       = {36},
      number       = {7},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2021-01884},
      pages        = {109522},
      year         = {2021},
      note         = {DKFZ-ZMBH Alliance},
      abstract     = {Neuro-vascular communication is essential to synchronize
                      central nervous system development. Here, we identify
                      angiopoietin/Tie2 as a neuro-vascular signaling axis
                      involved in regulating dendritic morphogenesis of Purkinje
                      cells (PCs). We show that in the developing cerebellum Tie2
                      expression is not restricted to blood vessels, but it is
                      also present in PCs. Its ligands angiopoietin-1 (Ang1) and
                      angiopoietin-2 (Ang2) are expressed in neural cells and
                      endothelial cells (ECs), respectively. PC-specific deletion
                      of Tie2 results in reduced dendritic arborization, which is
                      recapitulated in neural-specific Ang1-knockout and Ang2
                      full-knockout mice. Mechanistically, RNA sequencing reveals
                      that Tie2-deficient PCs present alterations in gene
                      expression of multiple genes involved in cytoskeleton
                      organization, dendritic formation, growth, and branching.
                      Functionally, mice with deletion of Tie2 in PCs present
                      alterations in PC network functionality. Altogether, our
                      data propose Ang/Tie2 signaling as a mediator of
                      intercellular communication between neural cells, ECs, and
                      PCs, required for proper PC dendritic morphogenesis and
                      function.},
      keywords     = {Purkinje cell (Other) / Tie2 (Other) / angiogenesis (Other)
                      / angipoietin (Other) / blood vessels (Other) / cerebellum
                      (Other) / dendritic branching (Other) / dendritic morphology
                      (Other) / neuro-vascular (Other) / neurodevelopment (Other)},
      cin          = {A190},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34407407},
      doi          = {10.1016/j.celrep.2021.109522},
      url          = {https://inrepo02.dkfz.de/record/170294},
}