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@ARTICLE{Rauner:153710,
      author       = {M. Rauner and U. Baschant and A. Roetto and R. M.
                      Pellegrino and S. Rother and J. Salbach-Hirsch and H.
                      Weidner and V. Hintze and G. Campbell and A. Petzold and R.
                      Lemaitre and I. Henry and T. Bellido and I. Theurl and S.
                      Altamura and S. Colucci and M. U. Muckenthaler and G. Schett
                      and D. Komla Ebri and J. H. D. Bassett and G. R. Williams
                      and U. Platzbecker and L. C. Hofbauer$^*$},
      title        = {{T}ransferrin receptor 2 controls bone mass and
                      pathological bone formation via {BMP} and {W}nt signaling.},
      journal      = {Nature metabolism},
      volume       = {1},
      number       = {1},
      issn         = {2522-5812},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2020-00408},
      pages        = {111 - 124},
      year         = {2019},
      abstract     = {Transferrin receptor 2 (Tfr2) is mainly expressed in the
                      liver and controls iron homeostasis. Here, we identify Tfr2
                      as a regulator of bone homeostasis that inhibits bone
                      formation. Mice lacking Tfr2 display increased bone mass and
                      mineralization independent of iron homeostasis and hepatic
                      Tfr2. Bone marrow transplantation experiments and studies of
                      cell-specific Tfr2 knockout mice demonstrate that Tfr2
                      impairs BMP-p38MAPK signaling and decreases expression of
                      the Wnt inhibitor sclerostin specifically in osteoblasts.
                      Reactivation of MAPK or overexpression of sclerostin rescues
                      skeletal abnormalities in Tfr2 knockout mice. We further
                      show that the extracellular domain of Tfr2 binds BMPs and
                      inhibits BMP-2-induced heterotopic ossification by acting as
                      a decoy receptor. These data indicate that Tfr2 limits bone
                      formation by modulating BMP signaling, possibly through
                      direct interaction with BMP either as a receptor or as a
                      co-receptor in a complex with other BMP receptors. Finally,
                      the Tfr2 extracellular domain may be effective in the
                      treatment of conditions associated with pathological bone
                      formation.},
      cin          = {L301},
      ddc          = {610},
      cid          = {I:(DE-He78)L301-20160331},
      pnm          = {899 - ohne Topic (POF3-899)},
      pid          = {G:(DE-HGF)POF3-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30886999},
      pmc          = {pmc:PMC6420074},
      doi          = {10.1038/s42255-018-0005-8},
      url          = {https://inrepo02.dkfz.de/record/153710},
}