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@ARTICLE{Nouri:154266,
      author       = {Nouri, Parivash and Götz, Sebastian and Rauser, Benedict
                      and Irmler, Martin and Peng, Changgeng and Trümbach,
                      Dietrich and Kempny, Christian and Lechermeier, Carina G and
                      Bryniok, Agnes and Dlugos, Andrea and Euchner, Ellen and
                      Beckers, Johannes and Brodski, Claude and Klümper, Claudia
                      and Wurst, Wolfgang and Prakash, Nilima},
      title        = {{D}ose-{D}ependent and {S}ubset-{S}pecific {R}egulation of
                      {M}idbrain {D}opaminergic {N}euron {D}ifferentiation by
                      {LEF}1-{M}ediated {WNT}1/b-{C}atenin {S}ignaling.},
      journal      = {Frontiers in cell and developmental biology},
      volume       = {8},
      issn         = {2296-634X},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DZNE-2021-00120},
      pages        = {587778},
      year         = {2020},
      note         = {ISSN 2296-634X not unique: **3 hits**.},
      abstract     = {The mesodiencephalic dopaminergic (mdDA) neurons, including
                      the nigrostriatal subset that preferentially degenerates in
                      Parkinson's Disease (PD), strongly depend on an accurately
                      balanced Wingless-type MMTV integration site family member 1
                      (WNT1)/beta-catenin signaling pathway during their
                      development. Loss of this pathway abolishes the generation
                      of these neurons, whereas excessive WNT1/b-catenin signaling
                      prevents their correct differentiation. The identity of the
                      cells responding to this pathway in the developing mammalian
                      ventral midbrain (VM) as well as the precise progression of
                      WNT/b-catenin action in these cells are still unknown. We
                      show that strong WNT/b-catenin signaling inhibits the
                      differentiation of WNT/b-catenin-responding mdDA progenitors
                      into PITX3+ and TH+ mdDA neurons by repressing the Pitx3
                      gene in mice. This effect is mediated by RSPO2, a
                      WNT/b-catenin agonist, and lymphoid enhancer binding factor
                      1 (LEF1), an essential nuclear effector of the WNT/b-catenin
                      pathway, via conserved LEF1/T-cell factor binding sites in
                      the Pitx3 promoter. LEF1 expression is restricted to a
                      caudolateral mdDA progenitor subset that preferentially
                      responds to WNT/b-catenin signaling and gives rise to a
                      fraction of all mdDA neurons. Our data indicate that an
                      attenuation of WNT/b-catenin signaling in mdDA progenitors
                      is essential for their correct differentiation into specific
                      mdDA neuron subsets. This is an important consideration for
                      stem cell-based regenerative therapies and in vitro models
                      of neuropsychiatric diseases.},
      keywords     = {Parkinson’s disease (Other) / dopamine (Other) / mouse
                      (Other) / nerve cell (Other) / regenerative therapy (Other)},
      cin          = {Ext HZM / AG Wurst},
      ddc          = {570},
      cid          = {I:(DE-2719)5000050 / I:(DE-2719)1140001},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33195246},
      pmc          = {pmc:PMC7649324},
      doi          = {10.3389/fcell.2020.587778},
      url          = {https://pub.dzne.de/record/154266},
}