A dual function of Bcl11b/Ctip2 in hippocampal neurogenesis

• Ruth Simon ^[5] ; Heike Brylka ^[6] ; Herbert Schwegler ^[1] ; Sathish Venkataramanappa ^[5] ; Jacqueline Andratschke ^[5] ; Christoph Wiegreffe ^[5] ; Pentao Liu ^[2] ; Elaine Fuchs ^[3] ; Nancy A Jenkins ^[7] ; Neal G Copeland ^[7] ; Carmen Birchmeier ^[4] ; Stefan Britsch ^[6]
  1. [1] Otto-von-Guericke University Magdeburg

     Otto-von-Guericke University Magdeburg

     Landeshauptstadt Magdeburg, Alemania

     
  2. [2] Wellcome Trust Sanger Institute

     Wellcome Trust Sanger Institute

     Cambridge District, Reino Unido

     
  3. [3] Rockefeller University

     Rockefeller University

     Estados Unidos

     
  4. [4] Max Delbrück Center for Molecular Medicine

     Max Delbrück Center for Molecular Medicine

     Berlin, Stadt, Alemania

     
  5. [5] Institute of Molecular and Cellular Anatomy, Ulm University, Ulm, Germany
  6. [6] Institute of Molecular and Cellular Anatomy, Ulm University, Ulm, Germany; Center for Anatomy, Georg-August-University, Goettingen, Germany; Max Delbrück Center for Molecular Medicine (MDC), Berlin-Buch, Germany
  7. [7] Cancer Research Program, The Methodist Hospital Research Institute, Houston, TX, USA

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• Localización: EMBO journal: European Molecular Biology Organization, ISSN 0261-4189, Vol. 31, Nº. 13, 2012, págs. 2922-2936
• Idioma: inglés
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• Resumen

  • The transcription factor Bcl11b/Ctip2 promotes hippocampal progenitor proliferation and neural differentiation in a non-cell autonomous manner by regulating the expression of the cell adhesion molecule Desmoplakin. Forebrain-specific ablation causes defective spatial learning and memory.