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COUP-TFI coordinates cortical patterning, neurogenesis, and laminar fate and modulates MAPK/ERK, AKT, and beta-catenin signaling.

A major unsolved question in cortical development is how proliferation, neurogenesis, regional growth, regional identity, and laminar fate specification are coordinated. Here we provide evidence, using loss-of-function and gain-of-function manipulations, that the COUP-TFI orphan nuclear receptor promotes ventral cortical fate, promotes cell cycle exit and neural differentiation, regulates the balance of early- and late-born neurons, and regulates the balanced production of different types of layer V cortical projection neurons. We suggest that COUP-TFI controls these processes by repressing Mapk/Erk, Akt, and beta-catenin signaling.

Pubmed ID: 18165280

Authors

  • Faedo A
  • Tomassy GS
  • Ruan Y
  • Teichmann H
  • Krauss S
  • Pleasure SJ
  • Tsai SY
  • Tsai MJ
  • Studer M
  • Rubenstein JL

Journal

Cerebral cortex (New York, N.Y. : 1991)

Publication Data

September 18, 2008

Associated Grants

  • Agency: NIMH NIH HHS, Id: K05 MH065670
  • Agency: NINDS NIH HHS, Id: NS34661
  • Agency: Telethon, Id: TGM06A04
  • Agency: Telethon, Id: TGM06S01

Mesh Terms

  • Animals
  • COUP Transcription Factor I
  • Cell Division
  • Extracellular Signal-Regulated MAP Kinases
  • Female
  • MAP Kinase Signaling System
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Mitogen-Activated Protein Kinases
  • Neocortex
  • Neurons
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • Stem Cells
  • beta Catenin