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Targeting of δ-catenin to postsynaptic sites through interaction with the Shank3 N-terminus.

Fatemeh Hassani NiaDaniel WoikeVictoria MartensMalte KlüssendorfHans-Hinrich HönckSönke HarderHans-Jürgen Kreienkamp
Published in: Molecular autism (2020)
Our data show that the interaction between Shank3 N-terminus and δ-catenin is required for the postsynaptic targeting of δ-catenin. Failure of proper targeting of δ-catenin to postsynaptic sites may contribute to the pathogenesis of autism spectrum disorder.
Keyphrases
  • epithelial mesenchymal transition
  • cell proliferation
  • autism spectrum disorder
  • cancer therapy
  • intellectual disability
  • attention deficit hyperactivity disorder
  • artificial intelligence