Papers

Peer-reviewed
May, 2012

The Dishevelled-associating protein Daple controls the non-canonical Wnt/Rac pathway and cell motility

NATURE COMMUNICATIONS
  • Maki Ishida-Takagishi
  • Atsushi Enomoto
  • Naoya Asai
  • Kaori Ushida
  • Takashi Watanabe
  • Takahiko Hashimoto
  • Takuya Kato
  • Liang Weng
  • Shinji Matsumoto
  • Masato Asai
  • Yoshiki Murakumo
  • Kozo Kaibuchi
  • Akira Kikuchi
  • Masahide Takahashi
  • Display all

Volume
3
Number
First page
859
Last page
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.1038/ncomms1861
Publisher
NATURE PUBLISHING GROUP

Dishevelled is the common mediator of canonical and non-canonical Wnt signalling pathways, which are important for embryonic development, tissue maintenance and cancer progression. In the non-canonical Wnt signalling pathway, the Rho family of small GTPases acting downstream of Dishevelled has essential roles in cell migration. The mechanisms by which the non-canonical Wnt signalling pathway regulates Rac activation remain unknown. Here we show that Daple (Dishevelled-associating protein with a high frequency of leucine residues) regulates Wnt5a-mediated activation of Rac and formation of lamellipodia through interaction with Dishevelled. Daple increases the association of Dishevelled with an isoform of atypical protein kinase C, consequently promoting Rac activation. Accordingly, Daple deficiency impairs migration of fibroblasts and epithelial cells during wound healing in vivo. These findings indicate that Daple interacts with Dishevelled to direct the Dishevelled/protein kinase. protein complex to activate Rac, which in turn mediates the non-canonical Wnt signalling pathway required for cell migration.

Link information
DOI
https://doi.org/10.1038/ncomms1861
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/22643886
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000304611400054&DestApp=WOS_CPL
ID information
  • DOI : 10.1038/ncomms1861
  • ISSN : 2041-1723
  • Pubmed ID : 22643886
  • Web of Science ID : WOS:000304611400054

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