Interaction with IQGAP1 links APC to Rac1, Cdc42, and actin filaments during cell polarization and migration

Takashi Watanabe, Shujie Wang, Jun Noritake, Kazumasa Sato, Masaki Fukata, Mikito Takefuji, Masato Nakagawa, Nanae Izumi, Tetsu Akiyama, Kozo Kaibuchi

研究成果: Article査読

370 被引用数 (Scopus)

抄録

Rho family GTPases, particularly Rac1 and Cdc42, are key regulators of cell polarization and directional migration. Adenomatous polyposis coli (APC) is also thought to play a pivotal role in polarized cell migration. We have found that IQGAP1, an effector of Rac1 and Cdc42, interacts directly with APC. IQGAP1 and APC localize interdependently to the leading edge in migrating Vero cells, and activated Rac1/Cdc42 form a ternary complex with IQGAP1 and APC. Depletion of either IQGAP1 or APC inhibits actin meshwork formation and polarized migration. Depletion of IQGAP1 or APC also disrupts localization of CLIP-170, a microtubule-stabilizing protein that interacts with IQGAP1. Taken together, these results suggest a model in which activation of Rac1 and Cdc42 in response to migration signals leads to recruitment of IQGAP1 and APC which, together with CLIP-170, form a complex that links the actin cytoskeleton and microtubule dynamics during cell polarization and directional migration.

本文言語English
ページ(範囲)871-883
ページ数13
ジャーナルDevelopmental Cell
7
6
DOI
出版ステータスPublished - 12-2004
外部発表はい

All Science Journal Classification (ASJC) codes

  • 分子生物学
  • 生化学、遺伝学、分子生物学(全般)
  • 発生生物学
  • 細胞生物学

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