CrkL directs ASAP1 to peripheral focal adhesions

Atsushi Oda*, Ikuo Wada, Koichi Miura, Katsuya Okawa, Toshihiko Kadoya, Takashi Kato, Hiroshi Nishihara, Masae Maeda, Shinya Tanaka, Kazuo Nagashima, Chiaki Nishitani, Kazuhiko Matsuno, Masaho Ishino, Laura M. Machesky, Hiroyoshi Fujita, Paul Randazzo

*この研究の対応する著者

研究成果: Article査読

38 被引用数 (Scopus)

抄録

Searching for proteins in platelets that can interact with the N-terminal SH3 domain of CrkL (using a combination of a pull-down assay followed by mass spectrometry), we have found that human platelets express an ADP-ribosylation factor (Arf)-specific GTPase-activating protein (GAP), ASAP1, as a CrkL-binding protein. In spreading platelets, most endogenous ASAP1 is localized at peripheral focal adhesions. To determine the physiologic significance of the CrkL-ASAP1 association, we overexpressed CrkL, ASAP1, or both in combination in COS7 cells. Unlike endogenous ASAP1 in platelets, overexpressed ASAP1 showed diffuse cytoplasmic distribution. However, when co-expressed with wild-type CrkL, both endogenous and expressed ASAP1 accumulated at CrkL-induced focal adhesions. An SH2-mutated CrkL, which cannot localize at focal adhesions, failed to recruit ASAP1 into focal adhesions. Thus, CrkL appears to be a lynchpin between ASAP1 and peripheral focal adhesions.

本文言語English
ページ(範囲)6456-6460
ページ数5
ジャーナルJournal of Biological Chemistry
278
8
DOI
出版ステータスPublished - 2003 2月 21

ASJC Scopus subject areas

  • 生化学
  • 分子生物学
  • 細胞生物学

フィンガープリント

「CrkL directs ASAP1 to peripheral focal adhesions」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル