論文種別	原著(症例報告除く)
言語種別	英語
査読の有無	その他(不明)
表題	Weak and Tunable Adhesion-Clutch Drives Rapid Cell Migration and Glioblastoma Invasion.
掲載誌名	正式名：Advanced science (Weinheim, Baden-Wurttemberg, Germany) 略　 称：Adv Sci (Weinh) ISSNコード：21983844/21983844
掲載区分	国外
巻・号・頁	pp.Online ahead of print
著者・共著者	Kentarou Baba, Ami Fukushi-Kumagai, Megumi Morisaki, Ryosuke Takeuchi, Zhize Xiao, Yoshikazu Nagashima, Mizuki Sakai, Yasuna Higashiguchi, Hiroko Katsuno-Kambe, Asako Katsuma, Yoshihiro Ueda, Yuji Kamioka, Daisuke Kawauchi, Tatsuo Kinashi, Yonehiro Kanemura, Naoyuki Inagaki
発行年月	2025/08
概要	To move forward, cells must exert backward forces against their surrounding environment. Recent studies have highlighted the importance of integrin-independent forces for cell migration; however, the molecular machinery that exerts forces remains unclear. This study shows that the clutch-linker molecule shootin1 and the cell adhesion molecule L1 transmit the backward force of treadmilling actin filaments to the environment, enabling rapid dendritic cell migration. Notably, shootin1 and L1 transmit weak traction forces, up to ∼100 times weaker than integrin-based forces, by constituting an integrin-independent slippery adhesion-clutch. This adhesion-clutch is tunable in response to the chemoattractant CCL19 and the adhesive ligand laminin, thereby enabling chemotaxis and haptokinesis. Furthermore, aberrant activity of this adhesion-clutch enhances glioblastoma cell invasion. The results show that the weak adhesion-clutch is well-suited for rapid cell migration, without forming strong adhesions that impede cell motility, and provides a potential target for inhibiting abnormal tumor invasion.
DOI	10.1002/advs.202502074
PMID	40804012