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ERK signaling promotes cell motility by inducing the localization of myosin 1E to lamellipodial tips

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Title: ERK signaling promotes cell motility by inducing the localization of myosin 1E to lamellipodial tips
Authors: Tanimura, Susumu / Hashizume, Junya / Arichika, Naoya / Watanabe, Kazushi / Ohyama, Kaname / Takeda, Kohsuke / Kohno, Michiaki
Issue Date: 8-Aug-2016
Publisher: Rockefeller University Press
Citation: The Journal of Cell Biology, 214(4), pp.475-489; 2016
Abstract: Signaling by extracellular signal-regulated kinase (ERK) plays an essential role in the induction of cell motility, but the precise mechanism underlying such regulation has remained elusive. We recently identified SH3P2 as a negative regulator of cell motility whose function is inhibited by p90 ribosomal S6 kinase (RSK)-mediated phosphorylation downstream of ERK. We here show that myosin 1E (Myo1E) is a binding partner of SH3P2 and that the interaction of the two proteins in the cytosol prevents the localization of Myo1E to the plasma membrane. Serum-induced phosphorylation of SH3P2 at Ser202 by RSK results in dissociation of Myo1E from SH3P2 in the cytosol and the subsequent localization of Myo1E to the tips of lamellipodia mediated by binding of its TH2 domain to F-actin. This translocation of Myo1E is essential for lamellipodium extension and consequent cell migration. The ERK signaling pathway thus promotes cell motility through regulation of the subcellular localization of Myo1E.
URI: http://hdl.handle.net/10069/37249
ISSN: 00219525
DOI: 10.1083/jcb.201503123
Rights: © 2016 Tanimura et al.This article is an open access article under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
Type: Journal Article
Text Version: publisher
Appears in Collections:Articles in academic journal

Citable URI : http://hdl.handle.net/10069/37249

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