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J Biol Chem, Vol. 275, Issue 15, 11333-11340, April 14, 2000
From the Department of Cell and Molecular Pharmacology, Medical
University of South Carolina,
Charleston, South Carolina 29425-2251
Intracellular signals can regulate cell adhesion
via several mechanisms in a process referred to as "inside-out"
signaling. In phorbol ester-sensitive EL4 thymoma cells,
phorbol-12-myristate 13-acetate (PMA) induces activation of
extracellular signal-regulated kinase (ERK) mitogen-activated protein
kinases and promotes cell adhesion. In this study, clonal EL4 cell
lines with varying abilities to activate ERKs in response to PMA were
used to examine signaling events occurring downstream of ERK
activation. Paxillin, a multifunctional docking protein involved in
cell adhesion, was phosphorylated on serine/threonine residues in
response to PMA treatment. This response was correlated with the extent
and time course of ERK activation. PMA-induced phosphorylation of
paxillin was inhibited by compounds that block the ERK activation
pathway in EL4 cells, primary murine thymocytes, and primary murine
splenocytes. Paxillin was phosphorylated in vitro by
purified active ERK2. Two-dimensional electrophoresis revealed that PMA
treatment generated a complex pattern of phosphorylated paxillin
species in intact cells, some of which were generated by ERK-mediated
phosphorylation in vitro. An ERK pathway inhibitor
interfered with PMA-induced adhesion of sensitive EL4 cells to
substrate. These findings describe a novel inside-out signaling pathway
by which the ERK cascade may regulate events involved in adhesion.
Phosphorylation of Paxillin via the ERK Mitogen-activated Protein
Kinase Cascade in EL4 Thymoma Cells*
*
This work was supported by National Science Foundation Grant
EPS-9630167, the University Research Committee of the Medical University of South Carolina, and U.S. Department of Defense Grant DAMD17-98-8524.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Cell and
Molecular Pharmacology, Medical University of South Carolina, P.O. Box
250505, 173 Ashley Ave., Charleston, SC 29425-2251. Tel.: 843-792-5853;
Fax: 843-792-2475; E-mail: meierke@musc.edu.
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