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J. Biol. Chem., Vol. 275, Issue 34, 26349-26358, August 25, 2000
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From the Laboratoire de Signalisation Cellulaire, Médiateurs
Lipidiques et Contrôle de l'Expression des Gènes, CNRS
UPRES-A 7079, Université Pierre et Marie Curie, 7 Quai
St-Bernard, Bâtiment A, 5ème étage, 75005 Paris,
France and the § Division of Hematology/Oncology, Vanderbilt
University School of Medicine, Nashville, Tennessee 37232
Angiotensin II (Ang II) binds to specific G
protein-coupled receptors and is mitogenic in Chinese hamster ovary
(CHO) cells stably expressing a rat vascular angiotensin II type 1A
receptor (CHO-AT1A). Cyclin D1 protein expression is
regulated by mitogens, and its assembly with the
cyclin-dependent kinases induces phosphorylation of the
retinoblastoma protein pRb, a critical step in G1 to S phase cell cycle progression contributing to the proliferative responses. In the present study, we found that in CHO-AT1A
cells, Ang II induced a rapid and reversible tyrosine phosphorylation of various intracellular proteins including the protein-tyrosine phosphatase SHP-2. Ang II also induced cyclin D1 protein expression in
a phosphatidylinositol 3-kinase and mitogen-activated protein kinase/extracellular signal-regulated kinase
(MAPK/ERK)-dependent manner. Using a pharmacological and a
co-transfection approach, we found that p21ras, Raf-1,
phosphatidylinositol 3-kinase and also the catalytic activity of
SHP-2 and its Src homology 2 domains are required for cyclin D1
promoter/reporter gene activation by Ang II through the regulation of
MAPK/ERK activity. Our findings suggest for the first time that
SHP-2 could play an important role in the regulation of a gene involved
in the control of cell cycle progression resulting from
stimulation of a G protein-coupled receptor independently of epidermal
growth factor receptor transactivation.
The Protein-tyrosine Phosphatase SHP-2 Is Required during
Angiotensin II-mediated Activation of Cyclin D1 Promoter in
CHO-AT1A Cells*
,
*
This work was supported by Association pour la Recherche sur
le Cancer Contract 9662, by CNRS, and by National Institutes of Health
Grants HL-57393 and CA75218 (to Z. J. Z.).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.
Supported by a doctoral fellowship from the French Ministère
de l'Education Nationale de l'Enseignement Supérieur et de la Recherche.
¶
To whom correspondence should be addressed. Tel.:
33-1-44-27-35-07; Fax: 33-1-44-27-51-40; E-mail:
rothhut@ccr.jussieu.fr.
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