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Luteinizing Hormone-Releasing Hormone-Signal Transduction and Stathmin Phosphorylation in the Gonadotrope T3–1 Cell Line¹

CNRS UMR 6544 (S.V.D., B.P.), Université de la Méditerranée, Faculté de Médecine Nord, Bd Pierre Dramard, 13916 Marseille Cedex 20, France; and Institut National de la Santé et de la Recherche Médicale, Unité 440 (V.M., A.S.), 75005 Paris, France

Address all correspondence and requests for reprints to: A. Sobel, Institut National de la Santé et de la Recherche Médicale, Unité 440, 17 Rue du Fer à Moulin, 75005 Paris, France. E-mail: sobel{at}infobiogen.fr

We have investigated the effects of GnRH (LHRH) and of the protein kinase C (PKC) activator 12-O-tetradecanoylphorbol-13-acetate on stathmin phosphorylation in the gonadotrope T3–1 cell line. Stathmin expression and its phosphorylation were maximal during the exponential phase of cell growth. LHRH stimulated stathmin phosphorylation through a specific receptor in a dose- and time-dependent manner, and TPA induced a similar extensive stathmin phosphorylation. Their effects were inhibited either in PKC-depleted T3–1 cells, or by the PKC inhibitor staurosporine. In the context of the known implication of PKC in LHRH-induced signal transduction, our results show that stathmin phosphorylation is involved in LHRH transduction, either as a result of direct activation of specific PKC isoforms or through a pathway involving kinases downstream to PKC activation.

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