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Blood, 1 November 2005, Vol. 106, No. 9, pp. 2962-2968. Prepublished online as a Blood First Edition Paper on July 5, 2005; DOI 10.1182/blood-2005-02-0526. This Article Full Text (PDF) All Versions of this Article: 2005-02-0526v1 106/9/2962    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by BERTHEBAUD, M. Articles by LOUACHE, F. Search for Related Content PubMed PubMed Citation Articles by BERTHEBAUD, M. Articles by LOUACHE, F. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted February 7, 2005 Accepted June 21, 2005 RGS16 is a negative regulator of SDF1-CXCR4 signaling in megakaryocytes Magali BERTHEBAUD, Christel RIVIERE, Peggy JARRIER, Adlen FOUDI, Yanyan ZHANG, Daniel COMPAGNO, Anne GALY, William VAINCHENKER, and Fawzia LOUACHE* INSERM U362, Institut Gustave Roussy, Villejuif, France Genethon, Evry, France * Corresponding author; email: fawl{at}igr.fr. Regulators of G-protein signaling (RGS) constitute a family of proteins involved in the negative regulation of signaling through heterotrimeric G protein-coupled receptors (GPCR). Several RGS proteins have been implicated in the down-regulation of chemokine signaling in hematopoietic cells. The chemokine SDF-1 activates migration of hematopoietic progenitors cells but fails to activate mature megakaryocytes in spite of high levels of CXCR4 receptor expression in these cells. This prompted us to analyze RGS expression and function during megakaryocyte differentiation. We found that RGS16 and RGS18 mRNA expression was upregulated during this process. Overexpressing RGS16 mRNA in the megakaryocytic MO7e cell line inhibited SDF-1-induced migration, AKT and MAPK activation, whereas RGS18 overexpression had no effect on CXCR4 signaling. Knocking-down RGS16 mRNA via lentiviral-mediated RNA interference increased CXCR4 signalling in MO7e cells and in primary megakaryocytes. Thus, our data reveal that RGS16 is a negative regulator of CXCR4 signaling in megakaryocytes. We postulate that RGS16 regulation is a mechanism that controls megakaryocyte maturation by regulating signals from the microenvironnement. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: RGS16 "tightens the reins" on CXCR4 Mariusz Z. Ratajczak Blood 2005 106: 2928-2929. [Full Text] [PDF] This article has been cited by other articles: A. Duces, R. Karaky, D. Martel-Renoir, L. Mir, Y. Hamma-Kourbali, I. Bieche, P. Opolon, J. Delbe, J. Courty, M. Perricaudet, et al. 16-kDa fragment of pleiotrophin acts on endothelial and breast tumor cells and inhibits tumor development Mol. Cancer Ther., September 1, 2008; 7(9): 2817 - 2827. [Abstract] [Full Text] [PDF] F. Bouilloux, G. Juban, N. Cohet, D. Buet, B. Guyot, W. Vainchenker, F. Louache, and F. Morle EKLF restricts megakaryocytic differentiation at the benefit of erythrocytic differentiation Blood, August 1, 2008; 112(3): 576 - 584. [Abstract] [Full Text] [PDF] M. H. Nisancioglu, W. M. Mahoney Jr., D. D. Kimmel, S. M. Schwartz, C. Betsholtz, and G. 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