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Blood, 1 June 2005, Vol. 105, No. 11, pp. 4492-4499. Prepublished online as a Blood First Edition Paper on February 3, 2005; DOI 10.1182/blood-2004-08-2985. This Article Full Text (PDF) All Versions of this Article: 2004-08-2985v1 105/11/4492    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 Carvajal-Vergara, X. Articles by Pandiella, A. Search for Related Content PubMed PubMed Citation Articles by Carvajal-Vergara, X. Articles by Pandiella, A. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted August 3, 2004 Accepted January 26, 2005 Multifunctional role of Erk5 in multiple myeloma Xonia Carvajal-Vergara, Soraya Tabera, Juan C Montero, Azucena Esparis-Ogando, Ricardo Lopez-Perez, Gema Mateo, Norma Gutierrez, Marisa Parmo-Cabanas, Joaquin Teixido, Jesus F San Miguel, and Atanasio Pandiella* Centro de Investigacion del Cancer, CSIC-Universidad de Salamanca, Salamanca, Spain Centro de Investigacion del Cancer, CSIC-Universidad de Salamanca, Salamanca, Spain; Hospital Universitario de Salamanca, Salamanca, Spain Centro de Investigaciones Biologicas, Madrid, Spain * Corresponding author; email: atanasio{at}usal.es. Multiple myeloma is characterized by the accumulation of terminally differentiated B-cells in the bone marrow, due to increased proliferation and restricted apoptosis of the myelomatous clone. Here we have studied the participation of a novel MAPK route, the Erk5 pathway, in the regulation of myeloma cell proliferation and apoptosis. Erk5 was expressed in cells isolated from patients and in myeloma cell lines. The myeloma growth factor Interleukin 6 (IL-6) activated Erk5, and this activation was Ras and Src-independent. Expression of a dominant-negative form of Erk5 restricted the proliferation of myeloma cells, and inhibited IL-6-dependent cell duplication. This dominant negative form also sensitized myeloma cells to the proapoptotic action of dexamethasone and PS341. The latter compound caused a profound decrease in the amount of endogenous Erk5, and was less effective in inducing apoptosis when the level of Erk5 was increased by transfection of Erk5. These results place the Erk5 route as a new regulatory signalling pathway that affects multiple myeloma proliferation and apoptosis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: E. J. Carter, R. A. Cosgrove, I. Gonzalez, J. H. Eisemann, F. A. Lovett, L. J. Cobb, and J. M. Pell MEK5 and ERK5 are mediators of the pro-myogenic actions of IGF-2 J. Cell Sci., September 1, 2009; 122(17): 3104 - 3112. [Abstract] [Full Text] [PDF] S. Charni, J. I. Aguilo, J. Garaude, G. de Bettignies, C. Jacquet, R. A. Hipskind, D. Singer, A. Anel, and M. Villalba ERK5 Knockdown Generates Mouse Leukemia Cells with Low MHC Class I Levels That Activate NK Cells and Block Tumorigenesis J. Immunol., March 15, 2009; 182(6): 3398 - 3405. [Abstract] [Full Text] [PDF] C. S. Mitsiades, E. M. Ocio, A. Pandiella, P. Maiso, C. Gajate, M. Garayoa, D. Vilanova, J. C. Montero, N. Mitsiades, C. J. McMullan, et al. Aplidin, a Marine Organism-Derived Compound with Potent Antimyeloma Activity In vitro and In vivo Cancer Res., July 1, 2008; 68(13): 5216 - 5225. [Abstract] [Full Text] [PDF] J. C. Montero, R. Lopez-Perez, J. F. San Miguel, and A. 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