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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Ottersbach, K. Articles by Graham, G. J. Search for Related Content PubMed PubMed Citation Articles by Ottersbach, K. Articles by Graham, G. J. Related Collections Brief Reports Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 December 2001, Vol. 98, No. 12, pp. 3476-3478 BRIEF REPORT Macrophage inflammatory protein-1 uses a novel receptor for primitive hemopoietic cell inhibition Katrin Ottersbach, Donald N. Cook, William A. Kuziel, Alison Humbles, Bao Lu, Craig Gerard, Amanda E. I. Proudfoot, and Gerard J. Graham From the Beatson Institute for Cancer Research, CRC Beatson Laboratories, Glasgow, Scotland; Schering-Plough Research Institute, Kenilworth, NJ; Department of Molecular Genetics and Microbiology and Institute for Cellular and Molecular Biology, University of Texas, Austin; The Ina Sue Perlmutter Laboratory, Childrens Hospital, Boston, MA; and Serono Pharmaceutical Research Institute, Geneva, Switzerland. Macrophage inflammatory protein-1 (MIP-1) is a member of the chemokine family of proinflammatory mediators. In addition to its inflammatory roles, MIP-1 has been shown to be active as an inhibitor of primitive hemopoietic cell proliferation. Indeed, a dysfunction in this inhibitory process has been postulated to contribute to leukemogenesis. Research has been aimed at characterizing the receptor involved in cellular inhibition by MIP-1. This study demonstrates that of all the -chemokines tested, only MIP-1 is capable of inhibiting primitive hemopoietic cell proliferation. Because no MIP-1-specific receptors have been identified, this suggests that inhibition is mediated by an uncharacterized receptor. Further evidence for the involvement of a novel receptor in this process is the equivalent potencies of MIP-1S and MIP-1P variants of human MIP-1 and the fact that primitive cells from bone marrow derived from individual MIP-1 receptor null mice display a full response to MIP-1 inhibition. © 2001 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. Mantel A helical turn makes an attractive inhibitor Blood, February 15, 2006; 107(4): 1245 - 1246. [Full Text] [PDF] K. Ottersbach, J. Mclean, N. W. Isaacs, and G. J. Graham A310 helical turn is essential for the proliferation-inhibiting properties of macrophage inflammatory protein-1 alpha (CCL3) Blood, February 15, 2006; 107(4): 1284 - 1291. [Abstract] [Full Text] [PDF] A. Panoskaltsis-Mortari, J. R. Hermanson, E. Taras, O. D. Wangensteen, J. S. Serody, and B. R. Blazar Acceleration of idiopathic pneumonia syndrome (IPS) in the absence of donor MIP-1alpha (CCL3) after allogeneic BMT in mice Blood, May 1, 2003; 101(9): 3714 - 3721. [Abstract] [Full Text] [PDF]

	Copyright © 2001 by American Society of Hematology         Online ISSN: 1528-0020