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Prepublished online as a Blood First Edition Paper on February 13, 2003; DOI 10.1182/blood-2002-07-2271. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-07-2271v1 101/11/4615    most recent 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 Santini, V. Articles by Schreiber, A. D. Search for Related Content PubMed PubMed Citation Articles by Santini, V. Articles by Schreiber, A. D. Related Collections Signal Transduction Phagocytes Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 June 2003, Vol. 101, No. 11, pp. 4615-4622 PHAGOCYTES The carboxy-terminal region of the granulocyte colony-stimulating factor receptor transduces a phagocytic signal Valeria Santini, Barbara Scappini, Zena K. Indik, Antonella Gozzini, Pierluigi Rossi Ferrini, and Alan D. Schreiber From the University of Florence, Department of Hematology, Florence, Italy; and University of Pennsylvania School of Medicine, Department of Medicine, Philadelphia. Granulocyte colony-stimulating factor (G-CSF) induces proliferation, maturation, and functional activities of myeloid progenitors and mature neutrophils through a specific receptor, the G-CSF-R. Different signals are mediated by distinct regions of the cytoplasmic domain of G-CSF-R, but the precise role of each region has not yet been fully clarified. We evaluated the involvement of Syk kinase, essential in mediating phagocytic signals by Fc receptors, in G-CSF–induced phagocytosis, using murine myeloid 32D cells transfected with wild-type (WT) human G-CSF-R (hG-CSF-R) or with a G-CSF-R mutant truncated at cytoplasmic amino acid 715. The G-CSF-R mutant lacks the immunoreceptor tyrosine-based activation motif (ITAM), putative binding site for Syk. Following treatment of WT hG-CSF-R transfectants with IgG-coated particles, there was a significant increase in phagocytosis in G-CSF–stimulated cells, in which Syk tyrosine phosphorylation occurred, paralleled by enhancement of its tyrosine kinase activity. In the mutant transfectants, no significant increase in phagocytosis or Syk tyrosine phosphorylation occurred after stimulation with G-CSF. We also demonstrated that tyrosine phosphorylation of the Src kinases Hck and Lyn occurs following G-CSF stimulation of cells expressing WT G-CSF-R, but that Hck is not phosphorylated in mutant G-CSF-R transfectants. The increase in phagocytosis following G-CSF stimulation cannot be attributed to a rapid de novo increase in expression of Fc receptors. G-CSF induced expression of Fc receptors only after prolonged stimulation. Our data provide evidence that the carboxy-terminal region of G-CSF-R plays a role in the phagocytosis of IgG-coated particles and that Syk and Hck kinase tyrosine phosphorylation is involved. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Metcalf Hematopoietic cytokines Blood, January 15, 2008; 111(2): 485 - 491. [Abstract] [Full Text] [PDF] C. H. Mermel, M. L. McLemore, F. Liu, S. Pereira, J. Woloszynek, C. A. Lowell, and D. C. Link Src family kinases are important negative regulators of G-CSF-dependent granulopoiesis Blood, October 15, 2006; 108(8): 2562 - 2568. [Abstract] [Full Text] [PDF] M. Ulanova, L. Puttagunta, M. Marcet-Palacios, M. Duszyk, U. Steinhoff, F. Duta, M.-K. Kim, Z. K. Indik, A. D. Schreiber, and A. D. Befus Syk tyrosine kinase participates in {beta}1-integrin signaling and inflammatory responses in airway epithelial cells Am J Physiol Lung Cell Mol Physiol, March 1, 2005; 288(3): L497 - L507. [Abstract] [Full Text] [PDF]

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