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Related Collections Signal Transduction Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 June 2001, Vol. 97, No. 12, pp. 3836-3845 HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Role of Fc receptor -chain in platelet glycoprotein Ib-mediated signaling Yi Wu, Katsue Suzuki-Inoue, Kaneo Satoh, Naoki Asazuma, Yutaka Yatomi, Michael C. Berndt, and Yukio Ozaki From the Department of Clinical and Laboratory Medicine, Yamanashi Medical University, Tamaho, Nakakoma, Yamanashi, Japan; and Baker Medical Research Institute, Prahran, Victoria, Australia. Interaction between von Willebrand factor (vWF) and glycoprotein Ib (GPIb) stimulates tyrosine kinases and subsequent tyrosine phosphorylation events in human platelets. This study found that the combination of vWF and botrocetin, by interacting with GPIb, induced tyrosine phosphorylation of Fc receptor -chain (FcR -chain), Syk, linker for activation of T cells (LAT), and phospholipase C 2 (PLC2). Pretreatment of platelets with 10 µM PP1 completely inhibited these tyrosine phosphorylation events. On GPIb stimulation, Src and Lyn formed a complex with FcR -chain and Syk, suggesting that Src and Lyn are involved in FcR -chain tyrosine phosphorylation and downstream signals. In spite of the PLC2 tyrosine phosphorylation, however, there was no intracellular calcium release and inositol 1,4,5-trisphosphate production. In Brij 35 lysates, FcR -chain was found to constitutively associate with GPIb. The number of GPIb expressed on FcR -chain-deficient platelets was comparable to that of the wild-type, as assessed by flow cytometry. However, tyrosine phosphorylation of Syk, LAT, and PLC2 in response to vWF plus botrocetin was significantly suppressed, suggesting that FcR -chain mediates activation signals related to GPIb. Compared with the aggregation response of wild-type platelets, that of FcR -chain-deficient platelets in response to vWF plus botrocetin was impaired, implying that FcR -chain is required for the full activation of platelets mediated by GPIb. © 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: D. Varga-Szabo, I. Pleines, and B. Nieswandt Cell Adhesion Mechanisms in Platelets Arterioscler. Thromb. Vasc. Biol., March 1, 2008; 28(3): 403 - 412. [Abstract] [Full Text] [PDF] H. Yin, A. Stojanovic, N. Hay, and X. Du The role of Akt in the signaling pathway of the glycoprotein Ib-IX induced platelet activation Blood, January 15, 2008; 111(2): 658 - 665. 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