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Blood, 1 October 2007, Vol. 110, No. 7, pp. 2449-2456. Prepublished online as a Blood First Edition Paper on June 19, 2007; DOI 10.1182/blood-2006-11-056069. This Article Full Text (PDF) All Versions of this Article: blood-2006-11-056069v1 110/7/2449    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 Kahner, B. N Articles by Kunapuli, S. P. Search for Related Content PubMed PubMed Citation Articles by Kahner, B. N Articles by Kunapuli, S. P. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted November 3, 2006 Accepted May 29, 2007 HS1 is a functionally important signaling molecule in platelet activation Bryan N Kahner, Robert T Dorsam, Sripal R Mada, Soochong Kim, Timothy J Stalker, Lawrence F Brass, James L Daniel, Daisuke Kitamura, and Satya P. Kunapuli* Department of Physiology, Temple University School of Medicine, Philadelphia, PA, United States Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA, United States Sol Sherry Thrombosis Research, Temple University School of Medicine, Philadelphia, PA, United States Department of Medicine, University of Pennsylvania, Philadelphia, PA, United States Research Institute for Biological Sciences, Tokyo University of Science, Noda, Japan * Corresponding author; email: spk{at}temple.edu. Collagen activates platelets through an intracellular signaling cascade downstream of glycoprotein VI (GPVI). We have investigated the contribution of hematopoietic lineage cell-specific protein-1 (HS1) downstream of GPVI in platelet activation. Stimulation of GPVI leads to tyrosine phosphorylation of HS1, which is blocked by Src family kinase inhibitors. HS1 null mice displayed increased bleeding times and increased time to occlusion in the FeCl3 in vivo thrombosis model compared to their wild type littermates. In addition, aggregation and secretion responses were diminished in HS1 null mouse platelets following stimulation with GPVI and PAR-4 agonists, compared to wild type littermate mouse platelets. Finally, Akt phosphorylation was diminished upon GPVI or PAR-4 stimulation in platelets from HS1 null mice compared to their wild type littermates. These results demonstrate that the phosphorylation of the HS1 protein occurs downstream of GPVI stimulation, that HS1 plays a significant functional role in platelet activation downstream of GPVI and PARs. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. Chari, T. Getz, B. Nagy Jr, K. Bhavaraju, Y. Mao, Y. S. Bynagari, S. Murugappan, K. Nakayama, and S. P. Kunapuli Protein Kinase C{delta} Differentially Regulates Platelet Functional Responses Arterioscler Thromb Vasc Biol, May 1, 2009; 29(5): 699 - 705. [Abstract] [Full Text] [PDF]

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