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JCI table of contents -- March 8, 2006

nction can therefore lead to uncontrolled bleeding or to the formation of thrombi, which can block blood vessels and, in the heart and brain, lead to heart attacks and strokes. In a new study appearing online on March 8 in advance of publication in the April print issue of the Journal of Clinical Investigation, Marie-Pierre Gratacap and colleagues from Toulouse, France, show that in mice, the protein SHIP1 is important for normal hemostasis. Mice lacking SHIP1 bled longer after tail injury and formed smaller thrombi that contained fewer platelets than normal mice. Consistent with these in vivo studies, when platelets from SHIP1-deficient mice were stimulated in vitro they formed smaller aggregates than platelets from normal mice. This study therefore identifies a new function for SHIP1 in regulating platelet function to sustain normal hemostasis.

TITLE: Deficiency of Src homology 2 domaincontaining inositol 5-phosphatase 1 affects platelet responses and thrombus growth

AUTHOR CONTACT:
Marie-Pierre Gratacap
Centre de Physiopathologie de Toulouse Purpan et Universit Paul Sabatier, Toulouse, France.
Phone: +33-562-74-45-22; Fax: +33-562-74-45-58; E-mail: marie-pierre.gratacap@toulouse.inserm.fr.

View the PDF of this article at: https://www.the-jci.org/article.php?id=29967


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Contact: Karen Honey
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
8-Mar-2007


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