A mutation in the β3 cytoplasmic tail causes variant Glanzmann thrombasthenia by abrogating transition of αIIbβ3 to an active state
Article first published online: 2 FEB 2012
© 2011 International Society on Thrombosis and Haemostasis
Journal of Thrombosis and Haemostasis
Volume 10, Issue 2, pages 289–297, February 2012
How to Cite
HAUSCHNER, H., MOR-COHEN, R., SELIGSOHN, U. and ROSENBERG, N. (2012), A mutation in the β3 cytoplasmic tail causes variant Glanzmann thrombasthenia by abrogating transition of αIIbβ3 to an active state. Journal of Thrombosis and Haemostasis, 10: 289–297. doi: 10.1111/j.1538-7836.2011.04577.x
- Issue published online: 2 FEB 2012
- Article first published online: 2 FEB 2012
- Accepted manuscript online: 3 DEC 2011 10:32AM EST
- Received 20 July 2011, accepted 24 November 2011
Figure S1. Actin and αIIbβ3 staining of WT and mutant cells.
Figure S2. AntiLIBS6 binding to αIIbβ3 expressing cells using flow cytometry.
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|JTH_4577_sm_Fig2.TIF||80K||Supporting info item|
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