Both TMEM16F-dependent and TMEM16F-independent pathways contribute to phosphatidylserine exposure in platelet apoptosis and platelet activation-Reference-Cited by-同舟云学术

Both TMEM16F-dependent and TMEM16F-independent pathways contribute to phosphatidylserine exposure in platelet apoptosis and platelet activation

Published:2013-03-07 Issue:10 Volume:121 Page:1850-1857
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

van Kruchten Roger¹,Mattheij Nadine J. A.¹,Saunders Christine²,Feijge Marion A. H.¹,Swieringa Frauke¹,Wolfs Jef L. N.¹,Collins Peter W.³,Heemskerk Johan W. M.¹,Bevers Edouard M.¹

Affiliation:

1. Department of Biochemistry, Cardiovascular Research Institute Maastricht, University of Maastricht, Maastricht, The Netherlands;

2. Welsh Blood Service, Pontyclun, United Kingdom; and

3. Arthur Bloom Haemophilia Centre, School of Medicine, Cardiff University, Cardiff, United Kingdom

Abstract

Key Points TMEM16F is not essential for apoptosis-induced phosphatidylserine exposure in platelets. Collagen plus thrombin-induced phosphatidylserine exposure in platelets results from 2 distinct pathways, one being TMEM16F dependent.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/121/10/1850/1364162/1850.pdf

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4. Exposure of platelet membrane phosphatidylserine regulates blood coagulation.;Lentz;Prog Lipid Res,2003

5. Platelet collagen receptors and coagulation. A characteristic platelet response as possible target for antithrombotic treatment.;Heemskerk;Trends Cardiovasc Med,2005

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