Combined In Vivo Depletion of Glycoprotein VI and C-Type Lectin-Like Receptor 2 Severely Compromises Hemostasis and Abrogates Arterial Thrombosis in Mice | Zendy

Markus Bender | Zendy; Frauke May | Zendy; Viola Lorenz | Zendy; Ina Thielmann | Zendy; Ina Hagedorn | Zendy; Brenda Finney | Zendy; Timo Vögtle | Zendy; Katharina A. Remer | Zendy; Attila Braun | Zendy; Michael R. Bösl | Zendy; Steve P. Watson | Zendy; Bernhard Nieswandt | Zendy

Open Access

Combined In Vivo Depletion of Glycoprotein VI and C-Type Lectin-Like Receptor 2 Severely Compromises Hemostasis and Abrogates Arterial Thrombosis in Mice

Author(s) -

Markus Bender,

Frauke May,

Viola Lorenz,

Ina Thielmann,

Ina Hagedorn,

Brenda Finney,

Timo Vögtle,

Katharina A. Remer,

Attila Braun,

Michael R. Bösl,

Steve P. Watson,

Bernhard Nieswandt

Publication year - 2013

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.112.300672

Subject(s) - gpvi , platelet membrane glycoprotein , platelet , hemostasis , platelet activation , receptor , chemistry , antithrombotic , in vivo , medicine , immunology , cancer research , microbiology and biotechnology , biology

Platelet inhibition is a major strategy to prevent acute ischemic cardiovascular and cerebrovascular events, which may, however, be associated with an increased bleeding risk. The (hem)immunoreceptor tyrosine activation motif-bearing platelet receptors, glycoprotein VI (GPVI) and C-type lectin-like receptor 2 (CLEC-2), might be promising antithrombotic targets because they can be depleted from circulating platelets by antibody treatment, leading to sustained antithrombotic protection, but only moderately increased bleeding times in mice.

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