Off-targets effects underlie the inhibitory effect of FAK inhibitors on platelet activation: studies using Fak -deficient mice

Author:

Roh M. E.1,Cosgrove M.1,Gorski K.1,Hitchcock I. S.1

Affiliation:

1. Department of Medicine; Stony Brook University; Stony Brook NY USA

Funder

American Heart Association

Publisher

Wiley

Subject

Hematology

Reference13 articles.

1. Protein kinase C regulates tyrosine phosphorylation of pp 125FAK in platelets adherent to fibrinogen;Haimovich;Blood,1996

2. Tyrosine phosphorylation of pp 125FAK in platelets requires coordinated signaling through integrin and agonist receptors;Shattil;J Biol Chem,1994

3. Tyrosine phosphorylation and cytoskeletal reorganization in platelets are triggered by interaction of integrin receptors with their immobilized ligands;Haimovich;J Biol Chem,1993

4. Roles of focal adhesion kinase (FAK) in megakaryopoiesis and platelet function: studies using a megakaryocyte lineage specific FAK knockout;Hitchcock;Blood,2008

5. Pf4-Cre transgenic mice allow the generation of lineage-restricted gene knockouts for studying megakaryocyte and platelet function in vivo;Tiedt;Blood,2007

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