Dual-specificity phosphatase 3 deficiency or inhibition limits platelet activation and arterial thrombosis.

ABSTRACT:

Background

A limitation of current antiplatelet therapies is their inability to separate thrombotic events from bleeding occurrences. A better understanding of the molecular mechanisms leading to platelet activation is important for the development of improved therapies. Recently, protein tyrosine phosphatases have emerged as critical regulators of platelet function.

Methods and results

This is the first report implicating the dual-specificity phosphatase 3 (DUSP3) in platelet signaling and thrombosis. This phosphatase is highly expressed in human and mouse platelets. Platelets from DUSP3-deficient mice displayed a selective impairment of aggregation and granule secretion mediated by the collagen receptor glycoprotein VI and the C-type lectin-like receptor 2. DUSP3-deficient

SUBMITTER: Musumeci L 

PROVIDER: S-EPMC4334727 | biostudies-literature | 2015 Feb

REPOSITORIES: biostudies-literature