Ontology highlight
ABSTRACT: Background
Immune complexes (ICs) bind to and activate platelets via FcγRIIA, causing patients to experience thrombocytopenia, as well as an increased risk of forming occlusive thrombi. Although platelets have been shown to mediate IC-induced pathologies, the mechanisms involved have yet to be fully elucidated. We identified that apoptosis signal-regulating kinase 1 (ASK1) is present in both human and mouse platelets and potentiates many platelet functions.Objectives
Here we set out to study ASK1's role in regulating IC-mediated platelet functions in vitro and IC-induced pathologies using an in vivo mouse model.Methods
Using human platelets treated with an ASK1-specific inhibitor and platelets from FCGR2A/Ask1-/- transgenic mice, we examined various plate
SUBMITTER: Patel P
PROVIDER: S-EPMC7831975 | biostudies-literature | 2020 Nov
REPOSITORIES: biostudies-literature