Browsing by Author "PRESTON, ROGER"
Now showing items 1-6 of 6
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Activated Factor X signaling via protease-activated receptor 2 suppresses pro-inflammatory cytokine prodution from LPS-stimulated myeloid cells.
PRESTON, ROGER; FALLON, PADRAIC (2014)Vitamin K-dependent proteases generated in response to vascular injury and infection enable fibrin clot formation, but also trigger distinct immuno-regulatory signaling pathways on myeloid cells. Factor Xa, a protease ... -
ADAMTS13 substrate recognition of von Willebrand factor A2 domain.
PRESTON, ROGER (2006)ADAMTS13 controls the multimeric size of circulating von Willebrand factor (VWF) by cleaving the Tyr1605?Met1606 bond in theA2 domain. To examine substrate recognition, we expressed in bacteria and purified three A2 ... -
Dissociation of activated protein C functions by elimination of protein S cofactor enhancement.
PRESTON, ROGER; O'DONNELL, JAMES; JOHNSON, JENNIFER; HARMON, SHONA; NI AINLE, FIONNUALA (2008)Activated protein C (APC) plays a critical anticoagulant role in vivo by inactivating procoagulant factor Va and factor VIIIa and thus down-regulating thrombin generation. In addition, APC bound to the endothelial cell ... -
Multifunctional specificity of the protein C/activated protein C Gla domain.
PRESTON, ROGER (American Society for Biochemistry and Molecular Biology, 2006)Activated protein C (APC) has potent anticoagulant and anti-inflammatory properties that are mediated in part by its interactions with its cofactor protein S and the endothelial cell protein C receptor (EPCR). The protein ... -
Platelet factor 4 impairs the anticoagulant activity of activated protein C.
PRESTON, ROGER; HARMON, SHONA; NI AINLE, FIONNUALA; O'DONNELL, JAMES; JOHNSON, JENNIFER (2009)Platelet factor 4 (PF4) is an abundant platelet -granule chemokine released following platelet activation. PF4 interacts with thrombomodulin and the -carboxyglutamic acid (Gla) domain of protein C, thereby enhancing ... -
Severe Plasmodium falciparum malaria is associated with circulating ultra-large von Willebrand multimers and ADAMTS13 inhibition.
PRESTON, ROGER; O'DONNELL, JAMES; JENKINS, P (2009)Plasmodium falciparum infection results in adhesion of infected erythrocytes to blood vessel endothelium, and acute endothelial cell activation, together with sequestration of platelets and leucocytes. We have previously ...