EC Number |
General Information |
Reference |
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3.4.21.69 | malfunction |
a recombinant APC variant (APCN329Q) mimicking the naturally occurring APC-beta plasma glycoform exhibits superior PAR1 proteolysis at a cleavage site that selectively mediates cytoprotective signaling.Mutant APCN329Q also enhances integrin aMb2-dependent PAR1 proteolysis to exert significantly improved anti-inflammatory activity on macrophages compared with wild-type APC |
753066 |
3.4.21.69 | malfunction |
a recombinant APC variant (APCN329Q) mimicking the naturally occurring APC-beta plasma glycoform exhibits superior PAR1 proteolysis at a cleavage site that selectively mediates cytoprotective signaling.Mutant APCN329Q also enhances integrin aMb2-dependent PAR1 proteolysis to exert significantly improved anti-inflammatory activity on macrophages compared with wild-type APC. Enhanced cytoprotective PAR1 signaling by APC-beta is a consequence of accelerated EPCR-dependent PAR1 proteolysis |
753066 |
3.4.21.69 | malfunction |
APC's cleavage in protease activated receptor 1 at a noncanonical Arg46 site through the APC mutant 3K3A-APC causes biased signaling that provides a major explanation for APC's in vivo mechanism of action for neuroprotective activities. Structure-activity relationships of protein C is used to analyse protein C dysfunction in venous thrombosis patients who have protein C mutations |
753070 |
3.4.21.69 | malfunction |
blocking Tie2 restricts endothelial barrier integrity. On blocking the Tie2 receptor, binding between APC and Tie2 is inhibited significantly irrespective of APC concentration |
753217 |
3.4.21.69 | malfunction |
coagulation factor V mediates inhibition of tissue factor signaling by activated protein C in mice. aPC resistance of factor (f)V due to the R506Q Leiden mutation protects against detrimental anticoagulant effects of aPC therapy but also abrogates the anti-inflammatory and mortality reducing effects of the signaling-selective 5A-aPC variant that has minimal anticoagulant function. aPC resistance of fV Leiden suppresses in vitro regulation of inflammatory gene expression by aPC, overview |
753065 |
3.4.21.69 | malfunction |
Mac-1 inhibition prevents APC attenuation of pro-inflammatory cytokine release from lipopolysaccharide (LPS)-stimulated murine macrophages. Furthermore, APC administration does not significantly reduce mortality in Mac-1 deficient endotoxemic mice, suggestive of an important role for Mac-1-dependent PAR1 activation on myeloid cells for the ability of APC to limit mortality in murine endotoxemia |
752736 |
3.4.21.69 | malfunction |
naturally occuring mutation G216D in the specificity pocket of the enzyme causes protein C deficiency. Superposition of the integrin binding motifs in wild-type and mutant forms suggests that the interaction with integrin can still occur and thus the mutant is likely to retain its antiseptic function related to the neutrophyl integrin binding |
732199 |
3.4.21.69 | malfunction |
potent neuroprotection in murine ischemic stroke models is linked to enzyme mutant 3K3A-APC-induced signaling that arises due to APC's cleavage in protease activated receptor 1 at a noncanonical Arg46 site. This cleavage causes biased signaling that provides a major explanation for APC's in vivo mechanism of action for neuroprotective activities. Mice carrying the 46QQ-PAR1 point mutation strongly support the concept that APC-induced, PAR1-dependent biased signaling following Arg46 cleavage is central to APC's in vivo neuroprotective benefits in this model of ischemic stroke |
753070 |
3.4.21.69 | malfunction |
severe thrombophilia occurs with deficiencies in phosphatidylcholine or phosphatidylserine and with a mutation in factor Va that prevents its inactivation by APC, known as Factor V Leiden |
717574 |
3.4.21.69 | metabolism |
activated protein C is the key effector molecule of the natural protein C pathway. Biological function and mechanism of the protein C pathway in which protein S and the aPC-cleaved form of factor V are cofactors for anti-inflammatory cell signaling by aPC in the context of endotoxemia and infection, overview |
753065 |