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Contribution of plasma protease inhibitors to the inactivation of kallikrein in plasma.
TLDR
It is demonstrated that Cl-INH and alpha(2)M are the only significant inhibitors of kallikrein in normal plasma confirming previous predictions based on experiments in purified systems. Expand
Cleavage of human high molecular weight kininogen by factor XIa in vitro. Effect on structure and function.
TLDR
Factor XIa has the potential to act as a regulator of contact-activated coagulation by virtue of its ability to destroy the cofactor function of HMWK after its generation by either kallikrein, factor XIIa, or to a lesser extent, factor XIa, itself. Expand
Prekallikrein activation and high-molecular-weight kininogen consumption in hereditary angioedema.
TLDR
Observations suggest that zymogens of the contact system are activated during attacks of hereditary angioedema and that some of the clinical manifestations may be mediated through products of this pathway, such as kinins. Expand
Protection of human plasma kallikrein from inactivation by C1 inhibitor and other protease inhibitors. The role of high molecular weight kininogen.
TLDR
Kinetic analysis indicated that the kallikrein-high Mr kininogen complex was formed by noncovalent interactions between the light chains of both kall Kikrein and high Mr kin inogen, which protected kallIKrein from inactivation by diisopropyl fluorophosphate. Expand
Function and immunochemistry of prekallikrein-high molecular weight kininogen complex in plasma.
TLDR
The influence of HMW kininogen on both functional and immunologic determinations of prekallikrein is emphasized, with findings that the functional and antigenic properties ofPrekallkrein in plasma from four other HMWKininogen-deficient individuals was similarly corrected to normal after adding HMW Kininogen. Expand
Activation of the contact system of plasma proteolysis in the adult respiratory distress syndrome.
TLDR
Findings showed that the proteins of the contact system were more extensively activated in ARDS than were the proteins that contribute to later reactions in intravascular coagulation and fibrinolysis. Expand
Williams trait. Human kininogen deficiency with diminished levels of plasminogen proactivator and prekallikrein associated with abnormalities of the Hageman factor-dependent pathways.
TLDR
Kininogen is a critical factor required for the functioning of Hageman factor-dependent coagulation and fibrinolysis and for the activation of prekallikrein. Expand
Human plasma kallikrein releases neutrophil elastase during blood coagulation.
TLDR
A series of experiments were carried out to determine if kallikrein was a major enzyme involved in neutrophil elastase release during blood coagulation, and suggest that kallIKrein may be a major enzymes responsible for the release of elastases during bloodCoagulation. Expand
Inactivation of factor XIa by plasma protease inhibitors: predominant role of alpha 1-protease inhibitor and protective effect of high molecular weight kininogen.
TLDR
It is confirmed that alpha(1)-protease inhibitor is the major inhibitor of Factor XIa in plasma, and that the formation of a reversible complex between Factor XI a and HMW kininogen decreases the rate of inactivation of the enzyme by its inhibitors. Expand
Alpha-1-antitrypsin-Pittsburgh. A potent inhibitor of human plasma factor XIa, kallikrein, and factor XIIf.
TLDR
In addition to its potential as an anticoagulant, this recently cloned protein may prove to be clinically valuable in the management of septic shock, hereditary angioedema, or other syndromes involving activation of the surface-mediated plasma proteolytic system. Expand
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