Active Hageman Factor: A Plasma Lysokinase of the Human Fibrinolytic System*

Iatridis, Sotirios G.; Ferguson, John H.

doi:10.1172/jci104590

Cited by 106 publications

(43 citation statements)

References 21 publications

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“…There were no contaminating proteins detected. Plasmin was prepared by activating 500 Al of plasminogen (100,g/ml) with 50 Al (1,500 U) of streptokinase for 30 min at 30'C and assayed on human fibrin plates (4).…”

Section: Isolation Of Components Of the Fibrinolytic Pathwaymentioning

confidence: 99%

“…The fibrinolytic pathway in human plasma is initiated by activation of Hageman factor (1,2). The prealbumin fragments of active Hageman factor isolated from serum or derived experimentally from activated Hageman factor have been shown to activate a plasma protein, the plasminogen proactivator to the plasminogen activator, which in turn converts plasminogen to plasmin (3,4).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Plasma Inhibitors of the Components of the Fibrinolytic Pathway in Man

Schreiber¹,

Kaplan²,

Austen³

1973

J. Clin. Invest.

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Section: Isolation Of Components Of the Fibrinolytic Pathwaymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Plasma Inhibitors of the Components of the Fibrinolytic Pathway in Man

Schreiber¹,

Kaplan²,

Austen³

1973

J. Clin. Invest.

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“…ILagemiian factor (Factor XII) is knoNvii to initiate the I)lasma coagulation (1), kinin-forming (2), and fibrinolytic pathways of human plasma (3,4) by activating the precursor proteins, plasma thromboplastin antecedent (Factor XI) (PTA) 1 (1), prekallikrein (Fletcher factor) (5), and plasminogein proactivator (6), respectivelv, to their respective active enzymes. Although patients with deficiency of Factor XII (Hageman trait) have no symptoms (7), in vitro testing of their plasmas reveals profound defects in surface-activated coagulation, kinin formation, and fibrinolysis.…”

Section: Introductionmentioning

confidence: 99%

Williams trait. Human kininogen deficiency with diminished levels of plasminogen proactivator and prekallikrein associated with abnormalities of the Hageman factor-dependent pathways.

Colman¹,

Bagdasarian²,

Talamo³

et al. 1975

J. Clin. Invest.

322

194

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A B S T R A C T An asymptomatic woman (Ms. \Vil-liams) was found to have a severe abnormality in the surface-activated intrinsic coagulation, fibrinolvtic, and kinin-generating pathways. Assays for known coagulation factors were normal while Fletcher factor (prekallikrein) was 45%, insufficient to account for the observed markedly prolonged partial thromboplastin time. Plasminogen proactivator was present at 20% of normal levels and addition of highly purified plasminogen proactivator containing 10% plasminogen activator partially corrected the coagulation and fibrinolytic abnormalities but not the kinin-generating defect. This effect was due to its plasminogen activator content. In addition, Williams trait plasma failed to convert prekallikrein to kallikrein or release kiniin upon incubation with kaolin. Kininogen

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“…Contact activation involves a sequence of events that is known to initiate intrinsic blood coagulation (1,2), fibrinolysis (3), and the kinin-forming pathway (4). Three other proteins in addition to Factor XI that participate in the contact phase of coagulation are Factor XII, prekallikrein, and high molecular weight (HMW)' kininogen.…”

Section: Introductionmentioning

confidence: 99%

“…During activation by Factor XIIa an internal peptide bond in each of the two 80,000-mol-wt chains is cleaved resulting in the formation of a pair of disulfide-linked heavy and light chains with molecular weights of 50,000 and 30,000 respectively ( [1][2][3][4][5][6][7][8][9][10][11][12][13], with each light chain containing one active site. Factor XI circulates in plasma noncovalently complexed with HMW kininogen (14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of activation of coagulation factor XI by factor XIIa studied with monoclonal antibodies.

Akiyama¹,

Sinha²,

Seaman³

et al. 1986

J. Clin. Invest.

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The interaction of Factor XIIa with Factor XI was investigated using two monoclonal antibodies, one (3C1) directed against the heavy chain of Factor Ma and the other (5F4) against its light chain. 3C1 either as intact IgG or as Fab' fragment, enhanced the rate of Factor Ma generation in the fluid phase but inhibited it in the presence of kaolin and high molecular weight (HMW) kininogen. In contrast, the Fab' fragments of 5F4 inhibited only the fluid phase activation and had no effect on the surface-mediated activation. 3C1 was found to block the binding of Factor XI to HMW kininogen, whereas 5F4 did not. We conclude: (a) a domain on the heavy chain region of Factor XI is essential for binding to HMW kininogen and for optimal surface-mediated activation by Factor MIa; and (b) binding of 3C1 to Factor XI changes its conformation rendering it a more favorable substrate for Factor XIIa in the fluid phase.

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Active Hageman Factor: A Plasma Lysokinase of the Human Fibrinolytic System*

Cited by 106 publications

References 21 publications

Plasma Inhibitors of the Components of the Fibrinolytic Pathway in Man

Plasma Inhibitors of the Components of the Fibrinolytic Pathway in Man

Williams trait. Human kininogen deficiency with diminished levels of plasminogen proactivator and prekallikrein associated with abnormalities of the Hageman factor-dependent pathways.

Mechanism of activation of coagulation factor XI by factor XIIa studied with monoclonal antibodies.

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