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Titolo:
Roles of platelets and factor XI in the initiation of blood coagulation bythrombin
Autore:
Walsh, PN;
Indirizzi:
Temple Univ, Sch Med, Sol Sherry Thrombosis Res Ctr, Dept Med, Philadelphia, PA 19140 USA Temple Univ Philadelphia PA USA 19140 ept Med, Philadelphia, PA 19140 USA Temple Univ, Sch Med, Dept Biochem, Sol Sherry Thrombosis Res Ctr, Philadelphia, PA 19122 USA Temple Univ Philadelphia PA USA 19122 Res Ctr, Philadelphia, PA 19122 USA
Titolo Testata:
THROMBOSIS AND HAEMOSTASIS
fascicolo: 1, volume: 86, anno: 2001,
pagine: 75 - 82
SICI:
0340-6245(200107)86:1<75:ROPAFX>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
MOLECULAR-WEIGHT KININOGEN; PLASMA THROMBOPLASTIN ANTECEDENT; AMYLOID PRECURSOR PROTEIN; ACTIVATED HAGEMAN-FACTOR; BINDING-SITE; FACTOR-IX; TISSUE FACTOR; FUNCTIONAL-CHARACTERIZATION; ANTITHROMBIN-III; POINT MUTATIONS;
Keywords:
factor XI; factor IX; protease nexin II; factor XII; high Mr kininogen;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
130
Recensione:
Indirizzi per estratti:
Indirizzo: Walsh, PN Temple Univ, Sch Med, Sol Sherry Thrombosis Res Ctr, Dept Med, 3400 N Broad St, Philadelphia, PA 19140 USA Temple Univ 3400 N Broad St Philadelphia PA USA 19140 19140 USA
Citazione:
P.N. Walsh, "Roles of platelets and factor XI in the initiation of blood coagulation bythrombin", THROMB HAEM, 86(1), 2001, pp. 75-82

Abstract

To account for the variable hemostatic defect in patients with factor XI (FXI) deficiency, with normal hemostasis in contact factor deficiencies, a coagulation paradigm is presented whereby trace quantities of thrombin, generated transiently by exposure of tissue factor at sites of vascular injury,activates FXI bound to the platelet surface in the presence of prothrombinor high Mr kininogen (HK). Tissue factor pathway inhibitor (TFPI) limits the flux of thrombin generated by the tissue factor pathway, and protease nexin II (PNII), released from activated platelets, inhibits solution phase FXIa and localizes FIX activation to the platelet surface where FXIa is protected from inactivation by PNII. Either prothrombin or HK binds to the Apple 1 (A1) domain of FXI, thereby exposing a platelet-binding site in the FXIA3 domain. Dimeric FXI binds to activated platelets directly through the A3 domain of one monomer. After proteolytic activation of platelet bound FXIby thrombin (or FXIIa), a substrate binding site for FIX is exposed in theopposite monomer that promotes FIX activation on the platelet surface resulting in the local explosive generation of thrombin and the formation of hemostatic thrombi at sites of vascular injury.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/01/20 alle ore 01:31:17