Factor XI activation in a revised model of blood coagulation

David Gailani; George J. Broze

doi:10.1126/science.1652157

Factor XI activation in a revised model of blood coagulation

David Gailani, George J. Broze

Division of Hematology

Research output: Contribution to journal › Article › peer-review

707 Scopus citations

Abstract

Coagulation factor XI is activated in vitro by factor XIIa in the presence of high molecular weight kininogen (HMWX) and a negatively charged surface. Factor XII deficiency is not associated with bleeding, which suggests that another mechanism for factor XI activation exists in vivo. A revised model of coagulation is proposed in which factor XI is activated by thrombin. In the absence of cofactors, thrombin is more effective (k_cat/K_m = 1.6 × 10⁵) than factor XIIa (1.7 × 10⁴) in activating factor XI. Dextran sulfate enhances activation of factor XI by thrombin 2000-fold; part of this effect is due to autoactivation of factor XI by activated factor XI.

Original language	English
Pages (from-to)	909-912
Number of pages	4
Journal	Science
Volume	253
Issue number	5022
DOIs	https://doi.org/10.1126/science.1652157
State	Published - 1991

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abstract = "Coagulation factor XI is activated in vitro by factor XIIa in the presence of high molecular weight kininogen (HMWX) and a negatively charged surface. Factor XII deficiency is not associated with bleeding, which suggests that another mechanism for factor XI activation exists in vivo. A revised model of coagulation is proposed in which factor XI is activated by thrombin. In the absence of cofactors, thrombin is more effective (kcat/Km = 1.6 × 105) than factor XIIa (1.7 × 104) in activating factor XI. Dextran sulfate enhances activation of factor XI by thrombin 2000-fold; part of this effect is due to autoactivation of factor XI by activated factor XI.",

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T1 - Factor XI activation in a revised model of blood coagulation

AU - Gailani, David

AU - Broze, George J.

PY - 1991

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N2 - Coagulation factor XI is activated in vitro by factor XIIa in the presence of high molecular weight kininogen (HMWX) and a negatively charged surface. Factor XII deficiency is not associated with bleeding, which suggests that another mechanism for factor XI activation exists in vivo. A revised model of coagulation is proposed in which factor XI is activated by thrombin. In the absence of cofactors, thrombin is more effective (kcat/Km = 1.6 × 105) than factor XIIa (1.7 × 104) in activating factor XI. Dextran sulfate enhances activation of factor XI by thrombin 2000-fold; part of this effect is due to autoactivation of factor XI by activated factor XI.

AB - Coagulation factor XI is activated in vitro by factor XIIa in the presence of high molecular weight kininogen (HMWX) and a negatively charged surface. Factor XII deficiency is not associated with bleeding, which suggests that another mechanism for factor XI activation exists in vivo. A revised model of coagulation is proposed in which factor XI is activated by thrombin. In the absence of cofactors, thrombin is more effective (kcat/Km = 1.6 × 105) than factor XIIa (1.7 × 104) in activating factor XI. Dextran sulfate enhances activation of factor XI by thrombin 2000-fold; part of this effect is due to autoactivation of factor XI by activated factor XI.

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U2 - 10.1126/science.1652157

DO - 10.1126/science.1652157

M3 - Article

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SN - 0036-8075

VL - 253

SP - 909

EP - 912

JO - Science

JF - Science

IS - 5022

ER -

Factor XI activation in a revised model of blood coagulation

Abstract

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