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Factor XI deficiency in animal models

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Factor XI deficiency in animal models. / Renné, T; Oschatz, C; Seifert, S; Müller, F; Antovic, J; Karlman, M; Benz, P M.

in: J THROMB HAEMOST, Jahrgang 7 Suppl 1, 01.07.2009, S. 79-83.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Renné, T, Oschatz, C, Seifert, S, Müller, F, Antovic, J, Karlman, M & Benz, PM 2009, 'Factor XI deficiency in animal models', J THROMB HAEMOST, Jg. 7 Suppl 1, S. 79-83. https://doi.org/10.1111/j.1538-7836.2009.03393.x

APA

Renné, T., Oschatz, C., Seifert, S., Müller, F., Antovic, J., Karlman, M., & Benz, P. M. (2009). Factor XI deficiency in animal models. J THROMB HAEMOST, 7 Suppl 1, 79-83. https://doi.org/10.1111/j.1538-7836.2009.03393.x

Vancouver

Renné T, Oschatz C, Seifert S, Müller F, Antovic J, Karlman M et al. Factor XI deficiency in animal models. J THROMB HAEMOST. 2009 Jul 1;7 Suppl 1:79-83. https://doi.org/10.1111/j.1538-7836.2009.03393.x

Bibtex

@article{0264e20315084f41a650b807ae759bfc,
title = "Factor XI deficiency in animal models",
abstract = "The blood coagulation system forms fibrin to limit blood loss from sites of injury, but also contributes to occlusive diseases such as deep vein thrombosis, myocardial infarction, and stroke. In the current model of a coagulation balance, normal hemostasis and thrombosis represent two sides of the same coin; however, data from coagulation factor XI-deficient animal models have challenged this dogma. Gene targeting of factor XI, a serine protease of the intrinsic pathway of coagulation, severely impairs arterial thrombus formation but is not associated with excessive bleeding. Mechanistically, factor XI may be activated by factor XII following contact activation or by thrombin in a feedback activation loop. This review focuses on the role of factor XI, and its deficiency states as novel target for prevention of thrombosis with low bleeding risk in animal models.",
keywords = "Animals, Disease Models, Animal, Factor XI Deficiency, Hemorrhage, Hemostasis, Thrombosis",
author = "T Renn{\'e} and C Oschatz and S Seifert and F M{\"u}ller and J Antovic and M Karlman and Benz, {P M}",
year = "2009",
month = jul,
day = "1",
doi = "10.1111/j.1538-7836.2009.03393.x",
language = "English",
volume = "7 Suppl 1",
pages = "79--83",
journal = "J THROMB HAEMOST",
issn = "1538-7933",
publisher = "Wiley-Blackwell",

}

RIS

TY - JOUR

T1 - Factor XI deficiency in animal models

AU - Renné, T

AU - Oschatz, C

AU - Seifert, S

AU - Müller, F

AU - Antovic, J

AU - Karlman, M

AU - Benz, P M

PY - 2009/7/1

Y1 - 2009/7/1

N2 - The blood coagulation system forms fibrin to limit blood loss from sites of injury, but also contributes to occlusive diseases such as deep vein thrombosis, myocardial infarction, and stroke. In the current model of a coagulation balance, normal hemostasis and thrombosis represent two sides of the same coin; however, data from coagulation factor XI-deficient animal models have challenged this dogma. Gene targeting of factor XI, a serine protease of the intrinsic pathway of coagulation, severely impairs arterial thrombus formation but is not associated with excessive bleeding. Mechanistically, factor XI may be activated by factor XII following contact activation or by thrombin in a feedback activation loop. This review focuses on the role of factor XI, and its deficiency states as novel target for prevention of thrombosis with low bleeding risk in animal models.

AB - The blood coagulation system forms fibrin to limit blood loss from sites of injury, but also contributes to occlusive diseases such as deep vein thrombosis, myocardial infarction, and stroke. In the current model of a coagulation balance, normal hemostasis and thrombosis represent two sides of the same coin; however, data from coagulation factor XI-deficient animal models have challenged this dogma. Gene targeting of factor XI, a serine protease of the intrinsic pathway of coagulation, severely impairs arterial thrombus formation but is not associated with excessive bleeding. Mechanistically, factor XI may be activated by factor XII following contact activation or by thrombin in a feedback activation loop. This review focuses on the role of factor XI, and its deficiency states as novel target for prevention of thrombosis with low bleeding risk in animal models.

KW - Animals

KW - Disease Models, Animal

KW - Factor XI Deficiency

KW - Hemorrhage

KW - Hemostasis

KW - Thrombosis

U2 - 10.1111/j.1538-7836.2009.03393.x

DO - 10.1111/j.1538-7836.2009.03393.x

M3 - SCORING: Journal article

C2 - 19630774

VL - 7 Suppl 1

SP - 79

EP - 83

JO - J THROMB HAEMOST

JF - J THROMB HAEMOST

SN - 1538-7933

ER -