PAI-1 Knockout Mouse Plasma and Organs from
 
Mouse PAI-1 genetically deficient brain
This organ is an ideal negative control for western blotting, immunoprecipitation, immunohistochemistry and other experiments involving PAI-1. Collected and flash frozen from homozygous PAI-1 knockout mice of strain B6.129S2-Serpine1 tm1Mlg /J. The targeted PAI-1 knockout mutation was made on the C57BL/6J background strain. Mice homozygous for this mutation develop normally and are viable and fertile. Compared to wild type mice, pulmonary clot lysis is increased in the heterozygote and further increased in the homozygote. Endotoxin induced venous thrombosis is decreased compared to wild type mice. Thus, disruption of the Serpine1 gene induces a mild hyperfibrinolytic state. Hemostasis is normal in homozygous mutants.

References:
Carmeliet P; Kieckens L; Schoonjans L; Ream B; van Nuffelen A; Prendergast G; Cole M; Bronson R; Collen D; Mulligan RC. 1993. Plasminogen activator inhibitor-1 gene-deficient mice. I. Generation by homologous recombination and characterization. J Clin Invest 92(6):2746-55.



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Mouse PAI-1 genetically deficient heart
This organ is an ideal negative control for western blotting, immunoprecipitation, immunohistochemistry and other experiments involving PAI-1. Collected and flash frozen from homozygous PAI-1 knockout mice of strain B6.129S2-Serpine1 tm1Mlg /J. The targeted PAI-1 knockout mutation was made on the C57BL/6J background strain. Mice homozygous for this mutation develop normally and are viable and fertile. Compared to wild type mice, pulmonary clot lysis is increased in the heterozygote and further increased in the homozygote. Endotoxin induced venous thrombosis is decreased compared to wild type mice. Thus, disruption of the Serpine1 gene induces a mild hyperfibrinolytic state. Hemostasis is normal in homozygous mutants.

References:
Carmeliet P; Kieckens L; Schoonjans L; Ream B; van Nuffelen A; Prendergast G; Cole M; Bronson R; Collen D; Mulligan RC. 1993. Plasminogen activator inhibitor-1 gene-deficient mice. I. Generation by homologous recombination and characterization. J Clin Invest 92(6):2746-55.



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Mouse PAI-1 genetically deficient kidney
This organ is an ideal negative control for western blotting, immunoprecipitation, immunohistochemistry and other experiments involving PAI-1. Collected and flash frozen from homozygous PAI-1 knockout mice of strain B6.129S2-Serpine1 tm1Mlg /J. The targeted PAI-1 knockout mutation was made on the C57BL/6J background strain. Mice homozygous for this mutation develop normally and are viable and fertile. Compared to wild type mice, pulmonary clot lysis is increased in the heterozygote and further increased in the homozygote. Endotoxin induced venous thrombosis is decreased compared to wild type mice. Thus, disruption of the Serpine1 gene induces a mild hyperfibrinolytic state. Hemostasis is normal in homozygous mutants.

References:
Carmeliet P; Kieckens L; Schoonjans L; Ream B; van Nuffelen A; Prendergast G; Cole M; Bronson R; Collen D; Mulligan RC. 1993. Plasminogen activator inhibitor-1 gene-deficient mice. I. Generation by homologous recombination and characterization. J Clin Invest 92(6):2746-55.



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Mouse PAI-1 genetically deficient lung
This organ is an ideal negative control for western blotting, immunoprecipitation, immunohistochemistry and other experiments involving PAI-1. Collected and flash frozen from homozygous PAI-1 knockout mice of strain B6.129S2-Serpine1 tm1Mlg /J. Each mouse lung consists of 5 lobes. The targeted PAI-1 knockout mutation was made on the C57BL/6J background strain. Mice homozygous for this mutation develop normally and are viable and fertile. Compared to wild type mice, pulmonary clot lysis is increased in the heterozygote and further increased in the homozygote. Endotoxin induced venous thrombosis is decreased compared to wild type mice. Thus, disruption of the Serpine1 gene induces a mild hyperfibrinolytic state. Hemostasis is normal in homozygous mutants.

References:
Carmeliet P; Kieckens L; Schoonjans L; Ream B; van Nuffelen A; Prendergast G; Cole M; Bronson R; Collen D; Mulligan RC. 1993. Plasminogen activator inhibitor-1 gene-deficient mice. I. Generation by homologous recombination and characterization. J Clin Invest 92(6):2746-55.



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Mouse PAI-1 genetically deficient liver
This organ is an ideal negative control for western blotting, immunoprecipitation, immunohistochemistry and other experiments involving PAI-1. Collected and flash frozen from homozygous PAI-1 knockout mice of strain B6.129S2-Serpine1 tm1Mlg /J. The targeted PAI-1 knockout mutation was made on the C57BL/6J background strain. Mice homozygous for this mutation develop normally and are viable and fertile. Compared to wild type mice, pulmonary clot lysis is increased in the heterozygote and further increased in the homozygote. Endotoxin induced venous thrombosis is decreased compared to wild type mice. Thus, disruption of the Serpine1 gene induces a mild hyperfibrinolytic state. Hemostasis is normal in homozygous mutants.

References:
Carmeliet P; Kieckens L; Schoonjans L; Ream B; van Nuffelen A; Prendergast G; Cole M; Bronson R; Collen D; Mulligan RC. 1993. Plasminogen activator inhibitor-1 gene-deficient mice. I. Generation by homologous recombination and characterization. J Clin Invest 92(6):2746-55.



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Mouse PAI-1 genetically deficient plasma, sodium citrate
This plasma is an ideal negative control for ELISA based assays and other experiments involving PAI-1. Collected from homozygous PAI-1 knockout mice of strain B6.129S2-Serpine1 tm1Mlg /J. Anticoagulated with sodium citrate and flash frozen. The targeted PAI-1 knockout mutation was made on the C57BL/6J background strain. Mice homozygous for this mutation develop normally and are viable and fertile. Compared to wild type mice, pulmonary clot lysis is increased in the heterozygote and further increased in the homozygote. Endotoxin induced venous thrombosis is decreased compared to wild type mice. Thus, disruption of the Serpine1 gene induces a mild hyperfibrinolytic state. Hemostasis is normal in homozygous mutants.

References:
Carmeliet P; Kieckens L; Schoonjans L; Ream B; van Nuffelen A; Prendergast G; Cole M; Bronson R; Collen D; Mulligan RC. 1993. Plasminogen activator inhibitor-1 gene-deficient mice. I. Generation by homologous recombination and characterization. J Clin Invest 92(6):2746-55.



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Mouse PAI-1 genetically deficient spleen
This organ is an ideal negative control for western blotting, immunoprecipitation, immunohistochemistry and other experiments involving PAI-1. Collected and flash frozen from homozygous PAI-1 knockout mice of strain B6.129S2-Serpine1 tm1Mlg /J. The targeted PAI-1 knockout mutation was made on the C57BL/6J background strain. Mice homozygous for this mutation develop normally and are viable and fertile. Compared to wild type mice, pulmonary clot lysis is increased in the heterozygote and further increased in the homozygote. Endotoxin induced venous thrombosis is decreased compared to wild type mice. Thus, disruption of the Serpine1 gene induces a mild hyperfibrinolytic state. Hemostasis is normal in homozygous mutants.

References:
Carmeliet P; Kieckens L; Schoonjans L; Ream B; van Nuffelen A; Prendergast G; Cole M; Bronson R; Collen D; Mulligan RC. 1993. Plasminogen activator inhibitor-1 gene-deficient mice. I. Generation by homologous recombination and characterization. J Clin Invest 92(6):2746-55.



Click to order!