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KNOCKOUT Maus Produkte

20.04.2015

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Mouse Factor XII genetically deficient plasma, sodium citrate
Art.Nr. 402194 - Art.Code MFXII-KO-SC - 0,05 ml
Art.Nr. 402195 - Art.Code MFXII-KO-SC -   0,1 ml

This plasma is an ideal negative control for ELISA based assays and other experiments involving Factor XII. collected from Homozygous Factor XII knockout mice, anticoagulated with sodium citrate and flash frozen. Collected from male mice. Female mouse plasma is also available. Freshly collected Factor XII knockout mouse organs are also available.
The targeted Factor XII knockout mutation was made on embryonic stem cells in 129SvJ chimeric mice then cross bred with C57BL/6 wild type mice. The Factor XII gene is totally inactivated by replacement of exons 3-8 with the neomycin resistance gene. Mice homozygous for this mutation develop normally and are viable and fertile. aPTT is greatly increased but PT is normal compared to wild type mice. Factor XII null mice were shown to be protected from ischemic stroke in a transient middle cerebral artery occlusion animal model of stroke.


Mouse PAI-1 genetically deficient plasma, sodium citrate
Art.Nr. 401424 - Art.Code MPAI-KO-SC - 0,05 ml
Art.Nr. 401425 - Art.Code MPAI-KO-SC -   0,1 ml

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. Collected from male mice. Female mouse plasma is also available.
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.


Mouse PAI-1 genetically deficient brain (Cryostat material)
Art.Nr. 401414 - Art.Code MPAI-KO-BR - 1 brain
Art.Nr. 401415 - Art.Code MPAI-KO-BR - 2 brains

Mouse PAI-1 genetically deficient heart (Cryostat material)
Art.Nr. 401416 - Art.Code MPAI-KO-HT - 1 heart
Art.Nr. 401417 - Art.Code MPAI-KO-HT - 2 hearts

Mouse PAI-1 genetically deficient kidney (Cryostat material)
Art.Nr. 401418 - Art.Code MPAI-KO-KD - 1 kidney
Art.Nr. 401419 - Art.Code MPAI-KO-KD - 2 kidneys

Mouse PAI-1 genetically deficient liver (Cryostat material)
Art.Nr. 401422 - Art.Code MPAI-KO-LR - 1 liver
Art.Nr. 401423 - Art.Code MPAI-KO-LR - 2 livers

Mouse PAI-1 genetically deficient lung (Cryostat material)
Art.Nr. 401420 - Art.Code MPAI-KO-LG - 1 lobe
Art.Nr. 401421 - Art.Code MPAI-KO-LG - whole lung

Mouse PAI-1 genetically deficient spleen (Cryostat material)
Art.Nr. 401426 - Art.Code MPAI-KO-SP - 1 spleen
Art.Nr. 401427 - Art.Code MPAI-KO-SP - 2 spleens

This organs are 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.

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