Strain Name:

C.129S2-Plautm1Mlg/J

Stock Number:

002328

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Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Specieslaboratory mouse
Background Strain BALB/c
Donor Strain 129S2 via D3 ES cell line
 
Donating InvestigatorDr. Peter Carmeliet,   University of Leuven

Description
Homozygotes develop normally, are fertile and have a normal life span. Rectal prolapse of a non-infectious origin develops in 9% of homozygotes and/or extensive non-healing ulcerations occur at the eyelids and around the face. Small, focal fibrin deposits are occasionally seen in the intestines and in the sinusoids of the liver, and excessive fibrin deposits are seen in ulcerated skin or prolapsed rectum. Pulmonary clot lysis is comparable to that seen in normal wildtype siblings. Endotoxin induced venous thrombosis is increased over normal wildtype siblings. Fibrin dissolution by PLAU-deficient macrophages is greatly reduced but macrophage invasion into the peritoneal cavity after thioglycollate injection is unaffected. Homozygous knockout mice have increased levels of Abeta42 and Abeta40 in plasma. Brain Abeta levels are not significantly different than controls. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Control Information

  Control
   000651 BALB/cJ
 
  Considerations for Choosing Controls

Related Strains

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014556   129S6/SvEv-Apoetm4Mae/J
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005708   B6.129-Apbb1tm1Quhu/J
004714   B6.129-Bace1tm1Pcw/J
004098   B6.129-Klc1tm1Gsn/J
004193   B6.129-Psen1tm1Mpm/J
003615   B6.129-Psen1tm1Shn/J
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005617   B6.129P-Psen2tm1Bdes/J
002609   B6.129P2-Nos2tm1Lau/J
007685   B6.129P2-Psen1tm1Vln/J
007999   B6.129P2-Sorl1Gt(Ex255)Byg/J
008087   B6.129S1-Bchetm1Loc/J
002509   B6.129S2-Plautm1Mlg/J
005301   B6.129S2-Tg(APP)8.9Btla/J
004163   B6.129S4-Cdk5r1tm1Lht/J
010959   B6.129S4-Grk5tm1Rjl/J
010960   B6.129S4-Grk5tm2Rjl/J
002213   B6.129S4-Ngfrtm1Jae/J
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006469   B6.129S4-Tg(PSEN1H163R)G9Btla/J
012564   B6.129S5-Dhcr24tm1Lex/SbpaJ
004142   B6.129S7-Aplp2tm1Dbo/J
004133   B6.129S7-Apptm1Dbo/J
007251   B6.129X1-Mapttm1Hnd/J
013040   B6.Cg-Apoetm1Unc Ins2Akita/J
005642   B6.Cg-Clutm1Jakh/J
005491   B6.Cg-Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
009126   B6.Cg-Nos2tm1Lau Tg(Thy1-APPSwDutIowa)BWevn/Mmjax
005866   B6.Cg-Tg(APP695)3Dbo Tg(PSEN1dE9)S9Dbo/Mmjax
008730   B6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax
005864   B6.Cg-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax
007575   B6.Cg-Tg(CAG-Ngb,-EGFP)1Dgrn/J
016197   B6.Cg-Tg(CAG-OTC/CAT)4033Prab/J
005855   B6.Cg-Tg(Camk2a-Prkaca)426Tabe/J
007004   B6.Cg-Tg(Camk2a-tTA)1Mmay/DboJ
004996   B6.Cg-Tg(DBH-Gal)1923Stei/J
007673   B6.Cg-Tg(Gad1-EGFP)3Gfng/J
004662   B6.Cg-Tg(PDGFB-APP)5Lms/J
006293   B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2Mmjax
006006   B6.Cg-Tg(Prnp-APP)A-2Dbo/J
008596   B6.Cg-Tg(Prnp-Abca1)EHol/J
006005   B6.Cg-Tg(Prnp-App/APPswe)E1-2Dbo/Mmjax
007180   B6.Cg-Tg(Prnp-ITM2B/APP695*40)1Emcg/J
007182   B6.Cg-Tg(Prnp-ITM2B/APP695*42)A12Emcg/J
005999   B6.Cg-Tg(SBE/TK-luc)7Twc/J
012597   B6.Cg-Tg(Thy1-COL25A1)861Yfu/J
007051   B6.Cg-Tg(tetO-APPSwInd)102Dbo/Mmjax
007052   B6.Cg-Tg(tetO-APPSwInd)107Dbo/Mmjax
007049   B6.Cg-Tg(tetO-APPSwInd)885Dbo/Mmjax
009337   B6.FVB-Tg(Prnp-RTN3)2Yanr/J
006394   B6;129-Apba2tm1Sud Apba3tm1Sud Apba1tm1Sud/J
008364   B6;129-Chattm1(cre/ERT)Nat/J
008476   B6;129-Ncstntm1Sud/J
004807   B6;129-Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa/Mmjax
007605   B6;129P-Psen1tm1Vln/J
005618   B6;129P2-Bace2tm1Bdes/J
008333   B6;129P2-Dldtm1Ptl/J
002596   B6;129P2-Nos2tm1Lau/J
003822   B6;129S-Psen1tm1Shn/J
012639   B6;129S4-Mapttm3(HDAC2)Jae/J
012869   B6;129S6-Apbb2tm1Her/J
006410   B6;129S6-Chattm2(cre)Lowl/J
005993   B6;129S6-Pcsk9tm1Jdh/J
008636   B6;C-Tg(Prnp-APP695*/EYFP)49Gsn/J
007002   B6;C3-Tg(Prnp-ITM2B/APP695*42)A12Emcg/Mmjax
008169   B6;C3-Tg(Prnp-MAPT*P301S)PS19Vle/J
000231   B6;C3Fe a/a-Csf1op/J
008850   B6;SJL-Tg(Mt1-LDLR)93-4Reh/AgnJ
003378   B6C3-Tg(APP695)3Dbo Tg(PSEN1)5Dbo/J
004462   B6C3-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax
003741   B6D2-Tg(Prnp-MAPT)43Vle/J
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018957   B6N.129S6(B6)-Chattm2(cre)Lowl/J
024841   B6N.Cg-Tg(Prnp-MAPT*P301S)PS19Vle/J
006554   B6SJL-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax
012621   C.129S(B6)-Chrna3tm1.1Hwrt/J
003375   C3B6-Tg(APP695)3Dbo/Mmjax
005087   C57BL/6-Tg(Camk2a-IDE)1Selk/J
005086   C57BL/6-Tg(Camk2a-MME)3Selk/J
008833   C57BL/6-Tg(Camk2a-UBB)3413-1Fwvl/J
007027   C57BL/6-Tg(Thy1-APPSwDutIowa)BWevn/Mmjax
010800   C57BL/6-Tg(Thy1-PTGS2)300Kand/J
010703   C57BL/6-Tg(Thy1-PTGS2)303Kand/J
005706   C57BL/6-Tg(tetO-CDK5R1/GFP)337Lht/J
006618   C57BL/6-Tg(tetO-COX8A/EYFP)1Ksn/J
007677   CB6-Tg(Gad1-EGFP)G42Zjh/J
007072   CByJ.129P2(B6)-Nos2tm1Lau/J
006472   D2.129(B6)-Tg(APPSw)40Btla/Mmjax
007067   D2.129P2(B6)-Apoetm1Unc/J
013719   D2.Cg-Apoetm1Unc Ins2Akita/J
003718   FVB-Tg(GadGFP)45704Swn/J
013732   FVB-Tg(NPEPPS)1Skar/J
013156   FVB-Tg(tetO-CDK5R1*)1Vln/J
015815   FVB-Tg(tetO-MAPT*P301L)#Kha/JlwsJ
002329   FVB.129S2-Plautm1Mlg/J
003753   FVB/N-Tg(Eno2CDK5R1)1Jdm/J
006143   FVB/N-Tg(Thy1-cre)1Vln/J
008051   NOD.129P2(B6)-Ctsbtm1Jde/RclJ
008390   STOCK Apptm1Sud/J
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004779   STOCK Mapttm1(EGFP)Klt/J
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View Alzheimer's Disease Models     (109 strains)

Strains carrying   Plautm1Mlg allele
002509   B6.129S2-Plautm1Mlg/J
002329   FVB.129S2-Plautm1Mlg/J
View Strains carrying   Plautm1Mlg     (2 strains)

Strains carrying other alleles of Plau
014557   C57BL/6-Plautm1.1Bug/J
View Strains carrying other alleles of Plau     (1 strain)

Additional Web Information

Visit the Alzheimer's Disease Mouse Model Resource site for helpful information on Alzheimer's Disease and research resources.

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Alzheimer Disease; AD
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Quebec Platelet Disorder; QPD   (PLAU)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Plautm1Mlg/Plautm1Mlg

        involves: 129S2/SvPas * C57BL/6
  • mortality/aging
  • *normal* mortality/aging
    • homozygotes display a normal lifespan relative to wild-type mice   (MGI Ref ID J:17427)
  • growth/size/body phenotype
  • *normal* growth/size/body phenotype
    • at 5 weeks of age, homozygotes exhibit a normal body weight relative to wild-type mice   (MGI Ref ID J:17427)
  • cardiovascular system phenotype
  • cardiac interstitial fibrosis
    • in response to pressure overload, homozygotes show only minimal signs of maladaptation (i.e. myolysis, fibrosis or increased intercapillary distance) relative to wild-type mice   (MGI Ref ID J:95236)
  • decreased susceptibility to induced choroidal neovascularization
    • in response to laser-induced injury of the Bruch's membrane, homozygotes display almost complete absence of choroidal neovascularization (CNV) at the site of trauma; in contrast, wild-type mice show a robust neovascular reaction   (MGI Ref ID J:82604)
    • resistance to CNV is associated with excessive fibrinogen-fibrin deposition at the site of choroidal trauma and in retinal vessels   (MGI Ref ID J:82604)
  • heart left ventricle hypertrophy
    • after transverse aortic banding (TAB), i.e. acute pressure overload, homozygotes remain significantly protected against LV hypertrophy for at least 7 weeks   (MGI Ref ID J:95236)
    • homozygotes display only a 20% increase in LV/body ratio and only a 22% increase in LV cardiomyocyte size relative to wild-type (~35% and ~40%, respectively)   (MGI Ref ID J:95236)
    • at 7 weeks after TAB, LV systolic dysfunction and dilatation are only marginally detectable without signs of pulmonary edema   (MGI Ref ID J:95236)
  • increased ventricle muscle contractility
    • at 7 weeks after TAB, homozygotes exhibit increased LV contractility, indicating normal fractional shortening with no cardiac failure or pulmonary congestion   (MGI Ref ID J:95236)
  • digestive/alimentary phenotype
  • rectal prolapse
    • at ~22 weeks of age, 9% of homozygotes display rectal prolapse of a non-infectious origin   (MGI Ref ID J:17427)
  • hearing/vestibular/ear phenotype
  • abnormal outer ear morphology
    • at ~26 weeks of age, 5% of homozygotes display severe non-healing ulcerations at the ears around the ear tag and the face   (MGI Ref ID J:17427)
  • hematopoietic system phenotype
  • *normal* hematopoietic system phenotype
    • homozygotes exhibit normal spontaneous lysis of a 125I-fibrin-labeled pulmonary plasma clot relative to wild-type   (MGI Ref ID J:17427)
    • abnormal macrophage physiology
      • in contrast to wild-type, homozygotes exhibit no plasminogen-dependent breakdown of 125I-fibrin-labeled matrix and of 3H-proline-labeled subendothelial breakdown by thioglycollate-activated macrohages; invasion of macrophages into the peritoneal cavity remains unaffected   (MGI Ref ID J:17427)
      • impaired macrophage chemotaxis
        • 5 days after bleomycin treatment, homozygotes display a peak in lung macrophage levels that coincides with the peak time observed in wild-type mice; however, their marcophage levels are significantly reduced relative to wild-type   (MGI Ref ID J:63134)
        • 7 days after bleomycin treatment, mutant and wild-type mice show a similar decrease in the number and percentage of macrophages found in the lung   (MGI Ref ID J:63134)
    • abnormal neutrophil physiology
      • 48 hours after intranasal inoculation with S. pneumoniae, homozygotes exhibit an enhanced antibacterial host defense, with less pneumococci in their lungs and increased neutrophil influx in the bronchoalveolar lavage fluid but no reduction in mortality relative to wild-type   (MGI Ref ID J:75573)
      • relative to wild-type, purified neutrophils from mutant mice exhibit a ~50% reduction in superoxide production in response to fMLP (a potent chemotaxin and activator of neutrophils) across the entire dose range tested; repletion with murine uPA completely reverses the defect in superoxide generation   (MGI Ref ID J:91980)
      • in response to fMLP, mutant neutrophils exhibit reduced neutrophil exocytosis of azurophilic granules (as shown by reduced myeloperoxidase release); however, this defect is not corrected by repletion with extracellular uPA   (MGI Ref ID J:91980)
      • in contrast, mutant neutrophils show normal agonist-stimulated release of specific granules relative to wild-type neutrophils   (MGI Ref ID J:91980)
      • impaired neutrophil phagocytosis
        • in vitro, purified neutrophils from mutant mice exhibit a significant reduction in phagocytosis of E. coli at all time points; repletion with murine uPA substantially reverses the defect in neutrophil phagocytosis   (MGI Ref ID J:91980)
    • impaired granulocyte bactericidal activity
      • in vitro, purified neutrophils from mutant mice display significant defects in several aspects of the antibacterial neutrophil activation process that lead to E. coli killing and effective host defense   (MGI Ref ID J:91980)
    • increased lymphocyte cell number
      • at day 7 post-treatment, the decline in macrophage counts coincides with an increase in the percentage of lymphocytes found in the lungs of bleomycin-treated mice   (MGI Ref ID J:63134)
  • immune system phenotype
  • abnormal acute phase protein level
    • bleomycin-treated homozygotes exhibit extensive areas of fibrin(ogen) deposition in the lung interstitium which are associated with areas of fibrosis   (MGI Ref ID J:63134)
    • after laser-induced injury of the Bruch's membrane, homozygotes show massive accumulation of fibrinogen-fibrin both in the retinal vessels, and in the bottom of the laser-induced trauma   (MGI Ref ID J:82604)
  • abnormal cell-mediated immunity
    • homozygotes fail to generate a type 2 immune response following schistosomal antigen challenge   (MGI Ref ID J:87817)
    • in response to schistosomal egg antigen (SEA), homozygotes fail to develop a delayed-type hypersensitivity response to SEA, do not polarize Ig production to IgE, fail to produce high levels of IL-4, IL-5, or IL-13 and generate pulmonary granulomas that are deficient in eosinophils   (MGI Ref ID J:87817)
    • homozygotes fail to generate a type 1 immune response in the lung during pulmonary fungal infection with C. neoformans   (MGI Ref ID J:95638)
    • in response to C. neoformans infection, homozygotes show impaired T cell proliferation in regional lymph nodes and fail to produce high levels of T1 cytokines (IFN-gamma and IL-12) in the lung; instead, mutants exhibit increased levels of IL-5, a T2 cytokine   (MGI Ref ID J:95638)
    • abnormal macrophage physiology
      • in contrast to wild-type, homozygotes exhibit no plasminogen-dependent breakdown of 125I-fibrin-labeled matrix and of 3H-proline-labeled subendothelial breakdown by thioglycollate-activated macrohages; invasion of macrophages into the peritoneal cavity remains unaffected   (MGI Ref ID J:17427)
      • impaired macrophage chemotaxis
        • 5 days after bleomycin treatment, homozygotes display a peak in lung macrophage levels that coincides with the peak time observed in wild-type mice; however, their marcophage levels are significantly reduced relative to wild-type   (MGI Ref ID J:63134)
        • 7 days after bleomycin treatment, mutant and wild-type mice show a similar decrease in the number and percentage of macrophages found in the lung   (MGI Ref ID J:63134)
    • abnormal neutrophil physiology
      • 48 hours after intranasal inoculation with S. pneumoniae, homozygotes exhibit an enhanced antibacterial host defense, with less pneumococci in their lungs and increased neutrophil influx in the bronchoalveolar lavage fluid but no reduction in mortality relative to wild-type   (MGI Ref ID J:75573)
      • relative to wild-type, purified neutrophils from mutant mice exhibit a ~50% reduction in superoxide production in response to fMLP (a potent chemotaxin and activator of neutrophils) across the entire dose range tested; repletion with murine uPA completely reverses the defect in superoxide generation   (MGI Ref ID J:91980)
      • in response to fMLP, mutant neutrophils exhibit reduced neutrophil exocytosis of azurophilic granules (as shown by reduced myeloperoxidase release); however, this defect is not corrected by repletion with extracellular uPA   (MGI Ref ID J:91980)
      • in contrast, mutant neutrophils show normal agonist-stimulated release of specific granules relative to wild-type neutrophils   (MGI Ref ID J:91980)
      • impaired neutrophil phagocytosis
        • in vitro, purified neutrophils from mutant mice exhibit a significant reduction in phagocytosis of E. coli at all time points; repletion with murine uPA substantially reverses the defect in neutrophil phagocytosis   (MGI Ref ID J:91980)
    • impaired granulocyte bactericidal activity
      • in vitro, purified neutrophils from mutant mice display significant defects in several aspects of the antibacterial neutrophil activation process that lead to E. coli killing and effective host defense   (MGI Ref ID J:91980)
  • increased lymphocyte cell number
    • at day 7 post-treatment, the decline in macrophage counts coincides with an increase in the percentage of lymphocytes found in the lungs of bleomycin-treated mice   (MGI Ref ID J:63134)
  • increased susceptibility to fungal infection
    • 21 days after inoculation with Cryptococcus neoformans, homozygotes contain significantly higher lung CFUs than wild-type mice   (MGI Ref ID J:95637)
    • C. neoformans-infected mutants disseminate the fungal pathogen to their spleen; eventually 15 out of 19 mutants (versus 3/19 wild-type) die from fungal meningitis   (MGI Ref ID J:95637)
  • increased susceptibility to parasitic infection
    • when primed homozygotes are challenged with schistosomal egg antigen (SEA) they exhibit a severe immune defect in response to this T2-eliciting antigen   (MGI Ref ID J:87817)
  • muscle phenotype
  • increased ventricle muscle contractility
    • at 7 weeks after TAB, homozygotes exhibit increased LV contractility, indicating normal fractional shortening with no cardiac failure or pulmonary congestion   (MGI Ref ID J:95236)
  • reproductive system phenotype
  • *normal* reproductive system phenotype
    • homozygotes display normal litter size and frequency of litters relative to wild-type mice   (MGI Ref ID J:17427)
  • respiratory system phenotype
  • pulmonary interstitial fibrosis
    • 14 days after bleomycin treatment, homozygotes exhibit an increase in lung hydroxyproline (collagen) content that is comparable to that observed in bleomycin-treated wild-type mice   (MGI Ref ID J:63134)
    • histological analysis 14 days after lung injury indicates extensive interstitial fibrosis in mutant mice relative to wild-type; however, no hemorrhage or extensive collagen deposition is observed   (MGI Ref ID J:63134)
    • 62% of bleomycin-treated homozygotes die as early as ~7 days after treatment, possibly as a result of extensive fibrosis   (MGI Ref ID J:63134)
  • vision/eye phenotype
  • abnormal eyelid morphology
    • at ~26 weeks of age, 5% homozygotes display severe non-healing ulcerations at the eyelids   (MGI Ref ID J:17427)
  • decreased susceptibility to induced choroidal neovascularization
    • in response to laser-induced injury of the Bruch's membrane, homozygotes display almost complete absence of choroidal neovascularization (CNV) at the site of trauma; in contrast, wild-type mice show a robust neovascular reaction   (MGI Ref ID J:82604)
    • resistance to CNV is associated with excessive fibrinogen-fibrin deposition at the site of choroidal trauma and in retinal vessels   (MGI Ref ID J:82604)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • homozygotes subjected to focal cerebral ischemia induced by persistent occlusion of the left middle cerebral artery produce an infarct with a size that is comparable to that produced in wild-type mice   (MGI Ref ID J:55243)
    • Abeta40 and 42 levels are not increased in mutant brains relative to controls   (MGI Ref ID J:104962)
  • homeostasis/metabolism phenotype
  • abnormal acute phase protein level
    • bleomycin-treated homozygotes exhibit extensive areas of fibrin(ogen) deposition in the lung interstitium which are associated with areas of fibrosis   (MGI Ref ID J:63134)
    • after laser-induced injury of the Bruch's membrane, homozygotes show massive accumulation of fibrinogen-fibrin both in the retinal vessels, and in the bottom of the laser-induced trauma   (MGI Ref ID J:82604)
  • abnormal circulating protein level
    • 3-6 month-old mice have elevated levels of plasma amyloid beta 42 (Abeta42) and Abeta40; by 11 months of age, difference in levels between mutants and controls has increased significantly   (MGI Ref ID J:104962)
  • thrombosis
    • homozygotes occasionally exhibit small, focal fibrin deposits in the intestines and in the sinusoids of the liver and extensive fibrin deposits in the ulcerated skin, ear or prolapsed rectum   (MGI Ref ID J:17427)
    • in response to injection of pro-inflammatory endotoxin in the footpad, homozygotes exhibit overt venous thrombosis at a significantly higher incidence (90% versus 54%) and to a much larger extent than wild-type mice (60% of mutants show >4 thrombosed veins per tissue section versus only 15% in wild-type)   (MGI Ref ID J:17427)
  • craniofacial phenotype
  • abnormal outer ear morphology
    • at ~26 weeks of age, 5% of homozygotes display severe non-healing ulcerations at the ears around the ear tag and the face   (MGI Ref ID J:17427)
  • cellular phenotype
  • impaired macrophage chemotaxis
    • 5 days after bleomycin treatment, homozygotes display a peak in lung macrophage levels that coincides with the peak time observed in wild-type mice; however, their marcophage levels are significantly reduced relative to wild-type   (MGI Ref ID J:63134)
    • 7 days after bleomycin treatment, mutant and wild-type mice show a similar decrease in the number and percentage of macrophages found in the lung   (MGI Ref ID J:63134)

Plautm1Mlg/Plautm1Mlg

        either: B6.Cg-Plautm1Mlg or (involves: Black Swiss * C57BL/6)
  • homeostasis/metabolism phenotype
  • reduced thrombolysis
    • in a model of pulmonary microembolism, wild-type mice are able to clear 125I-microemboli rapidly with complete lysis by 5 hours; in contrast, mutants remain unable to lyse pulmonary microemboli throughout the 5-hr experimental period   (MGI Ref ID J:64220)
    • in these mutants, impaired fibrinolysis can be rescued completely by providing urokinase exogenously   (MGI Ref ID J:64220)

Plautm1Mlg/Plautm1Mlg

        B6.Cg-Plautm1Mlg
  • tumorigenesis
  • altered tumor morphology
    • 3 weeks after implantation of T241 fibrosarcoma cells, primary tumors from mutant mice appear to be better delineated and less hemorrhagic than tumors from wild-type mice   (MGI Ref ID J:65383)
    • also, tumors from mutant mice show an increase in collagen deposition at the periphery of the lesion, forming a fibrous and thick pseudocapsule that is almost undetectable in tumors from wild-type mice   (MGI Ref ID J:65383)
    • ultrastructurally, fibrosarcoma tumor neovessels formed in mutant mice are larger and less mature than tumor vessels from wild-type mice   (MGI Ref ID J:65383)
    • decreased tumor growth/size
      • 3 weeks after implantation of T241 fibrosarcoma cells, primary tumors from mutant mice are significantly smaller than tumors from wild-type mice   (MGI Ref ID J:65383)
      • consistent with tumor growth suppression, tumor tissues from mutant mice exhibit lower proliferative and higher apoptotic indices relative to tumor tissues from wild-type mice   (MGI Ref ID J:65383)
  • decreased metastatic potential
    • following implantation of T241 fibrosarcoma cells, only a limited number of mutants develop metastatic lesions in the lung and brain; in contrast, almost all of wild-type mice display metastases to the same locations   (MGI Ref ID J:65383)
    • notably, only mutants that survive for longer periods (2 months) after the injection develop these lesions, indicating a delay in metastasis   (MGI Ref ID J:65383)
  • digestive/alimentary phenotype
  • abnormal perineum morphology
    • in males with rectal prolapse, the perineal region is swollen on both sides of the evaginated rectal mucosa   (MGI Ref ID J:73613)
  • abnormal rectum morphology
    • in males with rectal prolapse, the rectal mucosa is exteriorized and evaginated   (MGI Ref ID J:73613)
    • rectal prolapse
      • starting at 6 months, male (but not female) homozygotes show a high incidence of rectal prolapse   (MGI Ref ID J:73613)
      • in mutant males, rectal prolapse is irreducible and completely exteriorized by 12 months   (MGI Ref ID J:73613)
  • endocrine/exocrine gland phenotype
  • herniated seminal vesicle
    • males with rectal prolapse develop an irreducible hernia of the seminal vesicles through the pelvic outlet and through a hiatus found between the iliococcygeus (ISC), the bulbocavrnosus (BC), and the tail   (MGI Ref ID J:73613)
    • this hernia results in chronic stretching and thinning of the ISC, BC, and levator ani (LA) pelvic floor muscles   (MGI Ref ID J:73613)
  • immune system phenotype
  • abnormal acute phase protein level
    • at 9 days after glycerol-induced injury of skeletal muscles, homozygotes exhibit abundant fibrin deposits in degenerating muscle fibers   (MGI Ref ID J:68083)
  • abnormal cytokine level
    • in a model of collagen-induced arthritis, arthritic homozygotes exhibit a significant reduction in interleukin-1beta levels in the synovium relative to wild-type   (MGI Ref ID J:75303)
    • in a model of collagen-induced arthritis, arthritic homozygotes exhibit a significant reduction in TNF levels in the synovium relative to wild-type   (MGI Ref ID J:75303)
  • decreased T cell proliferation
    • despite a normal antibody response to type II collagen, T cells from arthritic homozygotes show a reduced proliferative response and produce less interferon-gamma on antigen stimulation in vitro   (MGI Ref ID J:75303)
  • decreased inflammatory response
    • in response to glycerol-induced muscle degeneration, homozygotes display significantly reduced numbers of macrophages and neutrophils at the site of injury relative to wild-type   (MGI Ref ID J:68083)
  • decreased susceptibility to induced arthritis
    • in a model of collagen-induced arthritis, homozygotes develop a significantly milder disease than wild-type mice, with little inflammation and joint destruction   (MGI Ref ID J:75303)
    • in this chronic systemic model, the affected limbs of mutants are rigid but not swollen; arthritis is largely confined to the ankle joint, with most joints in the feet appearing normal   (MGI Ref ID J:75303)
    • surprisingly, the joints of arthritic homozygotes display minimal fibrin(ogen) deposition relative to wild-type   (MGI Ref ID J:75303)
  • impaired macrophage chemotaxis
    • in response to skeletal muscle degeneration, homozygotes display a 50% reduction in macrophage recruitment at the injury site 48 hours after glycerol-induced injury   (MGI Ref ID J:68083)
  • muscle phenotype
  • abnormal muscle regeneration
    • in response to glycerol-induced injury, homozygotes exhibit a severe skeletal muscle regeneration defect relative to wild-type; this defect is apparent at 5 days but is most striking at 9 and 20 days after injury   (MGI Ref ID J:68083)
    • at 5 days after injury, skeletal muscles from mutant mice appear edematous; in contrast to wild-type, no uninucleated, small myofibers are yet formed   (MGI Ref ID J:68083)
    • at 7 days after injury, most injured skeletal muscles appear necrotic and show extensive fibrosis   (MGI Ref ID J:68083)
    • at 9 and 20 days, numerous degenerated myotubes and fibrosis are still visible in mutant muscles whereas no signs of previous damage are detectable in wild-type muscles   (MGI Ref ID J:68083)
    • systemic fibrinogen depletion via ancrod administration restores muscle regeneration: 9 days after injury, ancrod-treated mutants exhibit improved muscle regeneration, with centrally located nuclei inside the regenerated fibers   (MGI Ref ID J:68083)
  • myopathy
    • males with rectal prolapse, exhibit myopathic damage in the affected pelvic floor muscles (ISC, BC and LA)   (MGI Ref ID J:73613)
    • most affected myofibers have centrally located nuclei; some show basophilic degeneration in the absence of denervation, fibrosis or inflammation   (MGI Ref ID J:73613)
  • reproductive system phenotype
  • abnormal perineum morphology
    • in males with rectal prolapse, the perineal region is swollen on both sides of the evaginated rectal mucosa   (MGI Ref ID J:73613)
  • herniated seminal vesicle
    • males with rectal prolapse develop an irreducible hernia of the seminal vesicles through the pelvic outlet and through a hiatus found between the iliococcygeus (ISC), the bulbocavrnosus (BC), and the tail   (MGI Ref ID J:73613)
    • this hernia results in chronic stretching and thinning of the ISC, BC, and levator ani (LA) pelvic floor muscles   (MGI Ref ID J:73613)
  • skeleton phenotype
  • decreased susceptibility to induced arthritis
    • in a model of collagen-induced arthritis, homozygotes develop a significantly milder disease than wild-type mice, with little inflammation and joint destruction   (MGI Ref ID J:75303)
    • in this chronic systemic model, the affected limbs of mutants are rigid but not swollen; arthritis is largely confined to the ankle joint, with most joints in the feet appearing normal   (MGI Ref ID J:75303)
    • surprisingly, the joints of arthritic homozygotes display minimal fibrin(ogen) deposition relative to wild-type   (MGI Ref ID J:75303)
  • homeostasis/metabolism phenotype
  • abnormal acute phase protein level
    • at 9 days after glycerol-induced injury of skeletal muscles, homozygotes exhibit abundant fibrin deposits in degenerating muscle fibers   (MGI Ref ID J:68083)
  • abnormal cytokine level
    • in a model of collagen-induced arthritis, arthritic homozygotes exhibit a significant reduction in interleukin-1beta levels in the synovium relative to wild-type   (MGI Ref ID J:75303)
    • in a model of collagen-induced arthritis, arthritic homozygotes exhibit a significant reduction in TNF levels in the synovium relative to wild-type   (MGI Ref ID J:75303)
  • hematopoietic system phenotype
  • decreased T cell proliferation
    • despite a normal antibody response to type II collagen, T cells from arthritic homozygotes show a reduced proliferative response and produce less interferon-gamma on antigen stimulation in vitro   (MGI Ref ID J:75303)
  • impaired macrophage chemotaxis
    • in response to skeletal muscle degeneration, homozygotes display a 50% reduction in macrophage recruitment at the injury site 48 hours after glycerol-induced injury   (MGI Ref ID J:68083)
  • cellular phenotype
  • impaired macrophage chemotaxis
    • in response to skeletal muscle degeneration, homozygotes display a 50% reduction in macrophage recruitment at the injury site 48 hours after glycerol-induced injury   (MGI Ref ID J:68083)

Plautm1Mlg/Plautm1Mlg

        B6.129S2-Plautm1Mlg
  • mortality/aging
  • premature death
    • only 5 of 8 mice survive for a year   (MGI Ref ID J:164542)
  • immune system phenotype
  • chronic inflammation
    • chronic inflammation is secondary to fibrin deposition   (MGI Ref ID J:164542)
  • increased inflammatory response
    • in the liver and trachea   (MGI Ref ID J:164542)
    • however, leukocyte accumulation in standard models of inflammation is normal   (MGI Ref ID J:164542)
    • liver inflammation
      • the number of inflammatory foci is increased compared to in wild-type mice   (MGI Ref ID J:164542)
  • liver/biliary system phenotype
  • decreased liver glycogen level   (MGI Ref ID J:164542)
  • liver fibrosis
    • 2.5-fold more frequent in number compared with Plautm1.1Bug or Plaurtm1Jld homozygotes   (MGI Ref ID J:164542)
  • liver inflammation
    • the number of inflammatory foci is increased compared to in wild-type mice   (MGI Ref ID J:164542)
  • homeostasis/metabolism phenotype
  • abnormal response to injury
    • following treatment with carbon tetrachloride, substantial areas of necrosis persist in the liver unlike in similarly treated wild-type mice   (MGI Ref ID J:164542)
    • however, skin wound healing is normal   (MGI Ref ID J:164542)
  • decreased liver glycogen level   (MGI Ref ID J:164542)
  • respiratory system phenotype
  • abnormal trachea morphology
    • all mice exhibit inflammation in the tracheal with basement membrane hyperplasia and desquamation of the tracheal epithelium unlike in wild-type mice   (MGI Ref ID J:164542)
    • mice exhibit fibrosis in the trachea unlike wild-type mice   (MGI Ref ID J:164542)
  • adipose tissue phenotype
  • decreased total body fat amount   (MGI Ref ID J:164542)
  • growth/size/body phenotype
  • cachexia
    • some mice die before 1 year with a wasting syndrome   (MGI Ref ID J:164542)
  • decreased total body fat amount   (MGI Ref ID J:164542)
View Research Applications

Research Applications
This mouse can be used to support research in many areas including:

Plautm1Mlg related

Hematological Research
Clotting Defects

Metabolism Research

Neurobiology Research
Alzheimer's Disease

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Plautm1Mlg
Allele Name targeted mutation 1, Richard C Mulligan
Allele Type Targeted (knock-out)
Common Name(s) UPA-; u-PA-;
Mutation Made ByDr. Peter Carmeliet,   University of Leuven
Strain of Origin129S2/SvPas
ES Cell Line NameD3
ES Cell Line Strain129S2/SvPas
Gene Symbol and Name Plau, plasminogen activator, urokinase
Chromosome 14
Gene Common Name(s) ATF; BDPLT5; QPD; UPA; UPAM; URK; u-PA; urokinase-type plasminogen activator;
Molecular Note The gene was disrupted using neomycin resistance cassette. The vector replaced genomic sequences encompassing all but 23 amino acids of the coding sequence. Targeting was confirmed by the absence of gene specific mRNA and immunoreactivity. [MGI Ref ID J:17427]

Genotyping

Genotyping Information

Genotyping Protocols

Plautm1, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Carmeliet P; Schoonjans L; Kieckens L; Ream B; Degen J; Bronson R; De Vos R; van den Oord JJ; Collen D; Mulligan RC. 1994. Physiological consequences of loss of plasminogen activator gene function in mice. Nature 368(6470):419-24. [PubMed: 8133887]  [MGI Ref ID J:17427]

Additional References

Dewerchin M; Nuffelen AV; Wallays G; Bouche A; Moons L; Carmeliet P; Mulligan RC; Collen D. 1996. Generation and characterization of urokinase receptor-deficient mice. J Clin Invest 97(3):870-8. [PubMed: 8609247]  [MGI Ref ID J:31253]

Plautm1Mlg related

Abraham E; Gyetko MR; Kuhn K; Arcaroli J; Strassheim D; Park JS; Shetty S; Idell S. 2003. Urokinase-type plasminogen activator potentiates lipopolysaccharide-induced neutrophil activation. J Immunol 170(11):5644-51. [PubMed: 12759445]  [MGI Ref ID J:131136]

Bdeir K; Murciano JC; Tomaszewski J; Koniaris L; Martinez J; Cines DB; Muzykantov VR; Higazi AA. 2000. Urokinase mediates fibrinolysis in the pulmonary microvasculature Blood 96(5):1820-6. [PubMed: 10961882]  [MGI Ref ID J:64220]

Bergers G; Brekken R; McMahon G; Vu TH; Itoh T; Tamaki K; Tanzawa K; Thorpe P; Itohara S; Werb Z; Hanahan D. 2000. Matrix metalloproteinase-9 triggers the angiogenic switch during carcinogenesis Nat Cell Biol 2(10):737-44. [PubMed: 11025665]  [MGI Ref ID J:65019]

Bezerra JA; Currier AR; Melin-Aldana H; Sabla G; Bugge TH; Kombrinck KW; Degen JL. 2001. Plasminogen activators direct reorganization of the liver lobule after acute injury. Am J Pathol 158(3):921-9. [PubMed: 11238040]  [MGI Ref ID J:114282]

Bhandary YP; Shetty SK; Marudamuthu AS; Ji HL; Neuenschwander PF; Boggaram V; Morris GF; Fu J; Idell S; Shetty S. 2013. Regulation of Lung Injury and Fibrosis by p53-Mediated Changes in Urokinase and Plasminogen Activator Inhibitor-1. Am J Pathol 183(1):131-43. [PubMed: 23665346]  [MGI Ref ID J:197439]

Bryer SC; Fantuzzi G; Van Rooijen N; Koh TJ. 2008. Urokinase-type plasminogen activator plays essential roles in macrophage chemotaxis and skeletal muscle regeneration. J Immunol 180(2):1179-88. [PubMed: 18178858]  [MGI Ref ID J:130940]

Carmeliet P; Moons L; Dewerchin M; Rosenberg S; Herbert JM; Lupu F; Collen D. 1998. Receptor-independent role of urokinase-type plasminogen activator in pericellular plasmin and matrix metalloproteinase proteolysis during vascular wound healing in mice. J Cell Biol 140(1):233-45. [PubMed: 9425170]  [MGI Ref ID J:45379]

Carmeliet P; Moons L; Herbert JM; Crawley J; Lupu F; Lijnen R; Collen D. 1997. Urokinase but not tissue plasminogen activator mediates arterial neointima formation in mice. Circ Res 81(5):829-39. [PubMed: 9351457]  [MGI Ref ID J:95503]

Carmeliet P; Moons L; Lijnen R; Baes M; Lemaitre V; Tipping P; Drew A; Eeckhout Y; Shapiro S; Lupu F; Collen D. 1997. Urokinase-generated plasmin activates matrix metalloproteinases during aneurysm formation. Nat Genet 17(4):439-44. [PubMed: 9398846]  [MGI Ref ID J:44387]

Cho E; Lee KJ; Seo JW; Byun CJ; Chung SJ; Suh DC; Carmeliet P; Koh JY; Kim JS; Lee JY. 2012. Neuroprotection by urokinase plasminogen activator in the hippocampus. Neurobiol Dis 46(1):215-24. [PubMed: 22293605]  [MGI Ref ID J:182295]

Christie PD; Edelberg JM; Picard MH; Foulkes AS; Mamuya W; Weiler-Guettler H; Rubin RH; Gilbert P; Rosenberg RD. 1999. A murine model of myocardial microvascular thrombosis. J Clin Invest 104(5):533-9. [PubMed: 10487767]  [MGI Ref ID J:57461]

Connolly BM; Choi EY; Gardsvoll H; Bey AL; Currie BM; Chavakis T; Liu S; Molinolo A; Ploug M; Leppla SH; Bugge TH. 2010. Selective abrogation of the uPA-uPAR interaction in vivo reveals a novel role in suppression of fibrin-associated inflammation. Blood 116(9):1593-603. [PubMed: 20466854]  [MGI Ref ID J:164542]

Cook AD; Braine EL; Campbell IK; Hamilton JA. 2002. Differing roles for urokinase and tissue-type plasminogen activator in collagen-induced arthritis. Am J Pathol 160(3):917-26. [PubMed: 11891190]  [MGI Ref ID J:75303]

Daci E; Everts V; Torrekens S; Van Herck E; Tigchelaar-Gutterr W; Bouillon R; Carmeliet G. 2003. Increased bone formation in mice lacking plasminogen activators. J Bone Miner Res 18(7):1167-76. [PubMed: 12854826]  [MGI Ref ID J:111454]

Deindl E; Ziegelhoffer T; Kanse SM; Fernandez B; Neubauer E; Carmeliet P; Preissner KT; Schaper W. 2003. Receptor-independent role of the urokinase-type plasminogen activator during arteriogenesis. FASEB J 17(9):1174-6. [PubMed: 12692088]  [MGI Ref ID J:118013]

Deng GG; Martin-McNulty B; Sukovich DA; Freay A; Halks-Miller M; Thinnes T; Loskutoff DJ; Carmeliet P; Dole WP; Wang YX. 2003. Urokinase-type plasminogen activator plays a critical role in angiotensin II-induced abdominal aortic aneurysm. Circ Res 92(5):510-7. [PubMed: 12600880]  [MGI Ref ID J:115512]

Devy L; Blacher S; Grignet-Debrus C; Bajou K; Masson V; Gerard RD; Gils A; Carmeliet G; Carmeliet P; Declerck PJ; Noel A; Foidart JM. 2002. The pro- or antiangiogenic effect of plasminogen activator inhibitor 1 is dose dependent. FASEB J 16(2):147-54. [PubMed: 11818362]  [MGI Ref ID J:74281]

DiPasquale DM; Cheng M; Billich W; Huang SA; van Rooijen N; Hornberger TA; Koh TJ. 2007. Urokinase-type plasminogen activator and macrophages are required for skeletal muscle hypertrophy in mice. Am J Physiol Cell Physiol 293(4):C1278-85. [PubMed: 17652428]  [MGI Ref ID J:145128]

Ertekin-Taner N; Ronald J; Feuk L; Prince J; Tucker M; Younkin L; Hella M; Jain S; Hackett A; Scanlin L; Kelly J; Kihiko-Ehman M; Neltner M; Hersh L; Kindy M; Markesbery W; Hutton M; de Andrade M; Petersen RC; Graff-Radford N; Estus S; Brookes AJ; Younkin SG. 2005. Elevated amyloid beta protein (Abeta42) and late onset Alzheimer's disease are associated with single nucleotide polymorphisms in the urokinase-type plasminogen activator gene. Hum Mol Genet 14(3):447-60. [PubMed: 15615772]  [MGI Ref ID J:104962]

Gueler F; Rong S; Mengel M; Park JK; Kiyan J; Kirsch T; Dumler I; Haller H; Shushakova N. 2008. Renal urokinase-type plasminogen activator (uPA) receptor but not uPA deficiency strongly attenuates ischemia reperfusion injury and acute kidney allograft rejection. J Immunol 181(2):1179-89. [PubMed: 18606671]  [MGI Ref ID J:137466]

Guo Y; Li J; Hagstrom E; Ny T. 2011. Beneficial and detrimental effects of plasmin(ogen) during infection and sepsis in mice. PLoS One 6(9):e24774. [PubMed: 21931850]  [MGI Ref ID J:177689]

Gutierrez LS; Schulman A; Brito-Robinson T; Noria F; Ploplis VA; Castellino FJ. 2000. Tumor development is retarded in mice lacking the gene for urokinase-type plasminogen activator or its inhibitor, plasminogen activator inhibitor-1 Cancer Res 60(20):5839-47. [PubMed: 11059781]  [MGI Ref ID J:65383]

Gyetko MR; Aizenberg D; Mayo-Bond L. 2004. Urokinase-deficient and urokinase receptor-deficient mice have impaired neutrophil antimicrobial activation in vitro. J Leukoc Biol 76(3):648-56. [PubMed: 15240745]  [MGI Ref ID J:91980]

Gyetko MR; Chen GH; McDonald RA; Goodman R; Huffnagle GB; Wilkinson CC; Fuller JA; Toews GB. 1996. Urokinase is required for the pulmonary inflammatory response to Cryptococcus neoformans. A murine transgenic model. J Clin Invest 97(8):1818-26. [PubMed: 8621764]  [MGI Ref ID J:95637]

Gyetko MR; Libre EA; Fuller JA; Chen GH; Toews G. 1999. Urokinase is required for T lymphocyte proliferation and activation in vitro. J Lab Clin Med 133(3):274-88. [PubMed: 10072260]  [MGI Ref ID J:53238]

Gyetko MR; Sud S; Chen GH; Fuller JA; Chensue SW; Toews GB. 2002. Urokinase-type plasminogen activator is required for the generation of a type 1 immune response to pulmonary Cryptococcus neoformans infection. J Immunol 168(2):801-9. [PubMed: 11777975]  [MGI Ref ID J:95638]

Gyetko MR; Sud S; Chensue SW. 2004. Urokinase-deficient mice fail to generate a type 2 immune response following schistosomal antigen challenge. Infect Immun 72(1):461-7. [PubMed: 14688127]  [MGI Ref ID J:87817]

Gyetko MR; Sud S; Kendall T; Fuller JA; Newstead MW; Standiford TJ. 2000. Urokinase receptor-deficient mice have impaired neutrophil recruitment in response to pulmonary Pseudomonas aeruginosa infection. J Immunol 165(3):1513-9. [PubMed: 10903758]  [MGI Ref ID J:110728]

Heymans S; Lupu F; Terclavers S; Vanwetswinkel B; Herbert JM; Baker A; Collen D; Carmeliet P; Moons L. 2005. Loss or inhibition of uPA or MMP-9 attenuates LV remodeling and dysfunction after acute pressure overload in mice. Am J Pathol 166(1):15-25. [PubMed: 15631996]  [MGI Ref ID J:95236]

Heymans S; Luttun A; Nuyens D; Theilmeier G; Creemers E; Moons L; Dyspersin GD; Cleutjens JP; Shipley M; Angellilo A; Levi M; Nube O; Baker A; Keshet E; Lupu F; Herbert JM; Smits JF; Shapiro SD; Baes M; Borgers M; Collen D; Daemen MJ; Carmeliet P. 1999. Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure. Nat Med 5(10):1135-42. [PubMed: 10502816]  [MGI Ref ID J:124004]

Heymans S; Pauschinger M; De Palma A; Kallwellis-Opara A; Rutschow S; Swinnen M; Vanhoutte D; Gao F; Torpai R; Baker AH; Padalko E; Neyts J; Schultheiss HP; Van de Werf F; Carmeliet P; Pinto YM. 2006. Inhibition of urokinase-type plasminogen activator or matrix metalloproteinases prevents cardiac injury and dysfunction during viral myocarditis. Circulation 114(6):565-73. [PubMed: 16880329]  [MGI Ref ID J:123852]

Higazi AA; El-Haj M; Melhem A; Horani A; Pappo O; Alvarez CE; Muhanna N; Friedman SL; Safadi R. 2008. Immunomodulatory effects of plasminogen activators on hepatic fibrogenesis. Clin Exp Immunol 152(1):163-73. [PubMed: 18279442]  [MGI Ref ID J:133582]

Hovius JW; Bijlsma MF; van der Windt GJ; Wiersinga WJ; Boukens BJ; Coumou J; Oei A; de Beer R; de Vos AF; van 't Veer C; van Dam AP; Wang P; Fikrig E; Levi MM; Roelofs JJ; van der Poll T. 2009. The urokinase receptor (uPAR) facilitates clearance of Borrelia burgdorferi. PLoS Pathog 5(5):e1000447. [PubMed: 19461880]  [MGI Ref ID J:162185]

Ingram KG; Curtis CD; Silasi-Mansat R; Lupu F; Griffin CT. 2013. The NuRD chromatin-remodeling enzyme CHD4 promotes embryonic vascular integrity by transcriptionally regulating extracellular matrix proteolysis. PLoS Genet 9(12):e1004031. [PubMed: 24348274]  [MGI Ref ID J:207517]

Jogi A; Rono B; Lund IK; Nielsen BS; Ploug M; Hoyer-Hansen G; Romer J; Lund LR. 2010. Neutralisation of uPA with a monoclonal antibody reduces plasmin formation and delays skin wound healing in tPA-deficient mice. PLoS One 5(9):e12746. [PubMed: 20856796]  [MGI Ref ID J:165126]

Juncker-Jensen A; Lund LR. 2011. Phenotypic overlap between MMP-13 and the plasminogen activation system during wound healing in mice. PLoS One 6(2):e16954. [PubMed: 21326869]  [MGI Ref ID J:170892]

Kawasaki T; Dewerchin M; Lijnen HR; Vermylen J; Hoylaerts MF. 2000. Vascular release of plasminogen activator inhibitor-1 impairs fibrinolysis during acute arterial thrombosis in mice. Blood 96(1):153-60. [PubMed: 10891445]  [MGI Ref ID J:63087]

Kawasaki T; Dewerchin M; Lijnen HR; Vreys I; Vermylen J; Hoylaerts MF. 2001. Mouse carotid artery ligation induces platelet-leukocyte-dependent luminal fibrin, required for neointima development. Circ Res 88(2):159-66. [PubMed: 11157667]  [MGI Ref ID J:115383]

Koh TJ; Bryer SC; Pucci AM; Sisson TH. 2005. Mice deficient in plasminogen activator inhibitor-1 have improved skeletal muscle regeneration. Am J Physiol Cell Physiol 289(1):C217-23. [PubMed: 15716324]  [MGI Ref ID J:104684]

Kremen M; Krishnan R; Emery I; Hu JH; Slezicki KI; Wu A; Qian K; Du L; Plawman A; Stempien-Otero A; Dichek DA. 2008. Plasminogen mediates the atherogenic effects of macrophage-expressed urokinase and accelerates atherosclerosis in apoE-knockout mice. Proc Natl Acad Sci U S A 105(44):17109-14. [PubMed: 18957535]  [MGI Ref ID J:144061]

Lahtinen L; Ndode-Ekane XE; Barinka F; Akamine Y; Esmaeili MH; Rantala J; Pitkanen A. 2010. Urokinase-type plasminogen activator regulates neurodegeneration and neurogenesis but not vascular changes in the mouse hippocampus after status epilepticus. Neurobiol Dis 37(3):692-703. [PubMed: 20026272]  [MGI Ref ID J:158409]

Lazar MH; Christensen PJ; Du M; Yu B; Subbotina NM; Hanson KE; Hansen JM; White ES; Simon RH; Sisson TH. 2004. Plasminogen activator inhibitor-1 impairs alveolar epithelial repair by binding to vitronectin. Am J Respir Cell Mol Biol 31(6):672-8. [PubMed: 15308506]  [MGI Ref ID J:104660]

Leonardsson G; Peng XR; Liu K; Nordstrom L; Carmeliet P; Mulligan R; Collen D; Ny T. 1995. Ovulation efficiency is reduced in mice that lack plasminogen activator gene function: functional redundancy among physiological plasminogen activators. Proc Natl Acad Sci U S A 92(26):12446-50. [PubMed: 8618918]  [MGI Ref ID J:31086]

Levi M; Moons L; Bouche A; Shapiro SD; Collen D; Carmeliet P. 2001. Deficiency of urokinase-type plasminogen activator-mediated plasmin generation impairs vascular remodeling during hypoxia-induced pulmonary hypertension in mice. Circulation 103(15):2014-20. [PubMed: 11306532]  [MGI Ref ID J:135010]

Li J; Ny A; Leonardsson G; Nandakumar KS; Holmdahl R; Ny T. 2005. The Plasminogen Activator/Plasmin System Is Essential for Development of the Joint Inflammatory Phase of Collagen Type II-Induced Arthritis. Am J Pathol 166(3):783-92. [PubMed: 15743790]  [MGI Ref ID J:96720]

Liu K; Wahlberg P; Hagglund AC; Ny T. 2003. Expression pattern and functional studies of matrix degrading proteases and their inhibitors in the mouse corpus luteum. Mol Cell Endocrinol 205(1-2):131-40. [PubMed: 12890575]  [MGI Ref ID J:126215]

Liu Z; Li N; Diaz LA; Shipley M; Senior RM; Werb Z. 2005. Synergy between a plasminogen cascade and MMP-9 in autoimmune disease. J Clin Invest 115(4):879-887. [PubMed: 15841177]  [MGI Ref ID J:97324]

Lluis F; Roma J; Suelves M; Parra M; Aniorte G; Gallardo E; Illa I; Rodriguez L; Hughes SM; Carmeliet P; Roig M; Munoz-Canoves P. 2001. Urokinase-dependent plasminogen activation is required for efficient skeletal muscle regeneration in vivo. Blood 97(6):1703-11. [PubMed: 11238111]  [MGI Ref ID J:68083]

Lund IK; Nielsen BS; Almholt K; Rono B; Hald A; Illemann M; Green KA; Christensen IJ; Romer J; Lund LR. 2011. Concomitant lack of MMP9 and uPA disturbs physiological tissue remodeling. Dev Biol 358(1):56-67. [PubMed: 21802414]  [MGI Ref ID J:176606]

Lund LR; Bjorn SF; Sternlicht MD; Nielsen BS; Solberg H; Usher PA; Osterby R; Christensen IJ; Stephens RW; Bugge TH; Dano K; Werb Z. 2000. Lactational competence and involution of the mouse mammary gland require plasminogen Development 127(20):4481-92. [PubMed: 11003846]  [MGI Ref ID J:64966]

Lund LR; Green KA; Stoop AA; Ploug M; Almholt K; Lilla J; Nielsen BS; Christensen IJ; Craik CS; Werb Z; Dano K; Romer J. 2006. Plasminogen activation independent of uPA and tPA maintains wound healing in gene-deficient mice. EMBO J 25(12):2686-97. [PubMed: 16763560]  [MGI Ref ID J:119017]

Mahoney MG; Wang ZH; Stanley JR. 1999. Pemphigus vulgaris and pemphigus foliaceus antibodies are pathogenic in plasminogen activator knockout mice. J Invest Dermatol 113(1):22-5. [PubMed: 10417613]  [MGI Ref ID J:119605]

Matys T; Pawlak R; Strickland S. 2005. Tissue plasminogen activator in the bed nucleus of stria terminalis regulates acoustic startle. Neuroscience 135(3):715-22. [PubMed: 16125860]  [MGI Ref ID J:104429]

Minor KH; Seeds NW. 2008. Plasminogen activator induction facilitates recovery of respiratory function following spinal cord injury. Mol Cell Neurosci 37(1):143-52. [PubMed: 18042398]  [MGI Ref ID J:132690]

Morange PE; Bastelica D; Bonzi MF; Van Hoef B; Collen D; Juhan-Vague I; Lijnen HR. 2002. Influence of t-pA and u-PA on adipose tissue development in a murine model of diet-induced obesity. Thromb Haemost 87(2):306-10. [PubMed: 11858492]  [MGI Ref ID J:113728]

Nagai N; De Mol M; Lijnen HR; Carmeliet P; Collen D. 1999. Role of plasminogen system components in focal cerebral ischemic infarction: a gene targeting and gene transfer study in mice. Circulation 99(18):2440-4. [PubMed: 10318667]  [MGI Ref ID J:55243]

Nagai N; Okada K; Kawao N; Ishida C; Ueshima S; Collen D; Matsuo O. 2008. Urokinase-type plasminogen activator receptor (uPAR) augments brain damage in a murine model of ischemic stroke. Neurosci Lett 432(1):46-9. [PubMed: 18164548]  [MGI Ref ID J:141630]

Nassar T; Haj-Yehia A; Akkawi S; Kuo A; Bdeir K; Mazar A; Cines DB; Higazi AA. 2002. Binding of urokinase to low density lipoprotein-related receptor (LRP) regulates vascular smooth muscle cell contraction. J Biol Chem 277(43):40499-504. [PubMed: 12171938]  [MGI Ref ID J:118782]

Nassar T; Yarovoi S; Fanne RA; Akkawi S; Jammal M; Allen TC; Idell S; Cines DB; Higazi AA. 2010. Regulation of airway contractility by plasminogen activators through N-methyl-D-aspartate receptor-1. Am J Respir Cell Mol Biol 43(6):703-11. [PubMed: 20097831]  [MGI Ref ID J:179956]

Nishiuma T; Sisson TH; Subbotina N; Simon RH. 2004. Localization of plasminogen activator activity within normal and injured lungs by in situ zymography. Am J Respir Cell Mol Biol 31(5):552-8. [PubMed: 15284078]  [MGI Ref ID J:103595]

Oh CW; Hoover-Plow J; Plow EF. 2003. The role of plasminogen in angiogenesis in vivo. J Thromb Haemost 1(8):1683-7. [PubMed: 12911578]  [MGI Ref ID J:128184]

Piguet PF; Da Laperrousaz C; Vesin C; Tacchini-Cottier F; Senaldi G; Grau GE. 2000. Delayed mortality and attenuated thrombocytopenia associated with severe malaria in urokinase- and urokinase receptor-deficient mice. Infect Immun 68(7):3822-9. [PubMed: 10858190]  [MGI Ref ID J:62841]

Piguet PF; Vesin C; Da Laperousaz C; Rochat A. 2000. Role of plasminogen activators and urokinase receptor in platelet kinetics. Hematol J 1(3):199-205. [PubMed: 11920190]  [MGI Ref ID J:103182]

Pinsky DJ; Liao H; Lawson CA; Yan SF; Chen J; Carmeliet P; Loskutoff DJ; Stern DM. 1998. Coordinated induction of plasminogen activator inhibitor-1 (PAI-1) and inhibition of plasminogen activator gene expression by hypoxia promotes pulmonary vascular fibrin deposition. J Clin Invest 102(5):919-28. [PubMed: 9727060]  [MGI Ref ID J:112025]

Ploplis VA; Tipton H; Menchen H; Castellino FJ. 2007. A urokinase-type plasminogen activator deficiency diminishes the frequency of intestinal adenomas in ApcMin/+ mice. J Pathol 213(3):266-74. [PubMed: 17893885]  [MGI Ref ID J:126931]

Prager GW; Mihaly J; Brunner PM; Koshelnick Y; Hoyer-Hansen G; Binder BR. 2009. Urokinase mediates endothelial cell survival via induction of the X-linked inhibitor of apoptosis protein. Blood 113(6):1383-90. [PubMed: 18948573]  [MGI Ref ID J:145580]

Rakic JM; Lambert V; Munaut C; Bajou K; Peyrollier K; Alvarez-Gonzalez ML; Carmeliet P; Foidart JM; Noel A. 2003. Mice without uPA, tPA, or plasminogen genes are resistant to experimental choroidal neovascularization. Invest Ophthalmol Vis Sci 44(4):1732-9. [PubMed: 12657615]  [MGI Ref ID J:82604]

Reichel CA; Uhl B; Lerchenberger M; Puhr-Westerheide D; Rehberg M; Liebl J; Khandoga A; Schmalix W; Zahler S; Deindl E; Lorenzl S; Declerck PJ; Kanse S; Krombach F. 2011. Urokinase-type plasminogen activator promotes paracellular transmigration of neutrophils via Mac-1, but independently of urokinase-type plasminogen activator receptor. Circulation 124(17):1848-59. [PubMed: 21969013]  [MGI Ref ID J:189465]

Renckens R; Pater JM; van der Poll T. 2006. Plasminogen activator inhibitor type-1-deficient mice have an enhanced IFN-gamma response to lipopolysaccharide and staphylococcal enterotoxin B. J Immunol 177(11):8171-6. [PubMed: 17114493]  [MGI Ref ID J:140679]

Rijneveld AW; Levi M; Florquin S; Speelman P; Carmeliet P; van Der Poll T. 2002. Urokinase receptor is necessary for adequate host defense against pneumococcal pneumonia. J Immunol 168(7):3507-11. [PubMed: 11907112]  [MGI Ref ID J:75573]

Sato J; Schorey J; Ploplis VA; Haalboom E; Krahule L; Castellino FJ. 2003. The fibrinolytic system in dissemination and matrix protein deposition during a mycobacterium infection. Am J Pathol 163(2):517-31. [PubMed: 12875972]  [MGI Ref ID J:113588]

Schafer K; Konstantinides S; Riedel C; Thinnes T; Muller K; Dellas C; Hasenfuss G; Loskutoff DJ. 2002. Different mechanisms of increased luminal stenosis after arterial injury in mice deficient for urokinase- or tissue-type plasminogen activator. Circulation 106(14):1847-52. [PubMed: 12356640]  [MGI Ref ID J:103219]

Shanmukhappa K; Matte U; Degen JL; Bezerra JA. 2009. Plasmin-mediated proteolysis is required for hepatocyte growth factor activation during liver repair. J Biol Chem 284(19):12917-23. [PubMed: 19286661]  [MGI Ref ID J:149628]

Shapiro RL; Duquette JG; Nunes I; Roses DF; Harris MN; Wilson EL ; Rifkin DB. 1997. Urokinase-type plasminogen activator-deficient mice are predisposed to staphylococcal botryomycosis, pleuritis, and effacement of lymphoid follicles. Am J Pathol 150(1):359-69. [PubMed: 9006351]  [MGI Ref ID J:37695]

Shen Y; Guo Y; Du C; Wilczynska M; Hellstrom S; Ny T. 2012. Mice deficient in urokinase-type plasminogen activator have delayed healing of tympanic membrane perforations. PLoS One 7(12):e51303. [PubMed: 23236466]  [MGI Ref ID J:195678]

Shushakova N; Eden G; Dangers M; Zwirner J; Menne J; Gueler F; Luft FC; Haller H; Dumler I. 2005. The urokinase/urokinase receptor system mediates the IgG immune complex-induced inflammation in lung. J Immunol 175(6):4060-8. [PubMed: 16148155]  [MGI Ref ID J:116701]

Siconolfi LB; Seeds NW. 2001. Mice lacking tPA, uPA, or plasminogen genes showed delayed functional recovery after sciatic nerve crush. J Neurosci 21(12):4348-55. [PubMed: 11404420]  [MGI Ref ID J:123804]

Sisson TH; Nguyen MH; Yu B; Novak ML; Simon RH; Koh TJ. 2009. Urokinase-type plasminogen activator increases hepatocyte growth factor activity required for skeletal muscle regeneration. Blood 114(24):5052-61. [PubMed: 19812386]  [MGI Ref ID J:154983]

Suelves M; Vidal B; Serrano AL; Tjwa M; Roma J; Lopez-Alemany R; Luttun A; de Lagran MM; Diaz-Ramos A; Jardi M; Roig M; Dierssen M; Dewerchin M; Carmeliet P; Munoz-Canoves P. 2007. uPA deficiency exacerbates muscular dystrophy in MDX mice. J Cell Biol 178(6):1039-51. [PubMed: 17785520]  [MGI Ref ID J:134802]

Sulniute R; Lindh T; Wilczynska M; Li J; Ny T. 2011. Plasmin is essential in preventing periodontitis in mice. Am J Pathol 179(2):819-28. [PubMed: 21704601]  [MGI Ref ID J:174401]

Swaisgood CM; French EL; Noga C; Simon RH; Ploplis VA. 2000. The development of bleomycin-induced pulmonary fibrosis in mice deficient for components of the fibrinolytic system. Am J Pathol 157(1):177-87. [PubMed: 10880388]  [MGI Ref ID J:63134]

Teesalu T; Blasi F; Talarico D. 1996. Embryo implantation in mouse: fetomaternal coordination in the pattern of expression of uPA, uPAR, PAI-1 and alpha 2MR/LRP genes. Mech Dev 56(1-2):103-16. [PubMed: 8798151]  [MGI Ref ID J:33753]

Uchida HA; Poduri A; Subramanian V; Cassis LA; Daugherty A. 2011. Urokinase-type plasminogen activator deficiency in bone marrow-derived cells augments rupture of angiotensin II-induced abdominal aortic aneurysms. Arterioscler Thromb Vasc Biol 31(12):2845-52. [PubMed: 21868698]  [MGI Ref ID J:191466]

Uhrin P; Schofer C; Zaujec J; Ryban L; Hilpert M; Weipoltshammer K; Jerabek I; Pirtzkall I; Furtmuller M; Dewerchin M; Binder BR; Geiger M. 2007. Male fertility and protein C inhibitor/plasminogen activator inhibitor-3 (PCI): localization of PCI in mouse testis and failure of single plasminogen activator knockout to restore spermatogenesis in PCI-deficient mice. Fertil Steril 88(4 Suppl):1049-57. [PubMed: 17434507]  [MGI Ref ID J:129635]

Van Den Broeck T; Stevenaert F; Taveirne S; Debacker V; Vangestel C; Vandekerckhove B; Taghon T; Matthys P; Plum J; Held W; Dewerchin M; Yokoyama WM; Leclercq G. 2008. Ly49E-dependent inhibition of natural killer cells by urokinase plasminogen activator. Blood 112(13):5046-51. [PubMed: 18784372]  [MGI Ref ID J:143621]

Wei C; Moller CC; Altintas MM; Li J; Schwarz K; Zacchigna S; Xie L; Henger A; Schmid H; Rastaldi MP; Cowan P; Kretzler M; Parrilla R; Bendayan M; Gupta V; Nikolic B; Kalluri R; Carmeliet P; Mundel P; Reiser J. 2008. Modification of kidney barrier function by the urokinase receptor. Nat Med 14(1):55-63. [PubMed: 18084301]  [MGI Ref ID J:130835]

Weiler-Guettler H; Christie PD; Beeler DL; Healy AM; Hancock WW; Rayburn H; Edelberg JM; Rosenberg RD. 1998. A targeted point mutation in thrombomodulin generates viable mice with a prethrombotic state. J Clin Invest 101(9):1983-91. [PubMed: 9576763]  [MGI Ref ID J:47676]

Yamaguchi I; Lopez-Guisa JM; Cai X; Collins SJ; Okamura DM; Eddy AA. 2007. Endogenous urokinase lacks antifibrotic activity during progressive renal injury. Am J Physiol Renal Physiol 293(1):F12-9. [PubMed: 17356128]  [MGI Ref ID J:141660]

Yang YH; Carmeliet P; Hamilton JA. 2001. Tissue-type plasminogen activator deficiency exacerbates arthritis. J Immunol 167(2):1047-52. [PubMed: 11441114]  [MGI Ref ID J:120523]

Yepes M; Sandkvist M; Moore EG; Bugge TH; Strickland DK; Lawrence DA. 2003. Tissue-type plasminogen activator induces opening of the blood-brain barrier via the LDL receptor-related protein. J Clin Invest 112(10):1533-40. [PubMed: 14617754]  [MGI Ref ID J:119309]

Yiou R; Delmas V; Carmeliet P; Gherardi RK; Barlovatz-Meimon G; Chopin DK; Abbou CC; Lefaucheur JP. 2001. The pathophysiology of pelvic floor disorders: evidence from a histomorphologic study of the perineum and a mouse model of rectal prolapse. J Anat 199(Pt 5):599-607. [PubMed: 11760891]  [MGI Ref ID J:73613]

de Giorgio-Miller A; Bottoms S; Laurent G; Carmeliet P; Herrick S. 2005. Fibrin-induced skin fibrosis in mice deficient in tissue plasminogen activator. Am J Pathol 167(3):721-32. [PubMed: 16127152]  [MGI Ref ID J:100676]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3175.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Frozen Products

Price (US dollars $)
Frozen Embryo $1600.00

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • Cryorecovery - Standard.
    Progeny testing is not required.
    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice
    Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $4127.50
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Frozen Products

Price (US dollars $)
Frozen Embryo $2080.00

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • Cryorecovery - Standard.
    Progeny testing is not required.
    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice
    Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

  Control
   000651 BALB/cJ
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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