Overview

Also Known As:uPA-

These Plau knock-out mice exhibit occasional rectal prolapse and fibrin deposition.

Donating Investigator

Dr. Peter Carmeliet, University of Leuven

Genetic overview

Genetic Background	Generation

Plau^tm1Mlg

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Plau	plasminogen activator, urokinase

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Research Applications

Metabolism Research
Hematological Research
Neurobiology Research

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Base Price

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$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

Homozygotes develop normally, have a normal life span, and are poor breeders. Pups often need fostering. 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.

Development

This targeted mutant was made in the laboratories of Dr. Richard Mulligan of the Whitehead Institute for Biomedical Sciences, Cambridge Massachusetts and of Dr. Peter Carmellet at the Center for Molecular and Vascular Biology, University of Leuven, Leuven, Belgium. A targeting vector was used which resulted in the neomycin-resistant gene (neo) replacing all but 23 amino acids of the coding sequence. Targeting was done in 129S2/SvPas-derived D3 ES cells.

Control Suggestions

Wild-type from the colony
000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

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):419-24PubMed: 8133887 MGI: J:17427

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Genetics

Plau^tm1Mlg

Allele Symbol: Plau^tm1Mlg

Allele Name	targeted mutation 1, Richard C Mulligan
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	UPA-; u-PA^-
Gene Symbol and Name	Plau, plasminogen activator, urokinase
Gene Synonym(s)
Strain of Origin	129S2/SvPas
Chromosome	14
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.
Mutations Made By	Dr. Peter Carmeliet, University of Leuven

Disease/Phenotype

Disease Terms

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's disease

Research Areas By Phenotype

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

Genotype: Plau^tm1Mlg related

Metabolism Research
Hematological Research
- Clotting Defects
Neurobiology Research
- Alzheimer's Disease

Mammalian Phenotype Terms by Genotype

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

Genotype: Plau^tm1Mlg/Plau^tm1Mlg
B6.Cg-Plau

cellular 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

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

hematopoietic system 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

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

homeostasis/metabolism phenotype

abnormal cytokine level
- in a model of collagen-induced arthritis, arthritic homozygotes exhibit a significant reduction in TNF levels in the synovium relative to wild-type
- in a model of collagen-induced arthritis, arthritic homozygotes exhibit a significant reduction in interleukin-1beta levels in the synovium relative to wild-type

abnormal acute phase protein level
- at 9 days after glycerol-induced injury of skeletal muscles, homozygotes exhibit abundant fibrin deposits in degenerating muscle fibers

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

abnormal cytokine level
- in a model of collagen-induced arthritis, arthritic homozygotes exhibit a significant reduction in TNF levels in the synovium relative to wild-type
- in a model of collagen-induced arthritis, arthritic homozygotes exhibit a significant reduction in interleukin-1beta levels in the synovium relative to wild-type

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

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

decreased susceptibility to induced arthritis
- surprisingly, the joints of arthritic homozygotes display minimal fibrin(ogen) deposition relative to wild-type
- in a model of collagen-induced arthritis, homozygotes develop a significantly milder disease than wild-type mice, with little inflammation and joint destruction
- 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

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

muscle phenotype

impaired skeletal muscle regeneration
- at 7 days after injury, most injured skeletal muscles appear necrotic and show extensive fibrosis
- at 5 days after injury, skeletal muscles from mutant mice appear edematous; in contrast to wild-type, no uninucleated, small myofibers are yet formed
- 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
- 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
- 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

myopathy
- most affected myofibers have centrally located nuclei; some show basophilic degeneration in the absence of denervation, fibrosis or inflammation
- males with rectal prolapse, exhibit myopathic damage in the affected pelvic floor muscles (ISC, BC and LA)

digestive/alimentary phenotype

abnormal perineum morphology
- in males with rectal prolapse, the perineal region is swollen on both sides of the evaginated rectal mucosa

abnormal rectum morphology
- in males with rectal prolapse, the rectal mucosa is exteriorized and evaginated

rectal prolapse
- in mutant males, rectal prolapse is irreducible and completely exteriorized by 12 months
- starting at 6 months, male (but not female) homozygotes show a high incidence of rectal prolapse

neoplasm

decreased metastatic potential
- notably, only mutants that survive for longer periods (2 months) after the injection develop these lesions, indicating a delay in metastasis
- 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

abnormal tumor morphology
- 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
- ultrastructurally, fibrosarcoma tumor neovessels formed in mutant mice are larger and less mature than tumor vessels from wild-type mice
- 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

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
- 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

reproductive system 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
- this hernia results in chronic stretching and thinning of the ISC, BC, and levator ani (LA) pelvic floor muscles

abnormal perineum morphology
- in males with rectal prolapse, the perineal region is swollen on both sides of the evaginated rectal mucosa

skeleton phenotype

decreased susceptibility to induced arthritis
- 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
- surprisingly, the joints of arthritic homozygotes display minimal fibrin(ogen) deposition relative to wild-type
- in a model of collagen-induced arthritis, homozygotes develop a significantly milder disease than wild-type mice, with little inflammation and joint destruction

endocrine/exocrine gland phenotype

herniated seminal vesicle
- this hernia results in chronic stretching and thinning of the ISC, BC, and levator ani (LA) pelvic floor muscles
- 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

Genotype: Plau^tm1Mlg/Plau^tm1Mlg
involves: 129S2/SvPas * C57BL/6

craniofacial phenotype

abnormal facial skin morphology
- at ~26 weeks of age, 5% of homozygotes display severe non-healing ulcerations at the face

abnormal outer ear skin morphology
- at ~26 weeks of age, 5% of homozygotes display severe non-healing ulcerations at the ears around the eartag

digestive/alimentary phenotype

rectal prolapse
- at ~22 weeks of age, 9% of homozygotes display rectal prolapse of a non-infectious origin

growth/size/body region phenotype

heart left ventricle hypertrophy
- at 7 weeks after TAB, LV systolic dysfunction and dilatation are only marginally detectable without signs of pulmonary edema
- after transverse aortic banding (TAB), i.e. acute pressure overload, homozygotes remain significantly protected against LV hypertrophy for at least 7 weeks
- 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)

abnormal outer ear skin morphology
- at ~26 weeks of age, 5% of homozygotes display severe non-healing ulcerations at the ears around the eartag

abnormal facial skin morphology
- at ~26 weeks of age, 5% of homozygotes display severe non-healing ulcerations at the face

hearing/vestibular/ear phenotype

abnormal outer ear skin morphology
- at ~26 weeks of age, 5% of homozygotes display severe non-healing ulcerations at the ears around the eartag

hematopoietic system phenotype

abnormal macrophage physiology
- mains unaffected
- 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

abnormal neutrophil physiology
- reverses the defect in superoxide generation
- 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
- 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
- in contrast, mutant neutrophils show normal agonist-stimulated release of specific granules relative to wild-type neutrophils
- 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
- lative to wild-type

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
- 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

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

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

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

homeostasis/metabolism phenotype

abnormal acute phase protein level
- 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
- bleomycin-treated homozygotes exhibit extensive areas of fibrin(ogen) deposition in the lung interstitium which are associated with areas of fibrosis

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

increased susceptibility to induced thrombosis
- 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)

abnormal 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

cardiovascular system phenotype

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
- at 7 weeks after TAB, LV systolic dysfunction and dilatation are only marginally detectable without signs of pulmonary edema
- 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)

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

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
- resistance to CNV is associated with excessive fibrinogen-fibrin deposition at the site of choroidal trauma and in retinal vessels

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

immune system phenotype

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
- 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
- reverses the defect in superoxide generation
- in contrast, mutant neutrophils show normal agonist-stimulated release of specific granules relative to wild-type neutrophils
- lative to wild-type
- 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

abnormal cell-mediated immunity
- e deficient in eosinophils
- homozygotes fail to generate a type 1 immune response in the lung during pulmonary fungal infection with C. neoformans
- homozygotes fail to generate a type 2 immune response following schistosomal antigen challenge
- 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
- ine
- 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

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
- 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

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
- 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

increased susceptibility to fungal infection
- 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
- 21 days after inoculation with Cryptococcus neoformans, homozygotes contain significantly higher lung CFUs than wild-type mice

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
- mains unaffected

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

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

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

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

integument phenotype

abnormal facial skin morphology
- at ~26 weeks of age, 5% of homozygotes display severe non-healing ulcerations at the face

abnormal outer ear skin morphology
- at ~26 weeks of age, 5% of homozygotes display severe non-healing ulcerations at the ears around the eartag

mammalian phenotype

nervous system phenotype
- Abeta40 and 42 levels are not increased in mutant brains relative to controls
- Normal - 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

hematopoietic system phenotype
- Normal - homozygotes exhibit normal spontaneous lysis of a 125I-fibrin-labeled pulmonary plasma clot relative to wild-type

mortality/aging
- Normal - homozygotes display a normal lifespan relative to wild-type mice

reproductive system phenotype
- Normal - homozygotes display normal litter size and frequency of litters relative to wild-type mice

growth/size/body region phenotype
- Normal - at 5 weeks of age, homozygotes exhibit a normal body weight relative to wild-type mice

muscle phenotype

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
- 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)
- at 7 weeks after TAB, LV systolic dysfunction and dilatation are only marginally detectable without signs of pulmonary edema

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

respiratory system phenotype

pulmonary interstitial fibrosis
- 62% of bleomycin-treated homozygotes die as early as ~7 days after treatment, possibly as a result of extensive 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
- 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

vision/eye phenotype

abnormal eyelid morphology
- at ~26 weeks of age, 5% homozygotes display severe non-healing ulcerations at the eyelids

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
- resistance to CNV is associated with excessive fibrinogen-fibrin deposition at the site of choroidal trauma and in retinal vessels

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
- 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

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

The following phenotype relates to a compound genotype created using this strain

Genotype: Plau^tm1Mlg/Plau^tm1Mlg
B6.129S2-Plau

adipose tissue phenotype

decreased total body fat amount

liver/biliary system phenotype

liver fibrosis
- 2.5-fold more frequent in number compared with Plau^tm1.1Bug or Plaur^tm1Jld homozygotes

liver inflammation
- the number of inflammatory foci is increased compared to in wild-type mice

decreased liver glycogen level

mortality/aging

premature death
- only 5 of 8 mice survive for a year

respiratory system phenotype

abnormal trachea morphology
- all mice exhibit inflammation in the trachea with basement membrane hyperplasia and desquamation of the tracheal epithelium unlike in wild-type mice

trachea fibrosis
- mice exhibit fibrosis in the trachea unlike wild-type mice

trachea inflammation
- all mice exhibit inflammation in the trachea

growth/size/body region phenotype

cachexia
- some mice die before 1 year with a wasting syndrome

homeostasis/metabolism phenotype

abnormal response to injury
- Normal - however, skin wound healing is normal
- following treatment with carbon tetrachloride, substantial areas of necrosis persist in the liver unlike in similarly treated wild-type mice

decreased liver glycogen level

immune system phenotype

increased inflammatory response
- Normal - however, leukocyte accumulation in standard models of inflammation is normal
- in the liver and trachea

liver inflammation
- the number of inflammatory foci is increased compared to in wild-type mice

chronic inflammation
- chronic inflammation is secondary to fibrin deposition

trachea inflammation
- all mice exhibit inflammation in the trachea

Genotype: Plau^tm1Mlg/Plau^tm1Mlg
either: B6.Cg-Plau 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
- in these mutants, impaired fibrinolysis can be rescued completely by providing urokinase exogenously

References

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):419-24PubMed: 8133887 MGI: 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):870-8PubMed: 8609247 MGI: J:31253

Additional - Plau^tm1Mlg related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Genotyping resources and troubleshooting
Breeding Considerations

Homozygotes are poor breeders and pups often need fostering. Expected coat color from breeding:Black
- Additional Breeding and Husbandry Support
Appearance
- black
  Related Genotype: a/a
Citation
When using the uPA- mouse strain in a publication, please cite the originating article(s) and include JAX stock #002509 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

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

Pricing & Availability

Cryo Recovery

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Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous or wildtype for Plau<tm1Mlg>

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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. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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Questions about Terms of Use

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:uPA-

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Plautm1Mlg

Allele Symbol: Plautm1Mlg

Disease Terms

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).

Research Areas By Phenotype

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

Genotype: Plautm1Mlg related

Mammalian Phenotype Terms by Genotype

Genotype: Plautm1Mlg/Plautm1MlgB6.Cg-Plau

cellular phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

muscle phenotype

digestive/alimentary phenotype

neoplasm

reproductive system phenotype

skeleton phenotype

endocrine/exocrine gland phenotype

Genotype: Plautm1Mlg/Plautm1Mlginvolves: 129S2/SvPas * C57BL/6

craniofacial phenotype

digestive/alimentary phenotype

growth/size/body region phenotype

hearing/vestibular/ear phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

cardiovascular system phenotype

immune system phenotype

integument phenotype

mammalian phenotype

muscle phenotype

respiratory system phenotype

vision/eye phenotype

cellular phenotype

Genotype: Plautm1Mlg/Plautm1MlgB6.129S2-Plau

adipose tissue phenotype

liver/biliary system phenotype

mortality/aging

respiratory system phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

immune system phenotype

Genotype: Plautm1Mlg/Plautm1Mlgeither: B6.Cg-Plau or (involves: Black Swiss * C57BL/6)

homeostasis/metabolism phenotype

References

Additional References

Additional - Plautm1Mlg related

Genotyping Protocols

Breeding Considerations

Appearance

Citation

Animal Health Reports

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

Live Mouse

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

Plau^tm1Mlg

Allele Symbol: Plau^tm1Mlg

Genotype: Plau^tm1Mlg related

Genotype: Plau^tm1Mlg/Plau^tm1Mlg
B6.Cg-Plau

Genotype: Plau^tm1Mlg/Plau^tm1Mlg
involves: 129S2/SvPas * C57BL/6

Genotype: Plau^tm1Mlg/Plau^tm1Mlg
B6.129S2-Plau

Genotype: Plau^tm1Mlg/Plau^tm1Mlg
either: B6.Cg-Plau or (involves: Black Swiss * C57BL/6)

Additional - Plau^tm1Mlg related