Overview

Also Known As:t-PA^-

These plasminogen activator, tissue knock-out (Plat^tm1Mlg, also commonly referred to as tPA^-) mice may be useful in fibrosis, neurovascular and other studies involving the widespread physiological effects of plasminogen activator.

Donating Investigator

Dr. Peter Carmeliet, University of Leuven

Genetic overview

Genetic Background	Generation

Plat^tm1Mlg

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Plat	plasminogen activator, tissue

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Research Applications

Hematological Research

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

Homozygotes develop normally, are fertile and have a normal life span. There are no histological abnormalities. Pulmonary clot lysis is 21% that of normal wildtype siblings. Endotoxin induced venous thrombosis is increased over that seen in normal wildtype siblings. Fibrin dissolution by PLAT-deficient macrophages is unaffected.

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 genomic sequences encoding most of the kringle-2 domain and part of the proteinase domain, including the essential histidine-326 residue. Targeting was done in 129S2/SvPas derived D3 ES cells. The mice were backcrossed to C57BL/6 for 8 generations.

Control Suggestions

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

Plat^tm1Mlg

Allele Symbol: Plat^tm1Mlg

Allele Name	targeted mutation 1, Richard C Mulligan
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	Plat^tm1; t-PA^-; tPA^-
Gene Symbol and Name	Plat, plasminogen activator, tissue
Gene Synonym(s)
Strain of Origin	129S2/SvPas
Chromosome	8
Molecular Note	The gene was disrupted using neomycin resistance cassette. The vector replaced genomic sequences encoding most of the kringle-2 domain and part of the proteinase domain, including the catalytically essential histidine residue at position 326. 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

Research Areas By Phenotype

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

Genotype: Plat^tm1Mlg related

Hematological Research
- Clotting Defects

Mammalian Phenotype Terms by Genotype

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

Genotype: Plat^tm1Mlg/Plat^tm1Mlg
involves: 129S2/SvPas

hematopoietic system phenotype

abnormal microglial cell physiology
- significant decrease in the number of activated glial cells in ischemic tissue after transient middle cerebral artery occlusion

homeostasis/metabolism phenotype

abnormal response to CNS ischemic injury
- significant decrease in the number of activated glial cells in ischemic tissue after transient middle cerebral artery occlusion

immune system phenotype

abnormal microglial cell physiology
- significant decrease in the number of activated glial cells in ischemic tissue after transient middle cerebral artery occlusion

nervous system phenotype

abnormal response to CNS ischemic injury
- significant decrease in the number of activated glial cells in ischemic tissue after transient middle cerebral artery occlusion

abnormal microglial cell physiology
- significant decrease in the number of activated glial cells in ischemic tissue after transient middle cerebral artery occlusion

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

cellular phenotype

decreased retinal apoptosis
- at 12 and 24 h after intravitreal injection of low-dose (30 nmol/mouse) NMDA, homozygotes contain significantly less retinal apoptotic neurons in the ganglion cell layer (GCL) and inner nuclear layer (INL) relative to wild-type; no differences are noted at 72 h after low-dose NMDA injection
- t 72 h after low-dose NMDA injection
- at higher doses of NMDA, homozygotes show no differences in retinal damage relative to wild-type mice

growth/size/body region phenotype

heart left ventricle hypertrophy
- similar to wild-type mice, homozygotes display a ~35% increase in LV/body weight ratio and a ~40% increase in the LV cardiomyocyte size
- at 2 weeks after transverse aortic banding (TAB) i.e. acute pressure overload, homozygotes and wild-type mice exhibit a significant LV hypertrophy which persists for up to 7 weeks

hematopoietic system phenotype

increased macrophage cell number
- bleomycin-treated homozygotes display a delayed, but significant, increase in macrophage levels reaching wild-type levels at 9 days post-drug treatment

homeostasis/metabolism phenotype

abnormal thrombosis
- in response to injection of pro-inflammatory endotoxin in the footpad, homozygotes exhibit overt venous thrombosis at a significantly higher incidence (76% versus 54%) and to a much larger extent than wild-type mice (55% of mutants show >4 thrombosed veins per tissue section versus only 15% in wild-type)
- s per tissue section versus only 15% in wild-type)

decreased cerebral infarct size
- homozygotes subjected to focal cerebral ischemia induced by persistent occlusion of the left middle cerebral artery produce an infarct with a size that is significantly smaller than that produced in wild-type mice

abnormal acute phase protein level
- after bleomycin treatment, homozygotes exhibit areas of fibrin(ogen) deposits, especially in the vasculature of the lung, where fibrin thrombi are observed
- 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

reduced thrombolysis
- homozygotes exhibit a significant reduction in the rate of lysis of 125I-fibrin-labeled pulmonary plasma clots relative to wild-type mice

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 (76% versus 54%) and to a much larger extent than wild-type mice (55% of mutants show >4 thrombosed veins per tissue section versus only 15% in wild-type)

immune system 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
- after bleomycin treatment, homozygotes exhibit areas of fibrin(ogen) deposits, especially in the vasculature of the lung, where fibrin thrombi are observed

increased macrophage cell number
- bleomycin-treated homozygotes display a delayed, but significant, increase in macrophage levels reaching wild-type levels at 9 days post-drug treatment

mammalian phenotype

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
- Normal - no macroscopic or histologic abnormalities are observed up to 14 months of age

immune system phenotype
- Normal - homozygotes exhibit normal matrix degradation and invasion into the peritoneal cavity by thioglycollate-stimulated macrophages

muscle phenotype

heart left ventricle hypertrophy
- at 2 weeks after transverse aortic banding (TAB) i.e. acute pressure overload, homozygotes and wild-type mice exhibit a significant LV hypertrophy which persists for up to 7 weeks
- similar to wild-type mice, homozygotes display a ~35% increase in LV/body weight ratio and a ~40% increase in the LV cardiomyocyte size

decreased ventricle muscle contractility
- at 7 weeks after TAB, impaired fractional shortening and abnormal cardiac pump result in respiratory distress due to pulmonary congestion
- at 7 weeks after TAB, wild-type and mutant mice exhibit a similar degree of LV dilatation, obvious signs of LV systolic dysfunction, and pump failure

nervous system phenotype

intracerebral hemorrhage
- in a photothrombotic model of middle cerebral artery occlusion (MCAO), delayed heparin administration increases cerebral hemorrhage associated with ischemia in wild-type but NOT in mutant mice
- in this MCAO model, heparin administration induces tPA activity and mRNA expression in microglial cells, and enhances MMP9 expression and proteolytic activation in the ischemic brains of wild-type but NOT of mutant mice

decreased cerebral infarct size
- homozygotes subjected to focal cerebral ischemia induced by persistent occlusion of the left middle cerebral artery produce an infarct with a size that is significantly smaller than that produced in wild-type mice

respiratory system phenotype

pulmonary interstitial fibrosis
- bleomycin-treated homozygotes exhibit an enhanced increase in lung hydroxyproline (collagen) content relative to bleomycin-treated wild-type mice
- histological analysis after lung injury indicates extensive interstitial fibrosis in mutant mice relative to wild-type
- 75% of bleomycin-treated homozygotes die as early as 7 days after treatment, as a result of hemorrhage and extensive fibrotic lesions
- notably, homozygotes survive only 11 days post-drug treatment

pulmonary alveolar hemorrhage
- 11 days after bleomycin treatment, mutant lungs show areas of fibrosis surrounded by areas of extensive intra-alveolar hemorrhage
- hemorrhagic areas contain numerous hemosiderin-laden macrophages, indicating chronic pulmonary hemorrhage

vision/eye phenotype

decreased retinal apoptosis
- t 72 h after low-dose NMDA injection
- at 12 and 24 h after intravitreal injection of low-dose (30 nmol/mouse) NMDA, homozygotes contain significantly less retinal apoptotic neurons in the ganglion cell layer (GCL) and inner nuclear layer (INL) relative to wild-type; no differences are noted at 72 h after low-dose NMDA injection
- at higher doses of NMDA, homozygotes show no differences in retinal damage relative to wild-type mice

decreased susceptibility to induced retinal damage
- in contrast, neither intravitreal kainic acid nor transient ischemia results in significant differences in retinal damage in mutant vs. wild-type mice
- homozygotes are partially resistant to NMDA-induced retinal damage relative to wild-type mice

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

cardiovascular system phenotype

decreased ventricle muscle contractility
- at 7 weeks after TAB, wild-type and mutant mice exhibit a similar degree of LV dilatation, obvious signs of LV systolic dysfunction, and pump failure
- at 7 weeks after TAB, impaired fractional shortening and abnormal cardiac pump result in respiratory distress due to pulmonary congestion

heart left ventricle hypertrophy
- similar to wild-type mice, homozygotes display a ~35% increase in LV/body weight ratio and a ~40% increase in the LV cardiomyocyte size
- at 2 weeks after transverse aortic banding (TAB) i.e. acute pressure overload, homozygotes and wild-type mice exhibit a significant LV hypertrophy which persists for up to 7 weeks

intracerebral hemorrhage
- in a photothrombotic model of middle cerebral artery occlusion (MCAO), delayed heparin administration increases cerebral hemorrhage associated with ischemia in wild-type but NOT in mutant mice
- in this MCAO model, heparin administration induces tPA activity and mRNA expression in microglial cells, and enhances MMP9 expression and proteolytic activation in the ischemic brains of wild-type but NOT of mutant mice

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

pulmonary alveolar hemorrhage
- hemorrhagic areas contain numerous hemosiderin-laden macrophages, indicating chronic pulmonary hemorrhage
- 11 days after bleomycin treatment, mutant lungs show areas of fibrosis surrounded by areas of extensive intra-alveolar hemorrhage

cardiac interstitial fibrosis
- in response to pressure overload, wild-type and mutant mice display similar signs of maladaptation (i.e. myolysis, myocardial fibrosis and increased intercapillary distance)

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

cardiovascular system phenotype

decreased angiogenesis
- aortic vessel explants show almost complete inhibition of capillary sprouting in both collagen lattices and Matrigel

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

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

homeostasis/metabolism phenotype

abnormal acute phase protein level
- in a model of collagen-induced arthritis, severely affected joints from homozygotes display diffuse fibrin(ogen) deposition relative to wild-type
- within arthritic joints, higher fibrin levels appear to correlate with increased disease severity

decreased dopamine level
- homozygotes exhibit loss of morphine-induced dopamine release in the nucleus accumbens (Nacc)
- the defect of morphine-induced dopamine release is reversed by exogenous administration of tPA or plasmin into the Nacc but not into the ventral tegmental area (VTA)

increased circulating corticosterone level
- unlike wild-type mice, corticosterone levels in mutant mice do not return to pre-stress levels after a 90-min recovery period
- homozygotes show normal up-regulation of corticosterone in response to CRF but sustain elevation of corticosterone level during recovery
- after a 30-min restraint stress, homozygotes exhibit a 30% increase in corticosterone levels relative to wil-type

joint swelling
- in a model of collagen-induced arthritis, 60% of mutant mice have 3 or 4 affected limbs compared with only 18% of wild-type mice
- in arthritic mutants, 45% of affected individual limbs display severe swelling and/or rigidity compared with only 19% from wild-type
- there are no differences in the degree of swelling (i.e. paw thickness) between limbs from mutant and wild-type mice with the same clinical score

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

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

immune system phenotype

arthritis
- 95% of mutant mice develop arthritis compared with 68% of wild-type mice; no difference in the day of disease onset is observed
- in a model of collagen-induced arthritis, homozygotes develop a significantly more severe arthritis than wild-type mice
- severely affected joints from arthritic homozygotes exhibit higher cartilage damage and bone erosions than wild-type mice

chronic joint inflammation
- severely affected joints from arthritic homozygotes exhibit massive cell infiltration and higher proteoglycan depletion than wild-type mice
- in a model of collagen-induced arthritis, homozygotes develop significant joint inflammation and joint destruction relative to wild-type mice

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

abnormal acute phase protein level
- within arthritic joints, higher fibrin levels appear to correlate with increased disease severity
- in a model of collagen-induced arthritis, severely affected joints from homozygotes display diffuse fibrin(ogen) deposition relative to wild-type

mammalian phenotype

behavior/neurological phenotype
- Normal - homozygotes show normal footshock sensitivity thresholds relative to wild-type mice

muscle phenotype
- Normal - in response to glycerol-induced injury, homozygotes exhibit normal skeletal muscle regeneration after 5 days; regeneration is complete after 9 days
- Normal - at 7 days after injury, most injured fibers regenerate into groups of centrally nucleated myotubes, indicating advanced regeneration; only few necrotic fibers are observed
- Normal - at 20 days after injury, virtually no signs of muscle injury are detected, except for centrally located myonuclei inside the regenerated fibers

behavior/neurological phenotype

abnormal motor learning
- relative to wild-type, mutant mice exhibit a 28% reduction in both the rate and extent of learning a complex motor paradigm of irregular peg running, indicating impaired cerebellar motor learning

decreased anxiety-related response
- after up to 3 weeks of daily restraint, homozygotes exhibit absence of stress-induced anxiety in the elevated-plus maze; in wild-type, acute stress resuls in a decrease in open arm entries, with 21 days of daily restraint leading to some habituation
- in response to a high dose of CRF, homozygotes fail to explore the open arms but display a similar number of closed arms entries relative to wild-type mice, indicating normal locomotor activity
- in response to a low or middle dose of corticotropin-releasing factor (CRF), homozygotes exhibit reduced anxiety (lower number of open arm entries) in the elevated plus-maze, with an increased number of head dips (increased exploration) relative to wild-type
- ype

impaired behavioral response to morphine
- notably, homozygotes display a significant reduction in morphine-induced hyperlocomotion relative to wild-type
- Normal - homozygotes show no significant differences in the antinociceptive effect of morphine or development of its tolerance relative to wild-type mice
- the defect of morphine-induced hyperlocomotion is reversed by exogenous administration of tPA or plasmin into the nucleus accumbens (Nacc)

decreased exploration in new environment
- homozygotes display no habitation of object exploration relative to wild-type mice
- homozygotes show no reactivity to spatial change (measured as renewed exploration of displaced objects) relative to wild-type mice

abnormal active avoidance behavior
- homozygotes display poor active avoidance behavior relative to wild-type mice

impaired conditioned place preference behavior
- homozygotes display a significant reduction in morphine-induced conditioned place preference

abnormal contextual conditioning behavior
- homozygotes display poor contextual fear conditioning behavior relative to wild-type mice, indicating impaired hippocampal function

abnormal cued conditioning behavior
- homozygotes display enhanced cue fear conditioning behavior relative to wild-type mice

decreased vertical activity
- in an empty open field, homozygotes show normal horizontal activity but significantly reduced rearing activity relative to wild-type

nervous system phenotype

impaired synaptic plasticity
- after restraint, homozygotes show reduced neuronal remodeling in the medial amygdala, with absence of stress-induced ERK1/2 phosphorylation at all time points tested
- in response to CRF, homozygotes exhibit attenuated expression of Fos (an indicator of neuronal activation) in the central and medial amygdala but show normal Fos responses in paraventricular nuclei

reduced long term potentiation
- notably, a slight but significant reduction of the early phase of hippocampal LTP is also observed
- in response to tetanic stimulation, hippocampal CA1 slices from mutant mice show a significant reduction in the late phase of LTP relative to wild-type

absent long term depression
- in response to tetanic stimulation of corticostriatal fibers, homozygotes display absence of LTD in a significant portion of striatal neurons

skeleton phenotype

joint swelling
- in arthritic mutants, 45% of affected individual limbs display severe swelling and/or rigidity compared with only 19% from wild-type
- there are no differences in the degree of swelling (i.e. paw thickness) between limbs from mutant and wild-type mice with the same clinical score
- in a model of collagen-induced arthritis, 60% of mutant mice have 3 or 4 affected limbs compared with only 18% of wild-type mice

chronic joint inflammation
- in a model of collagen-induced arthritis, homozygotes develop significant joint inflammation and joint destruction relative to wild-type mice
- severely affected joints from arthritic homozygotes exhibit massive cell infiltration and higher proteoglycan depletion than wild-type mice

arthritis
- in a model of collagen-induced arthritis, homozygotes develop a significantly more severe arthritis than wild-type mice
- 95% of mutant mice develop arthritis compared with 68% of wild-type mice; no difference in the day of disease onset is observed
- severely affected joints from arthritic homozygotes exhibit higher cartilage damage and bone erosions than wild-type mice

Genotype: Plat^tm1Mlg/Plat^tm1Mlg
B6.129S2-Plat/J

immune system phenotype

abnormal susceptibility to Coronaviridae infection
- Normal - however, SARS-CoV MA15-infected mice show similar viral loads in the lung at 4 and 7 days post infection as wild-type controls
- mice infected with a lethal dose of SARS-CoV MA15 show early mortality compared to wild-type controls, although mice that survive early infection recover
- mice infected with a sublethal dose of mouse-adapted SARS-CoV MA15 show a slight, but not significant, acceleration in recovery of weight loss compared to controls
- SARS-CoV MA15 lethally infected mice show a trend toward less hemorrhage in the lungs

increased susceptibility to Coronaviridae infection induced morbidity/mortality
- mice infected with a lethal dose of SARS-CoV MA15 show early mortality compared to wild-type controls, although mice that survive early infection recover

mortality/aging

increased susceptibility to Coronaviridae infection induced morbidity/mortality
- mice infected with a lethal dose of SARS-CoV MA15 show early mortality compared to wild-type controls, although mice that survive early infection recover

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

Centonze D; Napolitano M; Saulle E; Gubellini P; Picconi B; Martorana A; Pisani A; Gulino A; Bernardi G; Calabresi P. 2002. Tissue plasminogen activator is required for corticostriatal long-term potentiation. Eur J Neurosci 16(4):713-21PubMed: 12270047 MGI: J:89414
Huang YY; Bach ME; Lipp HP; Zhuo M; Wolfer DP; Hawkins RD; Schoonjans L; Kandel ER; Godfraind JM; Mulligan R; Collen D; Carmeliet P. 1996. Mice lacking the gene encoding tissue-type plasminogen activator show a selective interference with late-phase long-term potentiation in both Schaffer collateral and mossy fiber pathways. Proc Natl Acad Sci U S A 93(16):8699-704PubMed: 8710934 MGI: J:34823
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):2440-4PubMed: 10318667 MGI: J:55243
Nagai T; Yamada K; Yoshimura M; Ishikawa K; Miyamoto Y; Hashimoto K; Noda Y; Nitta A; Nabeshima T. 2004. The tissue plasminogen activator-plasmin system participates in the rewarding effect of morphine by regulating dopamine release. Proc Natl Acad Sci U S A 101(10):3650-5PubMed: 14988509 MGI: J:88913

Additional - Plat^tm1Mlg related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Plat
- Separated PCR:Platalternate1
- Genotyping resources and troubleshooting
Breeding Considerations

When maintaining a live colony, these mice can be bred as homozygotes. the expected coat color from breeding is black.
- Additional Breeding and Husbandry Support
Mating System
- Homozygote x Homozygote
Appearance
- black
  Related Genotype: a/a
Citation
When using the t-PA^- mouse strain in a publication, please cite the originating article(s) and include JAX stock #002508 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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Age

Genotype

Price

weeks

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Frozen Mouse Embryo	B6.129S2-Plat<tm1Mlg>/J Frozen Embryos	$2595.00
Frozen Mouse Embryo	B6.129S2-Plat<tm1Mlg>/J Frozen Embryos	$2595.00
Frozen Mouse Embryo	B6.129S2-Plat<tm1Mlg>/J Frozen Embryos	$3373.50
Frozen Mouse Embryo	B6.129S2-Plat<tm1Mlg>/J Frozen Embryos	$3373.50

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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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General Terms and Conditions

Questions about Terms of Use

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:t-PA-

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Plattm1Mlg

Allele Symbol: Plattm1Mlg

Disease Terms

Research Areas By Phenotype

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

Genotype: Plattm1Mlg related

Mammalian Phenotype Terms by Genotype

Genotype: Plattm1Mlg/Plattm1Mlginvolves: 129S2/SvPas

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

nervous system phenotype

Genotype: Plattm1Mlg/Plattm1Mlginvolves: 129S2/SvPas * C57BL/6

cellular phenotype

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

mammalian phenotype

muscle phenotype

nervous system phenotype

respiratory system phenotype

vision/eye phenotype

cardiovascular system phenotype

Genotype: Plattm1Mlg/Plattm1Mlginvolves: 129S2/SvPas * C57BL/6J

cardiovascular system phenotype

Genotype: Plattm1Mlg/Plattm1MlgB6.Cg-Plat

homeostasis/metabolism phenotype

immune system phenotype

mammalian phenotype

behavior/neurological phenotype

nervous system phenotype

skeleton phenotype

Genotype: Plattm1Mlg/Plattm1MlgB6.129S2-Plat/J

immune system phenotype

mortality/aging

References

Additional References

Additional - Plattm1Mlg related

Genotyping Protocols

Breeding Considerations

Mating System

Appearance

Citation

Animal Health Reports

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

Live Mouse

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

Also Known As:t-PA^-

Plat^tm1Mlg

Allele Symbol: Plat^tm1Mlg

Genotype: Plat^tm1Mlg related

Genotype: Plat^tm1Mlg/Plat^tm1Mlg
involves: 129S2/SvPas

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

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

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

Genotype: Plat^tm1Mlg/Plat^tm1Mlg
B6.129S2-Plat/J

Additional - Plat^tm1Mlg related