Strain Name:

B6.129P2-Plgtm1Jld/J

Stock Number:

002830

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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 C57BL/6J
Donor Strain 129P2 via E14TG2a ES cell line
 
Donating InvestigatorDr. Thomas Bugge,   NIH/NIDCR

Appearance
black
Related Genotype: a/a

Description
Mice homozygous for the Plgtm1 targeted mutation are viable and fertile. They show a progressive multi-organ pathology and die around 6 months of age. The pathology is characterized by wasting, rectal prolapse, impaired skin wound healing, gastointestinal ulceration, and thrombosis. No details of mammary gland morphology have been provided.

Development
This mutation was generated by replacing a 9 kb fragment of the Plg gene with a vector containing Hprt. The 129-derived E14TG2a ES cell line was used.

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls

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).
Plasminogen Deficiency, Type I
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Plgtm1Jld/Plgtm1Jld

        B6.129P2-Plgtm1Jld
  • mortality/aging
  • decreased sensitivity to induced morbidity/mortality
    • show a moderate increase in survival after primary tumor resection at day 10   (MGI Ref ID J:44314)
  • premature death
    • median survival is 6 months   (MGI Ref ID J:120368)
  • reproductive system phenotype
  • reduced female fertility
    • exhibit more severe infertility than on a mixed 129P2/OlaHsd, Black Swiss, and C57BL/6J background, with fewer than 50% of females becoming pregnant   (MGI Ref ID J:64966)
    • second pregnancies are rare   (MGI Ref ID J:64966)
  • vision/eye phenotype
  • abnormal conjunctiva morphology   (MGI Ref ID J:46096)
    • abnormal conjunctival epithelium morphology
      • exhibit extensive disruption of the conjunctival epithelium in all lesions, associated with hypertrophy, disorganization, and reduplication consistent with chronic, recurrent ulceration and attempted re-epithelialization   (MGI Ref ID J:46096)
    • conjunctivitis
      • 100% of older mutants develop conjunctival lesions (palpebral and bulbar conjunctivitis) that are much more severe than on a mixed 129P2/OlaHsd and Black Swiss background   (MGI Ref ID J:46096)
      • incidence of lesion development increases with age and lesions develop into extensive, pedunculated plaques over time   (MGI Ref ID J:46096)
      • lesions contain acellular material rich in fibrin and are accompanied by a whitish, irregular surface of the palpebral conjunctiva, an increase in vascularization of the lid, and external accumulations of mucus   (MGI Ref ID J:46096)
      • acute inflammatory infiltrates with a predominance of neutrophils frequently accompany conjunctival lesions and occasionally see CD4+ and CD8+ lymphocytes in the infiltrates   (MGI Ref ID J:46096)
  • abnormal cornea morphology
    • occasionally observe corneal defects such as stromal haze in mutants with early conjunctival lesions, however lesions always occur in the palperbral conjunctiva prior to corneal defects   (MGI Ref ID J:46096)
    • form extensive fibrin rich plaques overlying the cornea, with associated epithelium ulceration, hypertrophy, and disorganization   (MGI Ref ID J:46096)
    • abnormal corneal epithelium morphology
      • corneal epithelium is frequently absent, necrotic, or hypertrophied   (MGI Ref ID J:46096)
    • abnormal corneal stroma morphology
      • ulceration or destruction of the stroma with extensive protruding plaques are seen overlying the cornea   (MGI Ref ID J:46096)
    • corneal vascularization
      • stromal vascularization is frequently associated with corneal lesions   (MGI Ref ID J:46096)
  • ectropion
    • palpebral conjunctival alterations result in hypertrophied, everted eyelids with ulceration and hemorrhage   (MGI Ref ID J:46096)
  • eye hemorrhage
    • palpebral conjunctival alterations result in hypertrophied, everted eyelids with ulceration and hemorrhage   (MGI Ref ID J:46096)
  • eye inflammation
    • formation of papillary or a retrocorneal membrane is seen in several mutants, consistent with chronic intraocular inflammation   (MGI Ref ID J:46096)
    • conjunctivitis
      • 100% of older mutants develop conjunctival lesions (palpebral and bulbar conjunctivitis) that are much more severe than on a mixed 129P2/OlaHsd and Black Swiss background   (MGI Ref ID J:46096)
      • incidence of lesion development increases with age and lesions develop into extensive, pedunculated plaques over time   (MGI Ref ID J:46096)
      • lesions contain acellular material rich in fibrin and are accompanied by a whitish, irregular surface of the palpebral conjunctiva, an increase in vascularization of the lid, and external accumulations of mucus   (MGI Ref ID J:46096)
      • acute inflammatory infiltrates with a predominance of neutrophils frequently accompany conjunctival lesions and occasionally see CD4+ and CD8+ lymphocytes in the infiltrates   (MGI Ref ID J:46096)
  • tumorigenesis
  • decreased tumor growth/size
    • homozygotes develop primary tumors with no difference in the rate of appearance or in lung metastasis when inoculated with a metastatic Lewis lung carcinoma expressing high levels of plasminogen activator, however the primary tumors are smaller, less hemorrhagic, display reduced skin ulceration, show delayed dissemination of the tumor to regional lymph nodes, and show a moderate increase in survival after primary tumor resection   (MGI Ref ID J:44314)
  • digestive/alimentary phenotype
  • abnormal rectum morphology
    • 71% developed rectal lesions   (MGI Ref ID J:46096)
  • cardiovascular system phenotype
  • corneal vascularization
    • stromal vascularization is frequently associated with corneal lesions   (MGI Ref ID J:46096)
  • eye hemorrhage
    • palpebral conjunctival alterations result in hypertrophied, everted eyelids with ulceration and hemorrhage   (MGI Ref ID J:46096)
  • liver/biliary system phenotype
  • increased hepatocyte proliferation
    • the number of proliferating hepatocyte is increased (126.6+/-3.9 compare to 95.2+/-3.7 in wild-type mice)   (MGI Ref ID J:120368)
  • endocrine/exocrine gland phenotype
  • abnormal lactation
    • more than 75% of females are unable to sustain lactation for 10 days, much higher percentage than on a mixed 129P2/OlaHsd, Black Swiss, and C57BL/6J background   (MGI Ref ID J:64966)
  • growth/size/body phenotype
  • decreased body weight
    • weight at 60 days of age is lower   (MGI Ref ID J:46096)
  • immune system phenotype
  • eye inflammation
    • formation of papillary or a retrocorneal membrane is seen in several mutants, consistent with chronic intraocular inflammation   (MGI Ref ID J:46096)
    • conjunctivitis
      • 100% of older mutants develop conjunctival lesions (palpebral and bulbar conjunctivitis) that are much more severe than on a mixed 129P2/OlaHsd and Black Swiss background   (MGI Ref ID J:46096)
      • incidence of lesion development increases with age and lesions develop into extensive, pedunculated plaques over time   (MGI Ref ID J:46096)
      • lesions contain acellular material rich in fibrin and are accompanied by a whitish, irregular surface of the palpebral conjunctiva, an increase in vascularization of the lid, and external accumulations of mucus   (MGI Ref ID J:46096)
      • acute inflammatory infiltrates with a predominance of neutrophils frequently accompany conjunctival lesions and occasionally see CD4+ and CD8+ lymphocytes in the infiltrates   (MGI Ref ID J:46096)
  • integument phenotype
  • abnormal lactation
    • more than 75% of females are unable to sustain lactation for 10 days, much higher percentage than on a mixed 129P2/OlaHsd, Black Swiss, and C57BL/6J background   (MGI Ref ID J:64966)
  • cellular phenotype
  • increased hepatocyte proliferation
    • the number of proliferating hepatocyte is increased (126.6+/-3.9 compare to 95.2+/-3.7 in wild-type mice)   (MGI Ref ID J:120368)

Plgtm1Jld/Plgtm1Jld

        B6.129P2-Plgtm1Jld/J
  • nervous system phenotype
  • abnormal microglial cell physiology
    • kainate acid-induced microglial migration is reduced compared to in similarly treated wild-type mice   (MGI Ref ID J:141739)
    • however, plasmin-mediated cleavage of Ccl2 restores kainate acid-induced microglial migration   (MGI Ref ID J:141739)
  • decreased susceptibility to neuronal excitotoxicity
    • kainate acid-treated mice exhibit reduced excitotoxicity compared with similarly treated wild-type mice   (MGI Ref ID J:141739)
    • however, plasmin-mediated cleavage of Ccl2 restores kainate acid-induced excitotoxicity   (MGI Ref ID J:141739)
  • homeostasis/metabolism phenotype
  • decreased susceptibility to neuronal excitotoxicity
    • kainate acid-treated mice exhibit reduced excitotoxicity compared with similarly treated wild-type mice   (MGI Ref ID J:141739)
    • however, plasmin-mediated cleavage of Ccl2 restores kainate acid-induced excitotoxicity   (MGI Ref ID J:141739)
  • immune system phenotype
  • abnormal microglial cell physiology
    • kainate acid-induced microglial migration is reduced compared to in similarly treated wild-type mice   (MGI Ref ID J:141739)
    • however, plasmin-mediated cleavage of Ccl2 restores kainate acid-induced microglial migration   (MGI Ref ID J:141739)
  • cellular phenotype
  • decreased susceptibility to neuronal excitotoxicity
    • kainate acid-treated mice exhibit reduced excitotoxicity compared with similarly treated wild-type mice   (MGI Ref ID J:141739)
    • however, plasmin-mediated cleavage of Ccl2 restores kainate acid-induced excitotoxicity   (MGI Ref ID J:141739)
  • hematopoietic system phenotype
  • abnormal microglial cell physiology
    • kainate acid-induced microglial migration is reduced compared to in similarly treated wild-type mice   (MGI Ref ID J:141739)
    • however, plasmin-mediated cleavage of Ccl2 restores kainate acid-induced microglial migration   (MGI Ref ID J:141739)

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

Plgtm1Jld/Plg+

        involves: 129P2/OlaHsd * C57BL/6J
  • cardiovascular system phenotype
  • decreased angiogenesis
    • aortic vessel explants show almost complete lack of capillary sprouting in collagen lattices   (MGI Ref ID J:108675)

Plgtm1Jld/Plgtm1Jld

        involves: 129P2/OlaHsd * NIH Black Swiss
  • homeostasis/metabolism phenotype
  • impaired wound healing
    • scab remains in place longer and once lost, the wound field is still gaping and red with a hard and often scaly surface lacking epidermal covering   (MGI Ref ID J:33897)
    • wounds appear to shrink and heal over several weeks, but about a third of the wounds are not healed 6 weeks after the original incision   (MGI Ref ID J:33897)
    • keratinocyte migration is impaired in skin wound healing experiments   (MGI Ref ID J:33897)
  • thrombosis
    • young mutants develop multiple spontaneous thrombotic lesions in liver, stomach, colon, rectum, lung, pancreas, and other tissues   (MGI Ref ID J:39419)
  • digestive/alimentary phenotype
  • abnormal colon morphology
    • 3 of 17 develop colonic ulcers, proximal to the rectum, at 7 and 10 weeks of age, showing a necrotic surface epithelium covered by exudates   (MGI Ref ID J:39419)
  • abnormal stomach morphology   (MGI Ref ID J:39419)
    • gastric ulcer
      • 10 of 17 show gastric ulcers at 5 to 21 weeks of age, including 7 with ulcerated lesions in the glandular portion of the stomach, 2 with an ulcer in the squamous portion of the stomach, and 1 with an ulcer at the junction of the two portions   (MGI Ref ID J:39419)
  • large intestinal inflammation
    • 7 of 43 develop inflammatory rectal lesions between 5 and 21 weeks of age   (MGI Ref ID J:39419)
  • perianal ulceration
    • exhibit anal-rectal tissue ulceration with surface exudates and surrounding fibrin deposition   (MGI Ref ID J:39419)
  • rectal prolapse
    • oldest of the mice that show inflammatory rectal lesions exhibit rectal prolapse   (MGI Ref ID J:39419)
  • immune system phenotype
  • large intestinal inflammation
    • 7 of 43 develop inflammatory rectal lesions between 5 and 21 weeks of age   (MGI Ref ID J:39419)
  • liver/biliary system phenotype
  • abnormal liver morphology
    • exhibit multiple hepatic fibrin deposits identified as fibrinogen that show varying degrees of organization with infiltration of spindle cells   (MGI Ref ID J:39419)
    • hepatic necrosis
      • necrosis is apparent within adjacent tissue in a fraction of hepatic lesions   (MGI Ref ID J:39419)
  • respiratory system phenotype
  • abnormal lung morphology
    • 7 of 17 show pulmonary lesions, with capillary fibrin thrombi in 4 mutants and organizing patches of alveolar fibrin in 4 mutants   (MGI Ref ID J:39419)
  • cardiovascular system phenotype
  • venoocclusion
    • young mutants exhibit vascular occlusions   (MGI Ref ID J:39419)

Plgtm1Jld/Plgtm1Jld

        involves: 129P2/OlaHsd * C57BL/6 * NIH Black Swiss
  • mortality/aging
  • premature death
    • only about 70% survive beyond 20 weeks of age   (MGI Ref ID J:42927)
  • growth/size/body phenotype
  • abnormal body weight
    • average body weight is 25% lower after 2 months of age   (MGI Ref ID J:42927)
  • cardiovascular system phenotype
  • *normal* cardiovascular system phenotype
    • do not develop atherosclerosis   (MGI Ref ID J:42927)

Plgtm1Jld/Plgtm1Jld

        involves: 129P2/OlaHsd
  • nervous system phenotype
  • abnormal nervous system physiology
    • exhibit resistance to hippocampal neuronal death induced by kainate injection   (MGI Ref ID J:42819)

Plgtm1Jld/Plgtm1Jld

        involves: 129P2/OlaHsd * Black Swiss
  • mortality/aging
  • premature death
    • mean survival time is 176 days and all died or had to be euthanized by 301 days; 40% die spontaneously   (MGI Ref ID J:36591)
  • growth/size/body phenotype
  • weight loss
    • exhibit a progressive weight loss starting around 2 months of age which becomes severe after 4 months of age   (MGI Ref ID J:36591)
    • cachexia
      • exhibit severe wasting   (MGI Ref ID J:36591)
  • digestive/alimentary phenotype
  • abnormal rectum morphology
    • 77% (10 of 13) show rectal ulceration   (MGI Ref ID J:36591)
    • rectal prolapse
      • develop spontaneous rectal ulcerations, which over a period of few weeks progress into rectal prolapse   (MGI Ref ID J:36591)
  • colitis
    • 8% (1 of 13) show colitis   (MGI Ref ID J:36591)
  • esophageal ulcer
    • 8% (1 of 13) show esophageal ulcer   (MGI Ref ID J:36591)
  • gastrointestinal ulcer
    • exhibit various ulcers in the gastrointestinal tract, including in the stomach, colon, and duodenum   (MGI Ref ID J:36591)
    • duodenal ulcer
      • 8% (1 of 13) show duodenal ulcers   (MGI Ref ID J:36591)
    • gastric ulcer
      • 70% (9 of 13) show glandular stomach ulcers   (MGI Ref ID J:36591)
      • 23% (3 of 13) show squamous stomach ulcers   (MGI Ref ID J:36591)
    • intestinal ulcer
      • 24% (3 of 13) exhibit colonic ulcers   (MGI Ref ID J:36591)
  • perianal ulceration
    • exhibit anal-rectal ulceration   (MGI Ref ID J:36591)
  • homeostasis/metabolism phenotype
  • impaired wound healing
    • scab is retained longer, and when lost, shows a large, gaping wound field lacking epidermal covering   (MGI Ref ID J:36591)
  • thrombosis
    • 8% (1 of 13) show larynx thrombi   (MGI Ref ID J:36591)
    • 23% (3 of 13) show tracheal thrombi   (MGI Ref ID J:36591)
    • kidney thrombosis
      • 8% (1 of 13) show kidney thrombi   (MGI Ref ID J:36591)
  • immune system phenotype
  • colitis
    • 8% (1 of 13) show colitis   (MGI Ref ID J:36591)
  • liver/biliary system phenotype
  • abnormal liver morphology
    • 100% exhibit multiple lesions scattered throughout the liver, characterized by sinusoidal deposits of fibrillar material   (MGI Ref ID J:36591)
  • renal/urinary system phenotype
  • kidney thrombosis
    • 8% (1 of 13) show kidney thrombi   (MGI Ref ID J:36591)
  • reproductive system phenotype
  • abnormal vagina morphology
    • 57% (4 of 7) virgin females show vaginal lesions   (MGI Ref ID J:36591)
  • respiratory system phenotype
  • abnormal larynx morphology
    • 8% (1 of 13) show larynx thrombi   (MGI Ref ID J:36591)
  • abnormal lung morphology
    • 39% (5 of 13) show pulmonary lesions   (MGI Ref ID J:36591)
  • abnormal trachea morphology
    • 8% (1 of 13) show tracheal necrosis   (MGI Ref ID J:36591)
    • 23% (3 of 13) show tracheal thrombi   (MGI Ref ID J:36591)
  • vision/eye phenotype
  • abnormal conjunctiva morphology
    • 17% (3 of 18) of older mutants develop conjunctival lesions that are milder than on C57BL/6J background   (MGI Ref ID J:46096)
  • cardiovascular system phenotype
  • kidney thrombosis
    • 8% (1 of 13) show kidney thrombi   (MGI Ref ID J:36591)

Plgtm1Jld/Plgtm1Jld

        involves: 129P2/OlaHsd * C57BL/6J
  • cardiovascular system phenotype
  • decreased angiogenesis
    • aortic vessel explants fail to form capillary sprouts in collagen lattices or Matrigel   (MGI Ref ID J:108675)
    • explants supplemented with either Plaur or Plat partially regain the ability to form capillary sprouts   (MGI Ref ID J:108675)

Plgtm1Jld/Plgtm1Jld

        involves: 129P2/OlaHsd * Black Swiss * C57BL/6J
  • reproductive system phenotype
  • reduced female fertility
    • fertility is reduced less than on a congenic C57BL/6J background, with 26% of females failing to give birth, even though exhibit normal estrus cycles   (MGI Ref ID J:64966)
    • second pregnancies are rare   (MGI Ref ID J:64966)
  • endocrine/exocrine gland phenotype
  • abnormal mammary gland connective tissue morphology
    • exhibit abnormal stromal extracellular matrix (ECM), with increased collagen deposition and absence of ECM degradation   (MGI Ref ID J:64966)
  • abnormal mammary gland development
    • mammary glands are underdeveloped   (MGI Ref ID J:64966)
    • mammary glands exhibit delayed epithelial regression accompanied by diminished adipocyte differentiation during involution; glands have less adipose tissue and stroma is instead filled with immature adipocytes and fibrotic tissue   (MGI Ref ID J:64966)
    • abnormal involution of the mammary gland
      • glands from lactating females are initially smaller and fail to involute after weaning   (MGI Ref ID J:64966)
      • during involution, the alveolar tissue shows only minimal regression, residual alveolar and ductal structures occupy larger volume fractions, collapsed alveoli with epithelial cells shed into the ducts, and uncollapsed necrotic alveoli are seen   (MGI Ref ID J:64966)
      • show decreased apoptosis in mammary glands at 5 days of involution, indicating delayed, but not completely blocked, alveolar regression   (MGI Ref ID J:64966)
    • abnormal mammary gland growth during lactation
      • in females capable of lactation, mammary glands are lighter and contain less total secretory alveolar tissue after 10 days of lactation, however after 10 days of lactation and 5 days of involution, glands do not show the same degree in gland size reduction as wild-type and are thus heavier   (MGI Ref ID J:64966)
      • mammary glands from 7 of 9 dams that were unable to nurse pups (do not lactate) contain almost no secretory alveolar epithelium, instead they have regions of prominent fibrosis, scattered areas of atypical adipose tissue, and sometimes abundant inflammatory cells   (MGI Ref ID J:64966)
      • exhibit an accumulation of activated macrophages in the stroma of lactating mammary glands   (MGI Ref ID J:64966)
  • lactation failure
    • 28% of females are unable to sustain lactation for 10 days, a much lower percentage than on a congenic C57BL/6J background   (MGI Ref ID J:64966)
    • lactation failure is more severe after a second pregnancy, with only 1 of 8 litters surviving   (MGI Ref ID J:64966)
  • integument phenotype
  • abnormal mammary gland connective tissue morphology
    • exhibit abnormal stromal extracellular matrix (ECM), with increased collagen deposition and absence of ECM degradation   (MGI Ref ID J:64966)
  • abnormal mammary gland development
    • mammary glands are underdeveloped   (MGI Ref ID J:64966)
    • mammary glands exhibit delayed epithelial regression accompanied by diminished adipocyte differentiation during involution; glands have less adipose tissue and stroma is instead filled with immature adipocytes and fibrotic tissue   (MGI Ref ID J:64966)
    • abnormal involution of the mammary gland
      • glands from lactating females are initially smaller and fail to involute after weaning   (MGI Ref ID J:64966)
      • during involution, the alveolar tissue shows only minimal regression, residual alveolar and ductal structures occupy larger volume fractions, collapsed alveoli with epithelial cells shed into the ducts, and uncollapsed necrotic alveoli are seen   (MGI Ref ID J:64966)
      • show decreased apoptosis in mammary glands at 5 days of involution, indicating delayed, but not completely blocked, alveolar regression   (MGI Ref ID J:64966)
    • abnormal mammary gland growth during lactation
      • in females capable of lactation, mammary glands are lighter and contain less total secretory alveolar tissue after 10 days of lactation, however after 10 days of lactation and 5 days of involution, glands do not show the same degree in gland size reduction as wild-type and are thus heavier   (MGI Ref ID J:64966)
      • mammary glands from 7 of 9 dams that were unable to nurse pups (do not lactate) contain almost no secretory alveolar epithelium, instead they have regions of prominent fibrosis, scattered areas of atypical adipose tissue, and sometimes abundant inflammatory cells   (MGI Ref ID J:64966)
      • exhibit an accumulation of activated macrophages in the stroma of lactating mammary glands   (MGI Ref ID J:64966)
  • lactation failure
    • 28% of females are unable to sustain lactation for 10 days, a much lower percentage than on a congenic C57BL/6J background   (MGI Ref ID J:64966)
    • lactation failure is more severe after a second pregnancy, with only 1 of 8 litters surviving   (MGI Ref ID J:64966)
View Research Applications

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

Internal/Organ Research
Wound Healing
      delayed/impaired

Plgtm1Jld related

Cancer Research
Other

Cardiovascular Research
Vascular Defects
      Thrombosis

Hematological Research
Clotting Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Plgtm1Jld
Allele Name targeted mutation 1, Jay L Degen
Allele Type Targeted (Null/Knockout)
Common Name(s) Plg-; Plg0;
Strain of Origin129P2/OlaHsd
ES Cell Line NameE14TG2a
ES Cell Line Strain129P2/OlaHsd
Gene Symbol and Name Plg, plasminogen
Chromosome 17
Gene Common Name(s) AI649309; Ab1-346; Pg; expressed sequence AI649309;
Molecular Note A PGK-HPRT minigene replaces proximal promoter sequences and the first two exons of the gene. Northern analysis and enzymatic activity assays were used to demonstrate the lack of a transcript and functional protein, respectively, in homozygous mutant animals. [MGI Ref ID J:39419]

Genotyping

Genotyping Information

Genotyping Protocols

Plgtm1Jld, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Bugge TH; Flick MJ; Daugherty CC; Degen JL. 1995. Plasminogen deficiency causes severe thrombosis but is compatible with development and reproduction. Genes Dev 9(7):794-807. [PubMed: 7705657]  [MGI Ref ID J:39419]

Additional References

Bannach FG; Gutierrez A; Fowler BJ; Bugge TH; Degen JL; Parmer RJ; Miles LA. 2002. Localization of regulatory elements mediating constitutive and cytokine-stimulated plasminogen gene expression. J Biol Chem 277(41):38579-88. [PubMed: 12149246]  [MGI Ref ID J:79462]

Bezerra JA; Carrick TL; Degen JL; Witte D; Degen SJF. 1998. Biological effects of targeted inactivation of hepatocyte growth factor-like protein in mice J Clin Invest 101(5):1175-83. [PubMed: 9486989]  [MGI Ref ID J:46185]

Bugge TH; Kombrinck KW; Flick MJ; Daugherty CC; Danton MJ; Degen JL. 1996. Loss of fibrinogen rescues mice from the pleiotropic effects of plasminogen deficiency. Cell 87(4):709-19. [PubMed: 8929539]  [MGI Ref ID J:36591]

Bugge TH; Kombrinck KW; Xiao Q; Holmback K; Daugherty CC; Witte DP; Degen JL. 1997. Growth and dissemination of Lewis lung carcinoma in plasminogen-deficient mice. Blood 90(11):4522-31. [PubMed: 9373263]  [MGI Ref ID J:44314]

Bugge TH; Lund LR; Kombrinck KK; Nielsen BS; Holmback K; Drew AF; Flick MJ; Witte DP; Dano K; Degen JL. 1998. Reduced metastasis of Polyoma virus middle T antigen-induced mammary cancer in plasminogen-deficient mice. Oncogene 16(24):3097-104. [PubMed: 9671388]  [MGI Ref ID J:48285]

Bugge TH; Suh TT; Flick MJ; Daugherty CC; Romer J; Solberg H; Ellis V; Dano K; Degen JL. 1995. The receptor for urokinase-type plasminogen activator is not essential for mouse development or fertility. J Biol Chem 270(28):16886-94. [PubMed: 7622505]  [MGI Ref ID J:26874]

Bugge TH; Xiao Q; Kombrinck KW; Flick MJ; Holmback K; Danton MJ; Colbert MC; Witte DP; Fujikawa K; Davie EW; Degen JL. 1996. Fatal embryonic bleeding events in mice lacking tissue factor, the cell-associated initiator of blood coagulation. Proc Natl Acad Sci U S A 93(13):6258-63. [PubMed: 8692802]  [MGI Ref ID J:33831]

Busso N; Peclat V; Van Ness K; Kolodziesczyk E; Degen J; Bugge T; So A. 1998. Exacerbation of antigen-induced arthritis in urokinase-deficient mice. J Clin Invest 102(1):41-50. [PubMed: 9649555]  [MGI Ref ID J:48540]

Gebbia JA; Monco JC; Degen JL; Bugge TH; Benach JL. 1999. The plasminogen activation system enhances brain and heart invasion in murine relapsing fever borreliosis. J Clin Invest 103(1):81-7. [PubMed: 9884337]  [MGI Ref ID J:51938]

Holmback K; Danton MJ; Suh TT; Daugherty CC; Degen JL. 1996. Impaired platelet aggregation and sustained bleeding in mice lacking the fibrinogen motif bound by integrin alpha IIb beta 3. EMBO J 15(21):5760-71. [PubMed: 8918453]  [MGI Ref ID J:36873]

Lijnen HR; Carmeliet P; Bouche A; Moons L; Ploplis VA; Plow EF; Collen D. 1996. Restoration of thrombolytic potential in plasminogen-deficient mice by bolus administration of plasminogen. Blood 88(3):870-6. [PubMed: 8704243]  [MGI Ref ID J:34531]

Ling Q; Jacovina AT; Deora A; Febbraio M; Simantov R; Silverstein RL; Hempstead B; Mark WH; Hajjar KA. 2004. Annexin II regulates fibrin homeostasis and neoangiogenesis in vivo. J Clin Invest 113(1):38-48. [PubMed: 14702107]  [MGI Ref ID J:87621]

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]

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):3650-5. [PubMed: 14988509]  [MGI Ref ID J:88913]

Nagashima M; Yin ZF; Zhao L; White K; Zhu Y; Lasky N; Halks-Miller M; Broze GJ Jr; Fay WP; Morser J. 2002. Thrombin-activatable fibrinolysis inhibitor (TAFI) deficiency is compatible with murine life. J Clin Invest 109(1):101-10. [PubMed: 11781355]  [MGI Ref ID J:73713]

Nordstrand A; Shamaei-Tousi A; Ny A; Bergstrom S. 2001. Delayed invasion of the kidney and brain by Borrelia crocidurae in plasminogen-deficient mice. Infect Immun 69(9):5832-9. [PubMed: 11500461]  [MGI Ref ID J:71225]

Ny A; Nordstrom L; Carmeliet P; Ny T. 1997. Studies of mice lacking plasminogen activator gene function suggest that plasmin production prior to ovulation exceeds the amount needed for optimal ovulation efficiency. Eur J Biochem 244(2):487-93. [PubMed: 9119016]  [MGI Ref ID J:39196]

Romer J; Bugge TH; Pyke C; Lund LR; Flick MJ; Degen JL; Dano K. 1996. Impaired wound healing in mice with a disrupted plasminogen gene [see comments] Nat Med 2(3):287-92. [PubMed: 8612226]  [MGI Ref ID J:33897]

Schuster V; Mingers AM; Seidenspinner S; Nussgens Z; Pukrop T; Kreth HW. 1997. Homozygous mutations in the plasminogen gene of two unrelated girls with ligneous conjunctivitis. Blood 90(3):958-66. [PubMed: 9242524]  [MGI Ref ID J:48307]

Sjoland H; Eitzman DT; Gordon D; Westrick R; Nabel EG; Ginsburg D. 2000. Atherosclerosis progression in LDL receptor-deficient and apolipoprotein E-deficient mice is independent of genetic alterations in plasminogen activator inhibitor-1. Arterioscler Thromb Vasc Biol 20(3):846-52. [PubMed: 10712412]  [MGI Ref ID J:61287]

Solberg H; Rinkenberger J; Dano K; Werb Z; Lund LR. 2003. A functional overlap of plasminogen and MMPs regulates vascularization during placental development. Development 130(18):4439-50. [PubMed: 12900459]  [MGI Ref ID J:84595]

Suh TT; Holmback K; Jensen NJ; Daugherty CC; Small K; Simon DI; Potter S; Degen JL. 1995. Resolution of spontaneous bleeding events but failure of pregnancy in fibrinogen-deficient mice. Genes Dev 9(16):2020-33. [PubMed: 7649481]  [MGI Ref ID J:28436]

Sun WY; Witte DP; Degen JL; Colbert MC; Burkart MC; Holmback K; Xiao Q; Bugge TH; Degen SJ. 1998. Prothrombin deficiency results in embryonic and neonatal lethality in mice. Proc Natl Acad Sci U S A 95(13):7597-602. [PubMed: 9636195]  [MGI Ref ID J:48273]

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]

Swaisgood CM; Schmitt D; Eaton D; Plow EF. 2002. In vivo regulation of plasminogen function by plasma carboxypeptidase B. J Clin Invest 110(9):1275-82. [PubMed: 12417566]  [MGI Ref ID J:80114]

Teesalu T; Blasi F; Talarico D. 1998. Expression and function of the urokinase type plasminogen activator during mouse hemochorial placental development. Dev Dyn 213(1):27-38. [PubMed: 9733098]  [MGI Ref ID J:49265]

Toft DJ; Linzer DI. 1999. Prolactin (PRL)-like protein J, a novel member of the PRL/growth hormone family, is exclusively expressed in maternal decidua. Endocrinology 140(11):5095-101. [PubMed: 10537137]  [MGI Ref ID J:58334]

Tsirka SE; Bugge TH; Degen JL; Strickland S. 1997. Neuronal death in the central nervous system demonstrates a non-fibrin substrate for plasmin. Proc Natl Acad Sci U S A 94(18):9779-81. [PubMed: 9275201]  [MGI Ref ID J:42819]

Tsirka SE; Rogove AD; Bugge TH; Degen JL; Strickland S. 1997. An extracellular proteolytic cascade promotes neuronal degeneration in the mouse hippocampus. J Neurosci 17(2):543-52. [PubMed: 8987777]  [MGI Ref ID J:37549]

Xiao Q; Danton MJ; Witte DP; Kowala MC; Valentine MT; Bugge TH ; Degen JL. 1997. Plasminogen deficiency accelerates vessel wall disease in mice predisposed to atherosclerosis. Proc Natl Acad Sci U S A 94(19):10335-40. [PubMed: 9294211]  [MGI Ref ID J:42927]

Xiao Q; Danton MJ; Witte DP; Kowala MC; Valentine MT; Degen JL. 1998. Fibrinogen deficiency is compatible with the development of atherosclerosis in mice. J Clin Invest 101(5):1184-94. [PubMed: 9486990]  [MGI Ref ID J:46186]

Plgtm1Jld related

An J; Zhang C; Polavarapu R; Zhang X; Zhang X; Yepes M. 2008. Tissue-type plasminogen activator and the low-density lipoprotein receptor-related protein induce Akt phosphorylation in the ischemic brain. Blood 112(7):2787-94. [PubMed: 18628488]  [MGI Ref ID J:140146]

Bolon I; Zhou HM; Charron Y; Wohlwend A; Vassalli JD. 2004. Plasminogen mediates the pathological effects of urokinase-type plasminogen activator overexpression. Am J Pathol 164(6):2299-304. [PubMed: 15161662]  [MGI Ref ID J:91071]

Brodsky S; Chen J; Lee A; Akassoglou K; Norman J; Goligorsky MS. 2001. Plasmin-dependent and -independent effects of plasminogen activators and inhibitor-1 on ex vivo angiogenesis. Am J Physiol Heart Circ Physiol 281(4):H1784-92. [PubMed: 11557572]  [MGI Ref ID J:108675]

Bugge TH; Kombrinck KW; Flick MJ; Daugherty CC; Danton MJ; Degen JL. 1996. Loss of fibrinogen rescues mice from the pleiotropic effects of plasminogen deficiency. Cell 87(4):709-19. [PubMed: 8929539]  [MGI Ref ID J:36591]

Bugge TH; Kombrinck KW; Xiao Q; Holmback K; Daugherty CC; Witte DP; Degen JL. 1997. Growth and dissemination of Lewis lung carcinoma in plasminogen-deficient mice. Blood 90(11):4522-31. [PubMed: 9373263]  [MGI Ref ID J:44314]

Bugge TH; Lund LR; Kombrinck KK; Nielsen BS; Holmback K; Drew AF; Flick MJ; Witte DP; Dano K; Degen JL. 1998. Reduced metastasis of Polyoma virus middle T antigen-induced mammary cancer in plasminogen-deficient mice. Oncogene 16(24):3097-104. [PubMed: 9671388]  [MGI Ref ID J:48285]

Chen PK; Chang BI; Kuo CH; Chen PS; Cho CF; Chang CF; Shi GY; Wu HL. 2013. Thrombomodulin functions as a plasminogen receptor to modulate angiogenesis. FASEB J 27(11):4520-31. [PubMed: 23943648]  [MGI Ref ID J:203849]

Chen ZL; Indyk JA; Bugge TH; Kombrinck KW; Degen JL; Strickland S. 1999. Neuronal death and blood-brain barrier breakdown after excitotoxic injury are independent processes. J Neurosci 19(22):9813-20. [PubMed: 10559390]  [MGI Ref ID J:119842]

Chen ZL; Indyk JA; Strickland S. 2003. The hippocampal laminin matrix is dynamic and critical for neuronal survival. Mol Biol Cell 14(7):2665-76. [PubMed: 12857855]  [MGI Ref ID J:126217]

Cheng Q; Zhao Y; Lawson WE; Polosukhin VV; Johnson JE; Blackwell TS; Gailani D. 2005. The effects of intrinsic pathway protease deficiencies on plasminogen-deficient mice. Blood 106(9):3055-7. [PubMed: 15985536]  [MGI Ref ID J:123906]

Chun TH; Sabeh F; Ota I; Murphy H; McDonagh KT; Holmbeck K; Birkedal-Hansen H; Allen ED; Weiss SJ. 2004. MT1-MMP-dependent neovessel formation within the confines of the three-dimensional extracellular matrix. J Cell Biol 167(4):757-67. [PubMed: 15545316]  [MGI Ref ID J:94371]

Cortes-Canteli M; Paul J; Norris EH; Bronstein R; Ahn HJ; Zamolodchikov D; Bhuvanendran S; Fenz KM; Strickland S. 2010. Fibrinogen and beta-amyloid association alters thrombosis and fibrinolysis: a possible contributing factor to Alzheimer's disease. Neuron 66(5):695-709. [PubMed: 20547128]  [MGI Ref ID J:167873]

Currier AR; Sabla G; Locaputo S; Melin-Aldana H; Degen JL; Bezerra JA. 2003. Plasminogen directs the pleiotropic effects of uPA in liver injury and repair. Am J Physiol Gastrointest Liver Physiol 284(3):G508-15. [PubMed: 12431907]  [MGI Ref ID J:107854]

Drew AF; Kaufman AH; Kombrinck KW; Danton MJ; Daugherty CC; Degen JL; Bugge TH. 1998. Ligneous conjunctivitis in plasminogen-deficient mice. Blood 91(5):1616-24. [PubMed: 9473227]  [MGI Ref ID J:46096]

Drew AF; Schiman HL; Kombrinck KW; Bugge TH; Degen JL; Kaufman AH. 2000. Persistent corneal haze after excimer laser photokeratectomy in plasminogen-deficient mice. Invest Ophthalmol Vis Sci 41(1):67-72. [PubMed: 10634603]  [MGI Ref ID J:115352]

Drew AF; Tucker HL; Kombrinck KW; Simon DI; Bugge TH; Degen JL. 2000. Plasminogen is a critical determinant of vascular remodeling in mice. Circ Res 87(2):133-9. [PubMed: 10903997]  [MGI Ref ID J:110280]

Echeverry R; Wu J; Haile WB; Guzman J; Yepes M. 2010. Tissue-type plasminogen activator is a neuroprotectant in the mouse hippocampus. J Clin Invest 120(6):2194-205. [PubMed: 20440070]  [MGI Ref ID J:161457]

Green KA; Almholt K; Ploug M; Rono B; Castellino FJ; Johnsen M; Bugge TH; Romer J; Lund LR. 2008. Profibrinolytic effects of metalloproteinases during skin wound healing in the absence of plasminogen. J Invest Dermatol 128(8):2092-101. [PubMed: 18337830]  [MGI Ref ID J:141615]

Green KA; Nielsen BS; Castellino FJ; Romer J; Lund LR. 2006. Lack of plasminogen leads to milk stasis and premature mammary gland involution during lactation. Dev Biol 299(1):164-75. [PubMed: 16949567]  [MGI Ref ID J:114391]

Hald A; Eickhardt H; Maerkedahl RB; Feldborg CW; Egerod KL; Engelholm LH; Laerum OD; Lund LR; Rono B. 2012. Plasmin-driven fibrinolysis facilitates skin tumor growth in a gender-dependent manner. FASEB J 26(11):4445-57. [PubMed: 22815383]  [MGI Ref ID J:192390]

Heissig B; Lund LR; Akiyama H; Ohki M; Morita Y; Romer J; Nakauchi H; Okumura K; Ogawa H; Werb Z; Dano K; Hattori K. 2007. The plasminogen fibrinolytic pathway is required for hematopoietic regeneration. Cell Stem Cell 1(6):658-70. [PubMed: 18371407]  [MGI Ref ID J:149807]

Ishihara M; Nishida C; Tashiro Y; Gritli I; Rosenkvist J; Koizumi M; Okaji Y; Yamamoto R; Yagita H; Okumura K; Nishikori M; Wanaka K; Tsuda Y; Okada Y; Nakauchi H; Heissig B; Hattori K. 2012. Plasmin inhibitor reduces T-cell lymphoid tumor growth by suppressing matrix metalloproteinase-9-dependent CD11b(+)/F4/80(+) myeloid cell recruitment. Leukemia 26(2):332-9. [PubMed: 21931322]  [MGI Ref ID J:181056]

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]

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]

List K; Jensen ON; Bugge TH; Lund LR; Ploug M; Dano K; Behrendt N. 2000. Plasminogen-independent initiation of the pro-urokinase activation cascade in vivo. Activation of pro-urokinase by glandular kallikrein (mGK-6) in plasminogen-deficient mice. Biochemistry 39(3):508-15. [PubMed: 10642175]  [MGI Ref ID J:60142]

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]

Lou XJ; Boonmark NW; Horrigan FT; Degen JL; Lawn RM. 1998. Fibrinogen deficiency reduces vascular accumulation of apolipoprotein(a) and development of atherosclerosis in apolipoprotein(a) transgenic mice. Proc Natl Acad Sci U S A 95(21):12591-5. [PubMed: 9770530]  [MGI Ref ID J:108651]

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]

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]

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):3650-5. [PubMed: 14988509]  [MGI Ref ID J:88913]

Ohki M; Ohki Y; Ishihara M; Nishida C; Tashiro Y; Akiyama H; Komiyama H; Lund LR; Nitta A; Yamada K; Zhu Z; Ogawa H; Yagita H; Okumura K; Nakauchi H; Werb Z; Heissig B; Hattori K. 2010. Tissue type plasminogen activator regulates myeloid-cell dependent neoangiogenesis during tissue regeneration. Blood 115(21):4302-12. [PubMed: 20110420]  [MGI Ref ID J:160268]

Okaji Y; Tashiro Y; Gritli I; Nishida C; Sato A; Ueno Y; Del Canto Gonzalez S; Ohki-Koizumi M; Akiyama H; Nakauchi H; Hattori K; Heissig B. 2012. Plasminogen deficiency attenuates postnatal erythropoiesis in male C57BL/6 mice through decreased activity of the LH-testosterone axis. Exp Hematol 40(2):143-54. [PubMed: 22056679]  [MGI Ref ID J:191393]

Otsuka G; Stempien-Otero A; Frutkin AD; Dichek DA. 2007. Mechanisms of TGF-beta1-induced intimal growth: plasminogen-independent activities of plasminogen activator inhibitor-1 and heterogeneous origin of intimal cells. Circ Res 100(9):1300-7. [PubMed: 17431190]  [MGI Ref ID J:137777]

Pang PT; Teng HK; Zaitsev E; Woo NT; Sakata K; Zhen S; Teng KK; Yung WH; Hempstead BL; Lu B. 2004. Cleavage of proBDNF by tPA/plasmin is essential for long-term hippocampal plasticity. Science 306(5695):487-91. [PubMed: 15486301]  [MGI Ref ID J:105428]

Passino MA; Adams RA; Sikorski SL; Akassoglou K. 2007. Regulation of hepatic stellate cell differentiation by the neurotrophin receptor p75NTR. Science 315(5820):1853-6. [PubMed: 17395831]  [MGI Ref ID J:120368]

Paul J; Strickland S; Melchor JP. 2007. Fibrin deposition accelerates neurovascular damage and neuroinflammation in mouse models of Alzheimer's disease. J Exp Med 204(8):1999-2008. [PubMed: 17664291]  [MGI Ref ID J:125949]

Pawlak R; Melchor JP; Matys T; Skrzypiec AE; Strickland S. 2005. Ethanol-withdrawal seizures are controlled by tissue plasminogen activator via modulation of NR2B-containing NMDA receptors. Proc Natl Acad Sci U S A 102(2):443-8. [PubMed: 15630096]  [MGI Ref ID J:96253]

Pawlak R; Rao BS; Melchor JP; Chattarji S; McEwen B; Strickland S. 2005. Tissue plasminogen activator and plasminogen mediate stress-induced decline of neuronal and cognitive functions in the mouse hippocampus. Proc Natl Acad Sci U S A 102(50):18201-6. [PubMed: 16330749]  [MGI Ref ID J:104368]

Pohl JF; Melin-Aldana H; Sabla G; Degen JL; Bezerra JA. 2001. Plasminogen deficiency leads to impaired lobular reorganization and matrix accumulation after chronic liver injury. Am J Pathol 159(6):2179-86. [PubMed: 11733368]  [MGI Ref ID J:108256]

Renckens R; Roelofs JJ; Florquin S; de Vos AF; Pater JM; Lijnen HR; Carmeliet P; van 't Veer C; van der Poll T. 2006. Endogenous tissue-type plasminogen activator is protective during Escherichia coli-induced abdominal sepsis in mice. J Immunol 177(2):1189-96. [PubMed: 16818777]  [MGI Ref ID J:134991]

Romer J; Bugge TH; Pyke C; Lund LR; Flick MJ; Degen JL; Dano K. 1996. Impaired wound healing in mice with a disrupted plasminogen gene [see comments] Nat Med 2(3):287-92. [PubMed: 8612226]  [MGI Ref ID J:33897]

Rono B; Engelholm LH; Lund LR; Hald A. 2013. Gender affects skin wound healing in plasminogen deficient mice. PLoS One 8(3):e59942. [PubMed: 23527289]  [MGI Ref ID J:199378]

Roszell NJ; Danton MJ; Jiang M; Witte D; Daugherty C; Grimes T; Girdler B; Anderson KP; Franco RS; Degen JL; Joiner CH. 2007. Fibrinogen deficiency, but not plasminogen deficiency, increases mortality synergistically in combination with sickle hemoglobin SAD in transgenic mice. Am J Hematol 82(12):1044-8. [PubMed: 17722076]  [MGI Ref ID J:146393]

Samara GJ; Schaffner AD; Eisenstat J; Nguyen HL. 2004. The effects of the plasminogen pathway on scar tissue formation. Laryngoscope 114(1):46-9. [PubMed: 14709993]  [MGI Ref ID J:105270]

Samson AL; Knaupp AS; Sashindranath M; Borg RJ; Au AE; Cops EJ; Saunders HM; Cody SH; McLean CA; Nowell CJ; Hughes VA; Bottomley SP; Medcalf RL. 2012. Nucleocytoplasmic coagulation: an injury-induced aggregation event that disulfide crosslinks proteins and facilitates their removal by plasmin. Cell Rep 2(4):889-901. [PubMed: 23041318]  [MGI Ref ID J:196219]

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]

Shanmukhappa K; Mourya R; Sabla GE; Degen JL; Bezerra JA. 2005. Hepatic to pancreatic switch defines a role for hemostatic factors in cellular plasticity in mice. Proc Natl Acad Sci U S A 102(29):10182-7. [PubMed: 16006527]  [MGI Ref ID J:100196]

Sheehan JJ; Zhou C; Gravanis I; Rogove AD; Wu YP; Bogenhagen DF; Tsirka SE. 2007. Proteolytic activation of monocyte chemoattractant protein-1 by plasmin underlies excitotoxic neurodegeneration in mice. J Neurosci 27(7):1738-45. [PubMed: 17301181]  [MGI Ref ID J:141739]

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]

Stempien-Otero A; Plawman A; Meznarich J; Dyamenahalli T; Otsuka G; Dichek DA. 2006. Mechanisms of cardiac fibrosis induced by urokinase plasminogen activator. J Biol Chem 281(22):15345-51. [PubMed: 16554301]  [MGI Ref ID J:113474]

Tsirka SE; Bugge TH; Degen JL; Strickland S. 1997. Neuronal death in the central nervous system demonstrates a non-fibrin substrate for plasmin. Proc Natl Acad Sci U S A 94(18):9779-81. [PubMed: 9275201]  [MGI Ref ID J:42819]

Tsirka SE; Rogove AD; Bugge TH; Degen JL; Strickland S. 1997. An extracellular proteolytic cascade promotes neuronal degeneration in the mouse hippocampus. J Neurosci 17(2):543-52. [PubMed: 8987777]  [MGI Ref ID J:37549]

Tucker HM; Simpson J; Kihiko-Ehmann M; Younkin LH; McGillis JP; Younkin SG; Degen JL; Estus S. 2004. Plasmin deficiency does not alter endogenous murine amyloid beta levels in mice. Neurosci Lett 368(3):285-9. [PubMed: 15364412]  [MGI Ref ID J:120020]

Xiao Q; Danton MJ; Witte DP; Kowala MC; Valentine MT; Bugge TH ; Degen JL. 1997. Plasminogen deficiency accelerates vessel wall disease in mice predisposed to atherosclerosis. Proc Natl Acad Sci U S A 94(19):10335-40. [PubMed: 9294211]  [MGI Ref ID J:42927]

Yepes M; Sandkvist M; Coleman TA; Moore E; Wu JY; Mitola D; Bugge TH; Lawrence DA. 2002. Regulation of seizure spreading by neuroserpin and tissue-type plasminogen activator is plasminogen-independent. J Clin Invest 109(12):1571-8. [PubMed: 12070304]  [MGI Ref ID J:120679]

Zhang C; An J; Strickland DK; Yepes M. 2009. The low-density lipoprotein receptor-related protein 1 mediates tissue-type plasminogen activator-induced microglial activation in the ischemic brain. Am J Pathol 174(2):586-94. [PubMed: 19147818]  [MGI Ref ID J:144185]

Zhang G; Kernan KA; Collins SJ; Cai X; Lopez-Guisa JM; Degen JL; Shvil Y; Eddy AA. 2007. Plasmin(ogen) promotes renal interstitial fibrosis by promoting epithelial-to-mesenchymal transition: role of plasmin-activated signals. J Am Soc Nephrol 18(3):846-59. [PubMed: 17267741]  [MGI Ref ID J:150559]

Zhang X; Polavarapu R; She H; Mao Z; Yepes M. 2007. Tissue-type plasminogen activator and the low-density lipoprotein receptor-related protein mediate cerebral ischemia-induced nuclear factor-kappaB pathway activation. Am J Pathol 171(4):1281-90. [PubMed: 17717150]  [MGI Ref ID J:125519]

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* $2525.00
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 $1650.00

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 10 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* $3283.00
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 $2145.00

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 10 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
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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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.


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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.
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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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