Strain Name:

B6.129P2-Plgtm1Jld/J

Stock Number:

002830

Availability:

Repository-Cryopreserved

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.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Specieslaboratory mouse
Background Strain C57BL/6J
Donor Strain 129P2 via E14TG2a ES cell line
GenerationN10F13N1p
 
Donating Investigator Thomas Bugge,  

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

Additional Web Information

Congenic Nomenclature

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms
Plasminogen Deficiency, Type I - Models with phenotypic similarity to human disease where etiologies involve orthologs.1
1 Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
View Mammalian Phenotype Terms

Mammalian Phenotype Terms
      assigned by genotype

Plgtm1Jld/Plgtm1Jld

        B6.129P2-Plgtm1Jld
  • life span-post-weaning/aging
  • abnormal induced morbidity/mortality (MGI Ref ID J:44314)
    • show a moderate increase in survival after primary tumor resection at day 10
  • premature death (MGI Ref ID J:120368)
    • median survival is 6 months
  • reproductive system phenotype
  • abnormal lactation (MGI Ref ID J:64966)
    • 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
  • reduced female fertility (MGI Ref ID J:64966)
    • exhibit more severe infertility than on a mixed 129P2/OlaHsd, Black Swiss, and C57BL/6J background, with fewer than 50% of females becoming pregnant
    • second pregnancies are rare
  • vision/eye phenotype
  • abnormal conjunctiva morphology (MGI Ref ID J:46096)
    • abnormal conjunctival epithelium (MGI Ref ID J:46096)
      • 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
    • conjunctivitis (MGI Ref ID J:46096)
      • 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
      • incidence of lesion development increases with age and lesions develop into extensive, pedunculated plaques over time
      • 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
      • acute inflammatory infiltrates with a predominance of neutrophils frequently accompany conjunctival lesions and occasionally see CD4+ and CD8+ lymphocytes in the infiltrates
  • abnormal cornea morphology (MGI Ref ID J:46096)
    • 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
    • form extensive fibrin rich plaques overlying the cornea, with associated epithelium ulceration, hypertrophy, and disorganization
    • abnormal corneal epithelium morphology (MGI Ref ID J:46096)
      • corneal epithelium is frequently absent, necrotic, or hypertrophied
    • abnormal corneal stroma morphology (MGI Ref ID J:46096)
      • ulceration or destruction of the stroma with extensive protruding plaques are seen overlying the cornea
    • corneal vascularization (MGI Ref ID J:46096)
      • stromal vascularization is frequently associated with corneal lesions
  • ectropion (MGI Ref ID J:46096)
    • palpebral conjunctival alterations result in hypertrophied, everted eyelids with ulceration and hemorrhage
  • eye inflammation (MGI Ref ID J:46096)
    • formation of papillary or a retrocorneal membrane is seen in several mutants, consistent with chronic intraocular inflammation
    • conjunctivitis (MGI Ref ID J:46096)
      • 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
      • incidence of lesion development increases with age and lesions develop into extensive, pedunculated plaques over time
      • 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
      • acute inflammatory infiltrates with a predominance of neutrophils frequently accompany conjunctival lesions and occasionally see CD4+ and CD8+ lymphocytes in the infiltrates
  • tumorigenesis
  • decreased tumor growth/size (MGI Ref ID J:44314)
    • 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
  • digestive/alimentary phenotype
  • abnormal rectum morphology (MGI Ref ID J:46096)
    • 71% developed rectal lesions
  • cardiovascular system phenotype
  • eye hemorrhage (MGI Ref ID J:46096)
    • palpebral conjunctival alterations result in hypertrophied, everted eyelids with ulceration and hemorrhage
  • liver/biliary system phenotype
  • abnormal hepatocyte morphology (MGI Ref ID J:120368)
    • the number of proliferating hepatocyte is increased (126.6+/-3.9 compare to 95.2+/-3.7 in wild-type mice)
  • endocrine/exocrine gland phenotype
  • abnormal lactation (MGI Ref ID J:64966)
    • 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
  • growth/size phenotype
  • decreased body weight (MGI Ref ID J:46096)
    • weight at 60 days of age is lower
  • immune system phenotype
  • eye inflammation (MGI Ref ID J:46096)
    • formation of papillary or a retrocorneal membrane is seen in several mutants, consistent with chronic intraocular inflammation
    • conjunctivitis (MGI Ref ID J:46096)
      • 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
      • incidence of lesion development increases with age and lesions develop into extensive, pedunculated plaques over time
      • 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
      • acute inflammatory infiltrates with a predominance of neutrophils frequently accompany conjunctival lesions and occasionally see CD4+ and CD8+ lymphocytes in the infiltrates

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Plgtm1Jld/Plg+

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

Plgtm1Jld/Plgtm1Jld

        involves: 129P2/OlaHsd * NIH Black Swiss
  • homeostasis/metabolism phenotype
  • impaired wound healing (MGI Ref ID J:33897)
    • 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
    • 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
    • keratinocyte migration is impaired in skin wound healing experiments
  • thrombosis (MGI Ref ID J:39419)
    • young mutants develop multiple spontaneous thrombotic lesions in liver, stomach, colon, rectum, lung, pancreas, and other tissues
  • digestive/alimentary phenotype
  • abnormal colon morphology (MGI Ref ID J:39419)
    • 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
  • abnormal stomach morphology (MGI Ref ID J:39419)
    • gastric ulcer (MGI Ref ID J:39419)
      • 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
  • large intestinal inflammation (MGI Ref ID J:39419)
    • 7 of 43 develop inflammatory rectal lesions between 5 and 21 weeks of age
  • perianal ulceration (MGI Ref ID J:39419)
    • exhibit anal-rectal tissue ulceration with surface exudates and surrounding fibrin deposition
  • rectal prolapse (MGI Ref ID J:39419)
    • oldest of the mice that show inflammatory rectal lesions exhibit rectal prolapse
  • immune system phenotype
  • large intestinal inflammation (MGI Ref ID J:39419)
    • 7 of 43 develop inflammatory rectal lesions between 5 and 21 weeks of age
  • liver/biliary system phenotype
  • abnormal liver morphology (MGI Ref ID J:39419)
    • exhibit multiple hepatic fibrin deposits identified as fibrinogen that show varying degrees of organization with infiltration of spindle cells
    • hepatic necrosis (MGI Ref ID J:39419)
      • necrosis is apparent within adjacent tissue in a fraction of hepatic lesions
  • respiratory system phenotype
  • abnormal lung morphology (MGI Ref ID J:39419)
    • 7 of 17 show pulmonary lesions, with capillary fibrin thrombi in 4 mutants and organizing patches of alveolar fibrin in 4 mutants
  • cardiovascular system phenotype
  • venoocclusion (MGI Ref ID J:39419)
    • young mutants exhibit vascular occlusions

Plgtm1Jld/Plgtm1Jld

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

Plgtm1Jld/Plgtm1Jld

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

Plgtm1Jld/Plgtm1Jld

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

Plgtm1Jld/Plgtm1Jld

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

Plgtm1Jld/Plgtm1Jld

        involves: 129P2/OlaHsd * Black Swiss * C57BL/6J
  • reproductive system phenotype
  • abnormal lactation (MGI Ref ID J:64966)
    • 28% of females are unable to sustain lactation for 10 days, a much lower percentage than on a congenic C57BL/6J background
    • lactation failure is more severe after a second pregnancy, with only 1 of 8 litters surviving
  • abnormal mammary gland morphology (MGI Ref ID J:64966)
    • exhibit abnormal stromal extracellular matrix (ECM), with increased collagen deposition and absence of ECM degradation
    • abnormal mammary gland development (MGI Ref ID J:64966)
      • mammary glands are underdeveloped
      • 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
      • abnormal involution of the mammary gland (MGI Ref ID J:64966)
        • glands from lactating females are initially smaller and fail to involute after weaning
        • 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
        • show decreased apoptosis in mammary glands at 5 days of involution, indicating delayed, but not completely blocked, alveolar regression
      • abnormal mammary gland growth during lactation (MGI Ref ID J:64966)
        • 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
        • 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
        • exhibit an accumulation of activated macrophages in the stroma of lactating mammary glands
  • reduced female fertility (MGI Ref ID J:64966)
    • 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
    • second pregnancies are rare
  • endocrine/exocrine gland phenotype
  • abnormal lactation (MGI Ref ID J:64966)
    • 28% of females are unable to sustain lactation for 10 days, a much lower percentage than on a congenic C57BL/6J background
    • lactation failure is more severe after a second pregnancy, with only 1 of 8 litters surviving
  • abnormal mammary gland morphology (MGI Ref ID J:64966)
    • exhibit abnormal stromal extracellular matrix (ECM), with increased collagen deposition and absence of ECM degradation
    • abnormal mammary gland development (MGI Ref ID J:64966)
      • mammary glands are underdeveloped
      • 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
      • abnormal involution of the mammary gland (MGI Ref ID J:64966)
        • glands from lactating females are initially smaller and fail to involute after weaning
        • 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
        • show decreased apoptosis in mammary glands at 5 days of involution, indicating delayed, but not completely blocked, alveolar regression
      • abnormal mammary gland growth during lactation (MGI Ref ID J:64966)
        • 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
        • 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
        • exhibit an accumulation of activated macrophages in the stroma of lactating mammary glands
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

 
Allele Symbol Plgtm1Jld
Allele Name targeted mutation 1, Jay L Degen
Allele Type Targeted (knock-out)
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; DKFZp779M0222; 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, STD PCR, vers. 1

Helpful Links

Optimizing PCR Protocols

References

References

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 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]

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]

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]

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]

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]

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]

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 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

Colony Maintenance

Diet Information LabDiet® 5K52/5K67

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Pricing for USA, Canada and Mexico shipping destinations View International pricing
Price (US dollars $)
Cryorecovery Fee $1900.00
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.

Additional Supply Details

Pricing for International shipping destinations View USA Canada and Mexico pricing
Price (US dollars $)
Cryorecovery Fee $2470.00
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.

Additional Supply Details

Supply Details

Standard SupplyCryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
Supply Notes
  • Cryorecovery - Standard.
    At least two mice that carry the mutation (if it is a mutant strain) will be provided. The total number of animals provided, their gender and genotype will vary. Please inquire if larger numbers of animals with specific genotypes and genders are needed. IMPORTANT NOTE: The genotypes of the 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 for possible genotypes for this specific strain. Animals typically ship within 13 to 16 weeks from your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will typically ship within 25 weeks.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice.
    One to two pairs will be recovered to establish a Dedicated Supply of mice. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 or 1-207-288-5845.

  • This strain is included in the Induced Mutant Resource Colony collection.
  • Genomic DNA is available for this strain from the Mouse DNA Resource.

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains.
  International - Control Pricing Information for Genetically Engineered Mutant Strains.

General Terms and Conditions


See Terms of Use


The Jackson Laboratory's Genotype Promise

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

      Purchasing Information
      JAX® Mice Orders
      Surgical Services

Contact Information
Orders & Technical Support
Tel: 800.422.6423 or 207.288.5845
Fax: 207.288.6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries

Contracts Administration

phone:207-288-6470
fax:207-288-6655

JAX® Mice & Services Conditions of Use

“Each recipient institution, including its employees and other researchers under its control (RECIPIENT), of mice or services using mice from The Jackson Laboratory (TJL) agrees that such mice, descendants of those mice derived by inbreeding or crossbreeding, including unmodified derivatives of those mice or their descendants (“MICE”) shall not be: (i) used for any purpose other than the internal research of the RECIPIENT, (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 with respect to MICE. Acceptance of MICE from TJL shall be deemed agreement by RECIPIENT to these conditions, and departure from these conditions requires The Jackson Laboratory’s prior written authorization.”

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. THE LABORATORY 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, The Jackson Laboratory will, at its option, provide credit or replacement for the MICE or product received or the services provided.

No Liability

In no event shall The Jackson Laboratory, 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 The Jackson Laboratory, its agents or employees. In purchasing or receiving MICE, products or services from The Jackson Laboratory, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges The Jackson Laboratory from all such causes of action or damages, and further agrees to defend and indemnify The Jackson Laboratory from any costs or damages arising out of any third party claims.

MICE and biological materials 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 The Jackson Laboratory’s MICE, products and services. In addition, special terms and conditions of sale of certain MICE, products and services may be set forth separately in The Jackson Laboratory 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 The Jackson Laboratory, 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 The Jackson Laboratory, 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 services by The Jackson Laboratory.


(3.4)