Strain Name:

B6.129S4-F2rtm1Ajc/J

Stock Number:

002862

Order this mouse

Availability:

Cryopreserved - Ready for recovery

Other products are available, see Purchasing Information for Cryopreserved Embryos

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 129S4 via RF8 ES cell line
 
Donating InvestigatorDr. Shaun Coughlin,   U. of California at San Francisco

Appearance
black
Related Genotype: a/a

Description
About half of the homozygous mice die at around embryonic day 9-10. The surviving homozygotes are fertile. Platelets from surviving homozygotes respond to thrombin while fibroblasts from the same mice are unable to respond to thrombin.

Control Information

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

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

F2rtm1Ajc/F2rtm1Ajc

        involves: 129S4/SvJae * C57BL/6J
  • mortality/aging
  • partial embryonic lethality during organogenesis
    • about 50% of homozygotes die between E9.0-10.0   (MGI Ref ID J:33380)
  • embryogenesis phenotype
  • abnormal placenta development
    • at E9.0-E9.5, homozygotes display a delay in placental development   (MGI Ref ID J:33380)
  • decreased embryo size
    • starting at E9.0, mutant embryos become uniformly smaller than wild-type embryos   (MGI Ref ID J:33380)
  • embryonic growth retardation
    • at E9.0-E9.5, homozygotes display a global developmental delay   (MGI Ref ID J:33380)
    • however, those that survive past E9.0-E10.0 catch up with control embryos by E11.5 and develop normally to birth   (MGI Ref ID J:33380)
  • cardiovascular system phenotype
  • absent heartbeat
    • by E9.5, approximately half of the mutant embryos display no heart beat   (MGI Ref ID J:33380)
    • however, E8.5 mutant embryos have beating hearts and a functional vitelline circulation   (MGI Ref ID J:33380)
  • cellular phenotype
  • abnormal cell physiology
    • in contrast to platelets, fibroblasts derived from E12.0 mutant embryos or adult lung fail to exhibit thrombin-induced phopshoinositide hydrolysis and calcium mobilization   (MGI Ref ID J:33380)
  • growth/size/body phenotype
  • decreased embryo size
    • starting at E9.0, mutant embryos become uniformly smaller than wild-type embryos   (MGI Ref ID J:33380)
  • embryonic growth retardation
    • at E9.0-E9.5, homozygotes display a global developmental delay   (MGI Ref ID J:33380)
    • however, those that survive past E9.0-E10.0 catch up with control embryos by E11.5 and develop normally to birth   (MGI Ref ID J:33380)
  • hematopoietic system phenotype
  • *normal* hematopoietic system phenotype
    • surviving homozygotes display normal tail bleeding times and no bleeding diathesis relative to wild-type   (MGI Ref ID J:33380)
    • in addition, mutant platelets display strong thrombin-induced responses   (MGI Ref ID J:33380)

F2rtm1Ajc/F2rtm1Ajc

        B6.129S4-F2rtm1Ajc
  • mortality/aging
  • partial embryonic lethality during organogenesis
    • by E12.5, 52% of mutant embryos are dead with extensive bleeding; the remaining embryos survive to adulthood and appear grossly normal   (MGI Ref ID J:71309)
  • tumorigenesis
  • *normal* tumorigenesis
    • when injected with B16-F10 melanoma cells via tail vein, homozygotes show no differences in hematogenous metastasis (tumor count or burden) relative to wild-type mice, indicating no protection against metastasis in this model   (MGI Ref ID J:92278)
  • cardiovascular system phenotype
  • abnormal sinus venosus morphology
    • at E9.5, 2 out of 3 mutant embryos exhibit a defect in the wall of the sinus venosus that is large enough to allow blood cells into the pericardial cavity   (MGI Ref ID J:71309)
  • abnormal vitelline vasculature morphology
    • at E8.75 to E10.5, embryos with gross bleeding are pale and display a disorganized yolk sac vasculature or delayed remodeling   (MGI Ref ID J:71309)
    • absent vitelline blood vessels
      • at E12.5, mutant yolk sacs lack blood-filled vessels   (MGI Ref ID J:71309)
  • distended pericardium
    • at E9.5, hemorrhagic embryos often display a dilated pericardial sac, indicating cardiovascular failure   (MGI Ref ID J:71309)
    • at this stage, 4 out of 19 mutant embryos with microscopic bleeding display normal pericardial sacs   (MGI Ref ID J:71309)
  • hemorrhage
    • by E9.5, ~66% of mutant embryos display microscopic bleeding in the pericardial and/or peritoneal, amniotic, and/or exocoelomic cavity   (MGI Ref ID J:71309)
    • live E9.5 to E10.5 embryos with both gross bleeding and vigorous heart beats are occasionally observed   (MGI Ref ID J:71309)
    • hemopericardium
      • at E9.5, 22% of mutant embryos exhibit hemorrhage in the exocoelomic and/or pericardial cavities   (MGI Ref ID J:71309)
  • cellular phenotype
  • abnormal cell physiology
    • relative to wild-type, mutant endothelial cells display a 20-30% reduction in F10 (coagulation protease factor Xa)-triggered phosphoinositide hydrolysis   (MGI Ref ID J:76348)
    • a similar reduction is observed when ERK1/2 phosphorylation is used to assess F10 signaling   (MGI Ref ID J:76348)
    • in contrast, mutant lung fibroblasts exhibit a complete absence of F10-induced phosphoinositide hydrolysis   (MGI Ref ID J:76348)
    • abnormal neuron apoptosis
      • cortical neurons from mutant fetuses exhibit a complete loss of activated protein C (APC)-mediated neuronal protection against NMDA-induced apoptosis   (MGI Ref ID J:89774)
  • embryogenesis phenotype
  • abnormal vitelline vasculature morphology
    • at E8.75 to E10.5, embryos with gross bleeding are pale and display a disorganized yolk sac vasculature or delayed remodeling   (MGI Ref ID J:71309)
    • absent vitelline blood vessels
      • at E12.5, mutant yolk sacs lack blood-filled vessels   (MGI Ref ID J:71309)
  • embryonic growth retardation
    • at E9.5, mutant embryos show a variable developmental delay but no gross vascular anomalies   (MGI Ref ID J:71309)
  • growth/size/body phenotype
  • embryonic growth retardation
    • at E9.5, mutant embryos show a variable developmental delay but no gross vascular anomalies   (MGI Ref ID J:71309)
  • nervous system phenotype
  • abnormal neuron apoptosis
    • cortical neurons from mutant fetuses exhibit a complete loss of activated protein C (APC)-mediated neuronal protection against NMDA-induced apoptosis   (MGI Ref ID J:89774)
  • homeostasis/metabolism phenotype
  • hemopericardium
    • at E9.5, 22% of mutant embryos exhibit hemorrhage in the exocoelomic and/or pericardial cavities   (MGI Ref ID J:71309)

F2rtm1Ajc/F2rtm1Ajc

        involves: 129S4/SvJae * C57BL/6
  • liver/biliary system phenotype
  • abnormal gallbladder physiology
    • the gallbladder fails to exhibit a normal short-circuit current response when stimulated with TFLLRN-NH2 and thrombin   (MGI Ref ID J:123689)
    • however, the short-circuit response to SLIGRL-NH2 and trypsin is normal   (MGI Ref ID J:123689)
  • immune system phenotype
  • *normal* immune system phenotype
    • mice exhibit a normal response to endotoxin treatment   (MGI Ref ID J:132733)

F2rtm1Ajc/F2rtm1Ajc

        involves: 129S4/SvJae
  • mortality/aging
  • partial embryonic lethality during organogenesis
    • ~50% of homozygotes die between E9.0-10.0   (MGI Ref ID J:33380)
  • limbs/digits/tail phenotype
  • curly tail
View Research Applications

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

F2rtm1Ajc related

Developmental Biology Research
Embryonic Lethality (Homozygous)
      incomplete

Hematological Research
Platelet Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol F2rtm1Ajc
Allele Name targeted mutation 1, Andrew J Connolly
Allele Type Targeted (Null/Knockout)
Common Name(s) PAR-1-; Par1-; Par1-; tr-;
Mutation Made ByDr. Andrew Connolly,   Palo Alto Medical Foundation
Strain of Origin129S4/SvJae
ES Cell Line NameRF8
ES Cell Line Strain129S4/SvJae
Gene Symbol and Name F2r, coagulation factor II (thrombin) receptor
Chromosome 13
Gene Common Name(s) AI482343; CF2R; Cf2r; HTR; PAR-1; PAR1; TR; TRGPC; ThrR; coagulation factor II, receptor; expressed sequence AI482343; thrombin receptor;
Molecular Note A neomycin resistance cassette replaced sequences in exon 2 encoding transmembrane domains 1-7. Northern blot analysis on RNA derived from E12 embryos and from embryonic fibroblasts demonstrated that no detectable transcript was produced from this allele. Furthermore, transcripts from this allele were not detected in various tissues of adult homozygous mice (data not shown). [MGI Ref ID J:33380]

Genotyping

Genotyping Information

Genotyping Protocols

F2rtm1Ajc, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Connolly AJ; Ishihara H; Kahn ML; Farese RV Jr; Coughlin SR. 1996. Role of the thrombin receptor in development and evidence for a second receptor. Nature 381(6582):516-9. [PubMed: 8632823]  [MGI Ref ID J:33380]

Additional References

Trejo J; Connolly AJ; Coughlin SR. 1996. The cloned thrombin receptor is necessary and sufficient for activation of mitogen-activated protein kinase and mitogenesis in mouse lung fibroblasts. Loss of responses in fibroblasts from receptor knockout mice. J Biol Chem 271(35):21536-41. [PubMed: 8702939]  [MGI Ref ID J:35136]

F2rtm1Ajc related

Almonte AG; Hamill CE; Chhatwal JP; Wingo TS; Barber JA; Lyuboslavsky PN; David Sweatt J; Ressler KJ; White DA; Traynelis SF. 2007. Learning and memory deficits in mice lacking protease activated receptor-1. Neurobiol Learn Mem 88(3):295-304. [PubMed: 17544303]  [MGI Ref ID J:128855]

Aronovich A; Nur Y; Shezen E; Rosen C; Zlotnikov Klionsky Y; Milman I; Yarimi L; Hagin D; Rechavi G; Martinowitz U; Nagasawa T; Frenette PS; Tchorsh-Yutsis D; Reisner Y. 2013. A novel role for factor VIII and thrombin/PAR1 in regulating hematopoiesis and its interplay with the bone structure. Blood 122(15):2562-71. [PubMed: 23982175]  [MGI Ref ID J:203434]

Burda JE; Radulovic M; Yoon H; Scarisbrick IA. 2013. Critical role for PAR1 in kallikrein 6-mediated oligodendrogliopathy. Glia 61(9):1456-70. [PubMed: 23832758]  [MGI Ref ID J:199448]

Camerer E; Cornelissen I; Kataoka H; Duong DN; Zheng YW; Coughlin SR. 2006. Roles of protease-activated receptors in a mouse model of endotoxemia. Blood 107(10):3912-21. [PubMed: 16434493]  [MGI Ref ID J:132733]

Camerer E; Kataoka H; Kahn M; Lease K; Coughlin SR. 2002. Genetic Evidence That Protease-activated Receptors Mediate Factor Xa Signaling in Endothelial Cells. J Biol Chem 277(18):16081-7. [PubMed: 11850418]  [MGI Ref ID J:76348]

Camerer E; Qazi AA; Duong DN; Cornelissen I; Advincula R; Coughlin SR. 2004. Platelets, protease-activated receptors, and fibrinogen in hematogenous metastasis. Blood 104(2):397-401. [PubMed: 15031212]  [MGI Ref ID J:92278]

Chen D; Shrivastava S; Ma L; Tham el-L; Abrahams J; Coe JD; Scott D; Lechler RI; McVey JH; Dorling A. 2012. Inhibition of thrombin receptor signaling on alpha-smooth muscle actin(+) CD34(+) progenitors leads to repair after murine immune vascular injury. Arterioscler Thromb Vasc Biol 32(1):42-9. [PubMed: 22034512]  [MGI Ref ID J:195975]

Connolly AJ; Suh DY; Hunt TK; Coughlin SR. 1997. Mice lacking the thrombin receptor, PAR1, have normal skin wound healing. Am J Pathol 151(5):1199-204. [PubMed: 9358744]  [MGI Ref ID J:43850]

Cunningham MA; Rondeau E; Chen X; Coughlin SR; Holdsworth SR; Tipping PG. 2000. Protease-activated receptor 1 mediates thrombin-dependent, cell-mediated renal inflammation in crescentic glomerulonephritis. J Exp Med 191(3):455-62. [PubMed: 10662791]  [MGI Ref ID J:60282]

Friedmann I; Hauben E; Yoles E; Kardash L; Schwartz M. 2001. T cell-mediated neuroprotection involves antithrombin activity. J Neuroimmunol 121(1-2):12-21. [PubMed: 11730935]  [MGI Ref ID J:102962]

Fukakusa A; Nagai T; Mizoguchi H; Otsuka N; Kimura H; Kamei H; Kim HC; Nabeshima T; Takuma K; Yamada K. 2008. Role of tissue plasminogen activator in the sensitization of methamphetamine-induced dopamine release in the nucleus accumbens. J Neurochem 105(2):436-44. [PubMed: 18036193]  [MGI Ref ID J:135451]

Griffin CT; Srinivasan Y; Zheng YW; Huang W; Coughlin SR. 2001. A role for thrombin receptor signaling in endothelial cells during embryonic development. Science 293(5535):1666-70. [PubMed: 11533492]  [MGI Ref ID J:71309]

Guo H; Liu D; Gelbard H; Cheng T; Insalaco R; Fernandez JA; Griffin JH; Zlokovic BV. 2004. Activated protein C prevents neuronal apoptosis via protease activated receptors 1 and 3. Neuron 41(4):563-72. [PubMed: 14980205]  [MGI Ref ID J:89774]

Hamilton JR; Cornelissen I; Coughlin SR. 2004. Impaired hemostasis and protection against thrombosis in protease-activated receptor 4-deficient mice is due to lack of thrombin signaling in platelets. J Thromb Haemost 2(8):1429-35. [PubMed: 15304051]  [MGI Ref ID J:102309]

Hirano K. 2007. The roles of proteinase-activated receptors in the vascular physiology and pathophysiology. Arterioscler Thromb Vasc Biol 27(1):27-36. [PubMed: 17095716]  [MGI Ref ID J:135066]

Howell DC; Johns RH; Lasky JA; Shan B; Scotton CJ; Laurent GJ; Chambers RC. 2005. Absence of proteinase-activated receptor-1 signaling affords protection from bleomycin-induced lung inflammation and fibrosis. Am J Pathol 166(5):1353-65. [PubMed: 15855637]  [MGI Ref ID J:98466]

Jenkins RG; Su X; Su G; Scotton CJ; Camerer E; Laurent GJ; Davis GE; Chambers RC; Matthay MA; Sheppard D. 2006. Ligation of protease-activated receptor 1 enhances alpha(v)beta6 integrin-dependent TGF-beta activation and promotes acute lung injury. J Clin Invest 116(6):1606-14. [PubMed: 16710477]  [MGI Ref ID J:110369]

Junge CE; Sugawara T; Mannaioni G; Alagarsamy S; Conn PJ; Brat DJ; Chan PH; Traynelis SF. 2003. The contribution of protease-activated receptor 1 to neuronal damage caused by transient focal cerebral ischemia. Proc Natl Acad Sci U S A 100(22):13019-24. [PubMed: 14559973]  [MGI Ref ID J:99736]

Kallis YN; Scotton CJ; Mackinnon AC; Goldin RD; Wright NA; Iredale JP; Chambers RC; Forbes SJ. 2014. Proteinase activated receptor 1 mediated fibrosis in a mouse model of liver injury: a role for bone marrow derived macrophages. PLoS One 9(1):e86241. [PubMed: 24475094]  [MGI Ref ID J:212718]

Kassel KM; Owens AP 3rd; Rockwell CE; Sullivan BP; Wang R; Tawfik O; Li G; Guo GL; Mackman N; Luyendyk JP. 2011. Protease-activated receptor 1 and hematopoietic cell tissue factor are required for hepatic steatosis in mice fed a Western diet. Am J Pathol 179(5):2278-89. [PubMed: 21907177]  [MGI Ref ID J:177385]

Kataoka H; Hamilton JR; McKemy DD; Camerer E; Zheng YW; Cheng A; Griffin C; Coughlin SR. 2003. Protease-activated receptors 1 and 4 mediate thrombin signaling in endothelial cells. Blood 102(9):3224-31. [PubMed: 12869501]  [MGI Ref ID J:115683]

Kirkland JG; Cottrell GS; Bunnett NW; Corvera CU. 2007. Agonists of protease-activated receptors 1 and 2 stimulate electrolyte secretion from mouse gallbladder. Am J Physiol Gastrointest Liver Physiol 293(1):G335-46. [PubMed: 17431214]  [MGI Ref ID J:123689]

Luyendyk JP; Sullivan BP; Guo GL; Wang R. 2010. Tissue factor-deficiency and protease activated receptor-1-deficiency reduce inflammation elicited by diet-induced steatohepatitis in mice. Am J Pathol 176(1):177-86. [PubMed: 20008134]  [MGI Ref ID J:156485]

Mannaioni G; Orr AG; Hamill CE; Yuan H; Pedone KH; McCoy KL; Berlinguer Palmini R; Junge CE; Lee CJ; Yepes M; Hepler JR; Traynelis SF. 2008. Plasmin potentiates synaptic N-methyl-D-aspartate receptor function in hippocampal neurons through activation of protease-activated receptor-1. J Biol Chem 283(29):20600-11. [PubMed: 18474593]  [MGI Ref ID J:138749]

Nagai T; Ito M; Nakamichi N; Mizoguchi H; Kamei H; Fukakusa A; Nabeshima T; Takuma K; Yamada K. 2006. The rewards of nicotine: regulation by tissue plasminogen activator-plasmin system through protease activated receptor-1. J Neurosci 26(47):12374-83. [PubMed: 17122062]  [MGI Ref ID J:116177]

Nicole O; Goldshmidt A; Hamill CE; Sorensen SD; Sastre A; Lyuboslavsky P; Hepler JR; McKeon RJ; Traynelis SF. 2005. Activation of protease-activated receptor-1 triggers astrogliosis after brain injury. J Neurosci 25(17):4319-29. [PubMed: 15858058]  [MGI Ref ID J:98744]

Redecha P; Franzke CW; Ruf W; Mackman N; Girardi G. 2008. Neutrophil activation by the tissue factor/Factor VIIa/PAR2 axis mediates fetal death in a mouse model of antiphospholipid syndrome. J Clin Invest 118(10):3453-61. [PubMed: 18802482]  [MGI Ref ID J:142729]

Reinhardt C; Bergentall M; Greiner TU; Schaffner F; Ostergren-Lunden G; Petersen LC; Ruf W; Backhed F. 2012. Tissue factor and PAR1 promote microbiota-induced intestinal vascular remodelling. Nature 483(7391):627-31. [PubMed: 22407318]  [MGI Ref ID J:182579]

Rullier A; Gillibert-Duplantier J; Costet P; Cubel G; Haurie V; Petibois C; Taras D; Dugot-Senant N; Deleris G; Bioulac-Sage P; Rosenbaum J. 2008. Protease-activated receptor 1 knockout reduces experimentally induced liver fibrosis. Am J Physiol Gastrointest Liver Physiol 294(1):G226-35. [PubMed: 17962354]  [MGI Ref ID J:130512]

Sevastos J; Kennedy SE; Davis DR; Sam M; Peake PW; Charlesworth JA; Mackman N; Erlich JH. 2007. Tissue factor deficiency and PAR-1 deficiency are protective against renal ischemia reperfusion injury. Blood 109(2):577-83. [PubMed: 16990608]  [MGI Ref ID J:144005]

Sevigny LM; Austin KM; Zhang P; Kasuda S; Koukos G; Sharifi S; Covic L; Kuliopulos A. 2011. Protease-activated receptor-2 modulates protease-activated receptor-1-driven neointimal hyperplasia. Arterioscler Thromb Vasc Biol 31(12):e100-6. [PubMed: 21940952]  [MGI Ref ID J:191453]

Song SJ; Pagel CN; Campbell TM; Pike RN; Mackie EJ. 2005. The role of protease-activated receptor-1 in bone healing. Am J Pathol 166(3):857-68. [PubMed: 15743797]  [MGI Ref ID J:96779]

Sood R; Sholl L; Isermann B; Zogg M; Coughlin SR; Weiler H. 2008. Maternal Par4 and platelets contribute to defective placenta formation in mouse embryos lacking thrombomodulin. Blood 112(3):585-91. [PubMed: 18490515]  [MGI Ref ID J:138440]

Szabo R; Uzzun Sales K; Kosa P; Shylo NA; Godiksen S; Hansen KK; Friis S; Gutkind JS; Vogel LK; Hummler E; Camerer E; Bugge TH. 2012. Reduced Prostasin (CAP1/PRSS8) Activity Eliminates HAI-1 and HAI-2 Deficiency-Associated Developmental Defects by Preventing Matriptase Activation. PLoS Genet 8(8):e1002937. [PubMed: 22952456]  [MGI Ref ID J:188121]

Trejo J; Connolly AJ; Coughlin SR. 1996. The cloned thrombin receptor is necessary and sufficient for activation of mitogen-activated protein kinase and mitogenesis in mouse lung fibroblasts. Loss of responses in fibroblasts from receptor knockout mice. J Biol Chem 271(35):21536-41. [PubMed: 8702939]  [MGI Ref ID J:35136]

Yang YH; Hall P; Little CB; Fosang AJ; Milenkovski G; Santos L; Xue J; Tipping P; Morand EF. 2005. Reduction of arthritis severity in protease-activated receptor-deficient mice. Arthritis Rheum 52(4):1325-32. [PubMed: 15818676]  [MGI Ref ID J:112513]

Zhong Z; Ilieva H; Hallagan L; Bell R; Singh I; Paquette N; Thiyagarajan M; Deane R; Fernandez JA; Lane S; Zlokovic AB; Liu T; Griffin JH; Chow N; Castellino FJ; Stojanovic K; Cleveland DW; Zlokovic BV. 2009. Activated protein C therapy slows ALS-like disease in mice by transcriptionally inhibiting SOD1 in motor neurons and microglia cells. J Clin Invest 119(11):3437-49. [PubMed: 19841542]  [MGI Ref ID J:154597]

van den Hengel LG; Hellingman AA; Nossent AY; van Oeveren-Rietdijk AM; de Vries MR; Spek CA; van Zonneveld AJ; Reitsma PH; Hamming JF; de Boer HC; Versteeg HH; Quax PH. 2013. Protease-activated receptor (PAR)2, but not PAR1, is involved in collateral formation and anti-inflammatory monocyte polarization in a mouse hind limb ischemia model. PLoS One 8(4):e61923. [PubMed: 23637930]  [MGI Ref ID J:200559]

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.
 

Payment Terms and Conditions

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


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

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

Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

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

No Warranty

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

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

No Liability

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

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

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

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


(6.8)