Strain Name:

129-Npr1tm1Gar/J

Stock Number:

004374

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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 Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse
 
Donating Investigator David L. Garbers,   U.T. Southwestern Medical Center

Description
Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) was detected. Homozygous mutant mice have elevated systolic, diastolic and mean blood pressure when compared to wildtype. Heterozygous mutant mice display systolic, diastolic and mean blood pressure that are slightly elevated above wildtype levels. Blood pressure in mutant mice remains elevated independent of salt content in diet. Infusion treatment of atrial natriuretic peptide in mutant mice does not result in the increased urine output or sodium excretion response seen in wildtype mice. Plasma volume expansion to release natriuretic/diuretic factors from the heart fails to induce increased urine output, sodium excretion and cyclic GMP excretion in the mutant. The same plasma volume expansion in wildtype mice results in a 12-fold increase in urine output, a 6-fold increase in sodium excretion and a 4-fold increase in cyclic GMP excretion in the urine. Mutant mice excrete only 30% of the normal level of urinary cyclic GMP. The Donating Investigator reports this mutant strain also exhibits cardiac hypertrophy and cardiac fibrosis. The phenotype of this mutant strain, salt insensitive hypertension, resembles that of half of all human patients with essential hypertension. This mutant mouse strain represents a model that may be useful in studies related to essential hypertension.

Development
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt exon 4 of the targeted gene. The construct was electroporated into 129S7/SvEvBrd-Hprt+ derived AB-1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts.

Control Information

  Control
   002448 129S1/SvImJ
 
  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.

Npr1tm1Gar/Npr1+

        involves: 129S7/SvEvBrd * C57BL/6J
  • cardiovascular system phenotype
  • increased systemic arterial blood pressure
    • on a standard rodent chow (0.7% NaCl), heterozygotes exhibit a 7.7 mm Hg increase in mean blood pressure relative to wild-type mice; no significant changes in heart rates are observed   (MGI Ref ID J:30007)
    • increased systemic arterial diastolic blood pressure
      • on a standard rodent chow (0.7% NaCl), heterozygotes exhibit a 5.9 mm Hg increase in diastolic blood pressure relative to wild-type mice   (MGI Ref ID J:30007)
    • increased systemic arterial systolic blood pressure
      • on a standard rodent chow (0.7% NaCl), heterozygotes exhibit a 10.5 mm Hg increase in systolic blood pressure relative to wild-type mice   (MGI Ref ID J:30007)
    • salt-resistant hypertension
      • heterozygotes display salt-resistant hypertension: on a low (0.008% NaCl), normal (0.7% NaCl) and high (8% NaCl) salt diet, their blood pressures and heart rates remain unchanged   (MGI Ref ID J:30007)
      • a high (8% NaCl) salt diet fails to change hematocrit or body weight, suggesting the possibility of increased natriuresis; no differences in aldosterone and atrial natriuretic peptide concentrations are observed   (MGI Ref ID J:30007)

Npr1tm1Gar/Npr1tm1Gar

        involves: 129S7/SvEvBrd * C57BL/6J
  • mortality/aging
  • *normal* mortality/aging
    • at 3 weeks, homozygotes are slightly (but significantly) underrepresented, at least partly due to the presence of hydrops fetalis in 10% of mutant embryos; however, stage of lethality is not speficied   (MGI Ref ID J:30007)
    • no histological abnormalities are detected in heart, vasculature or kidneys at less than 5 months of age   (MGI Ref ID J:30007)
  • cardiovascular system phenotype
  • abnormal systemic arterial blood pressure
    • in wild-type mice, ANP evoked a significant reduction in BP at 500 ng/kg/min, a rate which resulted in a plasma concentration of 0.8 nM; in contrast, ANP failed to lower BP in mutant mice even at infusion rates of 50 g/kg/min   (MGI Ref ID J:42893)
    • CNP evoked a significant reduction in BP at much higher infusion rates (50 g/kg/min), resulting in a plasma concentration of 18.3 nM, with no significant differences between wild-type and mutant mice   (MGI Ref ID J:42893)
    • increased systemic arterial blood pressure
      • on a standard rodent chow (0.7% NaCl), homozygotes exhibit a 19.7 mm Hg increase in mean blood pressure relative to wild-type mice; no significant changes in heart rates are observed   (MGI Ref ID J:30007)
      • increased systemic arterial diastolic blood pressure
        • on a standard rodent chow (0.7% NaCl), homozygotes exhibit a 15.3 mm Hg increase in diastolic blood pressure relative to wild-type mice   (MGI Ref ID J:30007)
      • increased systemic arterial systolic blood pressure
        • on a standard rodent chow (0.7% NaCl), homozygotes exhibit a 27.4 mm Hg increase in systolic blood pressure relative to wild-type mice   (MGI Ref ID J:30007)
      • salt-resistant hypertension
        • homozygotes display salt-resistant hypertension: on a low (0.008% NaCl), normal (0.7% NaCl) and high (8% NaCl) salt diet, their blood pressures and heart rates remain unchanged   (MGI Ref ID J:30007)
        • a high (8% NaCl) salt diet fails to change hematocrit or body weight, suggesting the possibility of increased natriuresis; no differences in aldosterone and atrial natriuretic peptide concentrations are observed   (MGI Ref ID J:30007)
  • abnormal vasodilation
    • atrial natriuretic peptide (ANP) or B-type natriuretic peptide (BNP) half-maximally relaxed KCl-precontracted aortic rings in wild-type mice at ~24 nM, but failed to relax aortas in mutant mice, even at micromolar concentrations   (MGI Ref ID J:42893)
    • in contrast, C-type natriuretic peptide (CNP) caused half-maximal relaxation at 335 and 146 nM in aortas from either wild-type or null mice, respectively (no significant difference)   (MGI Ref ID J:42893)
  • homeostasis/metabolism phenotype
  • hydrops fetalis
    • ~10% of homozygotes exhibit hydrops fetalis   (MGI Ref ID J:30007)
  • increased circulating atrial natriuretic factor
    • homozygous mutant mice exhibit increased basal concentrations of ANP relative to wild-type mice (~279 109 pM vs ~159 111 pM, respectively)   (MGI Ref ID J:42893)
    • in contrast, basal concentrations of circulating CNP are below the detectable limit in both wild-type and mutant mice   (MGI Ref ID J:42893)
  • muscle phenotype
  • abnormal vasodilation
    • atrial natriuretic peptide (ANP) or B-type natriuretic peptide (BNP) half-maximally relaxed KCl-precontracted aortic rings in wild-type mice at ~24 nM, but failed to relax aortas in mutant mice, even at micromolar concentrations   (MGI Ref ID J:42893)
    • in contrast, C-type natriuretic peptide (CNP) caused half-maximal relaxation at 335 and 146 nM in aortas from either wild-type or null mice, respectively (no significant difference)   (MGI Ref ID J:42893)

Npr1tm1Gar/Npr1tm1Gar

        B6.129S7-Npr1tm1Gar
  • cardiovascular system phenotype
  • decreased myocardial infarction size
    • at 2 days after myocardial ischemia/reperfusion, homozygotes exhibit a 20% reduction in myocardial infarct size relative to wild-type mice   (MGI Ref ID J:70496)
    • reduced infarct size is associated with concomitant reductions in PMN infiltration, coronary endothelial cell expression of P-selectin, and activation of NF-kappaB   (MGI Ref ID J:70496)
  • immune system phenotype
  • impaired neutrophil chemotaxis
    • in response to myocardial ischemia/reperfusion, homozygotes exhibit a significant reduction in the number of PMNs infiltrating the myocardium relative to wild-type mice   (MGI Ref ID J:70496)
    • reduced PMN emigration is corroborated by reduced cardiac MPO activity in infarct areas of mutant mice   (MGI Ref ID J:70496)
  • homeostasis/metabolism phenotype
  • decreased myocardial infarction size
    • at 2 days after myocardial ischemia/reperfusion, homozygotes exhibit a 20% reduction in myocardial infarct size relative to wild-type mice   (MGI Ref ID J:70496)
    • reduced infarct size is associated with concomitant reductions in PMN infiltration, coronary endothelial cell expression of P-selectin, and activation of NF-kappaB   (MGI Ref ID J:70496)
  • cellular phenotype
  • impaired neutrophil chemotaxis
    • in response to myocardial ischemia/reperfusion, homozygotes exhibit a significant reduction in the number of PMNs infiltrating the myocardium relative to wild-type mice   (MGI Ref ID J:70496)
    • reduced PMN emigration is corroborated by reduced cardiac MPO activity in infarct areas of mutant mice   (MGI Ref ID J:70496)
  • hematopoietic system phenotype
  • impaired neutrophil chemotaxis
    • in response to myocardial ischemia/reperfusion, homozygotes exhibit a significant reduction in the number of PMNs infiltrating the myocardium relative to wild-type mice   (MGI Ref ID J:70496)
    • reduced PMN emigration is corroborated by reduced cardiac MPO activity in infarct areas of mutant mice   (MGI Ref ID J:70496)
View Research Applications

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

Npr1tm1Gar related

Cardiovascular Research
Heart Abnormalities
Hypertension

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Npr1tm1Gar
Allele Name targeted mutation 1, David L Garbers
Allele Type Targeted (knock-out)
Common Name(s) GC-A KO; GC-A-;
Mutation Made By David Garbers,   U.T. Southwestern Medical Center
Strain of Origin129S7/SvEvBrd-Hprt<+>
ES Cell Line NameAB1
ES Cell Line Strain129S7/SvEvBrd-Hprt<+>
Gene Symbol and Name Npr1, natriuretic peptide receptor 1
Chromosome 3
Gene Common Name(s) AI893888; ANPRA; ANPa; GC-A; GUC2A; GUCY2A; Gca; NPR-A; NPRA; Pndr; expressed sequence AI893888; guanylyl cyclase-A;
Molecular Note Insertion of a neomycin resistance cassette into exon 4, which encodes part of the extra-cellular putative ligand-binding domain, disrupted the gene. Stable, wild-type size transcript was not detected in liver or kidney from homozygous mutant mice. [MGI Ref ID J:30007]

Genotyping

Genotyping Information

Genotyping Protocols

NEOTD (Generic Neo), Standard PCR
Npr1tm1Gar, Separated PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Lopez MJ; Wong SK; Kishimoto I; Dubois S; Mach V; Friesen J; Garbers DL; Beuve A. 1995. Salt-resistant hypertension in mice lacking the guanylyl cyclase-A receptor for atrial natriuretic peptide. Nature 378(6552):65-8. [PubMed: 7477288]  [MGI Ref ID J:30007]

Additional References

Npr1tm1Gar related

Chen S; Grigsby CL; Law CS; Ni X; Nekrep N; Olsen K; Humphreys MH; Gardner DG. 2009. Tonicity-dependent induction of Sgk1 expression has a potential role in dehydration-induced natriuresis in rodents. J Clin Invest 119(6):1647-58. [PubMed: 19436108]  [MGI Ref ID J:150581]

Chusho H; Ogawa Y; Tamura N; Suda M; Yasoda A; Miyazawa T; Kishimoto I; Komatsu Y; Itoh H; Tanaka K; Saito Y; Garbers DL; Nakao K. 2000. Genetic models reveal that brain natriuretic peptide can signal through different tissue-specific receptor-mediated pathways. Endocrinology 141(10):3807-13. [PubMed: 11014237]  [MGI Ref ID J:108806]

Dubois SK; Kishimoto I; Lillis TO; Garbers DL. 2000. A genetic model defines the importance of the atrial natriuretic peptide receptor (guanylyl cyclase-A) in the regulation of kidney function. Proc Natl Acad Sci U S A 97(8):4369-73. [PubMed: 10760303]  [MGI Ref ID J:126140]

Hunt LM; Hogeland EW; Henry MK; Swoap SJ. 2004. Hypotension and bradycardia during caloric restriction in mice are independent of salt balance and do not require ANP receptor. Am J Physiol Heart Circ Physiol 287(4):H1446-51. [PubMed: 15191892]  [MGI Ref ID J:95588]

Izumi T; Saito Y; Kishimoto I; Harada M; Kuwahara K; Hamanaka I; Takahashi N; Kawakami R; Li Y; Takemura G; Fujiwara H; Garbers DL; Mochizuki S; Nakao K. 2001. Blockade of the natriuretic peptide receptor guanylyl cyclase-A inhibits NF-kappaB activation and alleviates myocardial ischemia/reperfusion injury. J Clin Invest 108(2):203-13. [PubMed: 11457873]  [MGI Ref ID J:70496]

Kilic A; Velic A; De Windt LJ; Fabritz L; Voss M; Mitko D; Zwiener M; Baba HA; van Eickels M; Schlatter E; Kuhn M. 2005. Enhanced activity of the myocardial Na+/H+ exchanger NHE-1 contributes to cardiac remodeling in atrial natriuretic peptide receptor-deficient mice. Circulation 112(15):2307-17. [PubMed: 16216978]  [MGI Ref ID J:116814]

Kinoshita H; Kuwahara K; Nishida M; Jian Z; Rong X; Kiyonaka S; Kuwabara Y; Kurose H; Inoue R; Mori Y; Li Y; Nakagawa Y; Usami S; Fujiwara M; Yamada Y; Minami T; Ueshima K; Nakao K. 2010. Inhibition of TRPC6 channel activity contributes to the antihypertrophic effects of natriuretic peptides-guanylyl cyclase-A signaling in the heart. Circ Res 106(12):1849-60. [PubMed: 20448219]  [MGI Ref ID J:175052]

Kirchhof P; Fabritz L; Kilic A; Begrow F; Breithardt G; Kuhn M. 2004. Ventricular arrhythmias, increased cardiac calmodulin kinase II expression, and altered repolarization kinetics in ANP receptor deficient mice. J Mol Cell Cardiol 36(5):691-700. [PubMed: 15135664]  [MGI Ref ID J:102133]

Kong X; Wang X; Xu W; Behera S; Hellermann G; Kumar A; Lockey RF; Mohapatra S; Mohapatra SS. 2008. Natriuretic peptide receptor a as a novel anticancer target. Cancer Res 68(1):249-56. [PubMed: 18172317]  [MGI Ref ID J:131033]

Kuhn M; Volker K; Schwarz K; Carbajo-Lozoya J; Flogel U; Jacoby C; Stypmann J; van Eickels M; Gambaryan S; Hartmann M; Werner M; Wieland T; Schrader J; Baba HA. 2009. The natriuretic peptide/guanylyl cyclase--a system functions as a stress-responsive regulator of angiogenesis in mice. J Clin Invest 119(7):2019-30. [PubMed: 19487812]  [MGI Ref ID J:152580]

Li Y; Kishimoto I; Saito Y; Harada M; Kuwahara K; Izumi T; Hamanaka I; Takahashi N; Kawakami R; Tanimoto K; Nakagawa Y; Nakanishi M; Adachi Y; Garbers DL; Fukamizu A; Nakao K. 2004. Androgen contributes to gender-related cardiac hypertrophy and fibrosis in mice lacking the gene encoding guanylyl cyclase-A. Endocrinology 145(2):951-8. [PubMed: 14592959]  [MGI Ref ID J:88703]

Li Y; Kishimoto I; Saito Y; Harada M; Kuwahara K; Izumi T; Takahashi N; Kawakami R; Tanimoto K; Nakagawa Y; Nakanishi M; Adachi Y; Garbers DL; Fukamizu A; Nakao K. 2002. Guanylyl cyclase-A inhibits angiotensin II type 1A receptor-mediated cardiac remodeling, an endogenous protective mechanism in the heart. Circulation 106(13):1722-8. [PubMed: 12270869]  [MGI Ref ID J:103221]

Li Y; Saito Y; Kuwahara K; Rong X; Kishimoto I; Harada M; Adachi Y; Nakanishi M; Kinoshita H; Horiuchi M; Murray M; Nakao K. 2009. Guanylyl cyclase-A inhibits angiotensin II type 2 receptor-mediated pro-hypertrophic signaling in the heart. Endocrinology 150(8):3759-65. [PubMed: 19372206]  [MGI Ref ID J:158158]

Lopez MJ; Garbers DL; Kuhn M. 1997. The guanylyl cyclase-deficient mouse defines differential pathways of natriuretic peptide signaling. J Biol Chem 272(37):23064-8. [PubMed: 9287305]  [MGI Ref ID J:42893]

Madhani M; Hall AR; Cuello F; Charles RL; Burgoyne JR; Fuller W; Hobbs AJ; Shattock MJ; Eaton P. 2010. Phospholemman Ser69 phosphorylation contributes to sildenafil-induced cardioprotection against reperfusion injury. Am J Physiol Heart Circ Physiol 299(3):H827-36. [PubMed: 20543084]  [MGI Ref ID J:164509]

Miyashita K; Itoh H; Tsujimoto H; Tamura N; Fukunaga Y; Sone M; Yamahara K; Taura D; Inuzuka M; Sonoyama T; Nakao K. 2009. Natriuretic peptides/cGMP/cGMP-dependent protein kinase cascades promote muscle mitochondrial biogenesis and prevent obesity. Diabetes 58(12):2880-92. [PubMed: 19690065]  [MGI Ref ID J:158488]

Nakanishi M; Saito Y; Kishimoto I; Harada M; Kuwahara K; Takahashi N; Kawakami R; Nakagawa Y; Tanimoto K; Yasuno S; Usami S; Li Y; Adachi Y; Fukamizu A; Garbers DL; Nakao K. 2005. Role of natriuretic peptide receptor guanylyl cyclase-A in myocardial infarction evaluated using genetically engineered mice. Hypertension 46(2):441-7. [PubMed: 15998711]  [MGI Ref ID J:114365]

Ropero AB; Soriano S; Tuduri E; Marroqui L; Tellez N; Gassner B; Juan-Pico P; Montanya E; Quesada I; Kuhn M; Nadal A. 2010. The atrial natriuretic peptide and guanylyl cyclase-A system modulates pancreatic beta-cell function. Endocrinology 151(8):3665-74. [PubMed: 20555029]  [MGI Ref ID J:168515]

Schreier B; Borner S; Volker K; Gambaryan S; Schafer SC; Kuhlencordt P; Gassner B; Kuhn M. 2008. The heart communicates with the endothelium through the guanylyl cyclase-A receptor: acute handling of intravascular volume in response to volume expansion. Endocrinology 149(8):4193-9. [PubMed: 18450968]  [MGI Ref ID J:145509]

Soriano S; Ropero AB; Alonso-Magdalena P; Ripoll C; Quesada I; Gassner B; Kuhn M; Gustafsson JA; Nadal A. 2009. Rapid regulation of K(ATP) channel activity by 17{beta}-estradiol in pancreatic {beta}-cells involves the estrogen receptor {beta} and the atrial natriuretic peptide receptor. Mol Endocrinol 23(12):1973-82. [PubMed: 19855088]  [MGI Ref ID J:154658]

Steinmetz M; Potthast R; Sabrane K; Kuhn M. 2004. Diverging vasorelaxing effects of C-type natriuretic peptide in renal resistance arteries and aortas of GC-A-deficient mice. Regul Pept 119(1-2):31-7. [PubMed: 15093694]  [MGI Ref ID J:102436]

Tokudome T; Horio T; Kishimoto I; Soeki T; Mori K; Kawano Y; Kohno M; Garbers DL; Nakao K; Kangawa K. 2005. Calcineurin-nuclear factor of activated T cells pathway-dependent cardiac remodeling in mice deficient in guanylyl cyclase A, a receptor for atrial and brain natriuretic peptides. Circulation 111(23):3095-104. [PubMed: 15939815]  [MGI Ref ID J:112245]

Tokudome T; Kishimoto I; Horio T; Arai Y; Schwenke DO; Hino J; Okano I; Kawano Y; Kohno M; Miyazato M; Nakao K; Kangawa K. 2008. Regulator of G-protein signaling subtype 4 mediates antihypertrophic effect of locally secreted natriuretic peptides in the heart. Circulation 117(18):2329-39. [PubMed: 18443239]  [MGI Ref ID J:155088]

Tokudome T; Kishimoto I; Yamahara K; Osaki T; Minamino N; Horio T; Sawai K; Kawano Y; Miyazato M; Sata M; Kohno M; Nakao K; Kangawa K. 2009. Impaired recovery of blood flow after hind-limb ischemia in mice lacking guanylyl cyclase-A, a receptor for atrial and brain natriuretic peptides. Arterioscler Thromb Vasc Biol 29(10):1516-21. [PubMed: 19628785]  [MGI Ref ID J:167805]

Yasuno S; Usami S; Kuwahara K; Nakanishi M; Arai Y; Kinoshita H; Nakagawa Y; Fujiwara M; Murakami M; Ueshima K; Harada M; Nakao K. 2009. Endogenous cardiac natriuretic peptides protect the heart in a mouse model of dilated cardiomyopathy and sudden death. Am J Physiol Heart Circ Physiol 296(6):H1804-10. [PubMed: 19346456]  [MGI Ref ID J:150878]

Zhao L; Long L; Morrell NW; Wilkins MR. 1999. NPR-A-Deficient mice show increased susceptibility to hypoxia-induced pulmonary hypertension. Circulation 99(5):605-7. [PubMed: 9950655]  [MGI Ref ID J:53666]

Health & husbandry

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.

Health & Colony Maintenance Information

Animal Health Reports

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

Colony Maintenance

Breeding & HusbandryThis strain originated on a 129S7 background and is maintained on the 129S6/SvEvTac background as a heterozygote.

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* $2450.00
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 $1600.00

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 11 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* $3185.00
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 $2080.00

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 11 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
   002448 129S1/SvImJ
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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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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