Strain Name:

B6.129P2-Sod3tm1Mrkl/J

Stock Number:

009654

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Availability:

Cryopreserved - Ready for recovery

Mice that are homozygous for this targeted mutation of Sod3 (superoxide dismutase 3, extracellular) have increased extracellular superoxide radical concentration and exhibit increased sensitivity to experimentally induced hyperoxia, diabetes, inflammation, fibrosis, and hypertension. This mutant mouse strain may be useful in studies of oxidative stress and damage, inflammatory response, hypoxia, ischemia and reperfusion (I/R) injury, and alloxan-induced diabetes.

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
 
Donating Investigator James D Crapo,   Natl Jewish Med & Res Ctr

Description
Mice that are homozygous for the targeted mutation are viable, fertile, normal in size, but reproductive performance is inconsistent for homozygous X homozygous crosses. No gene product (EC-SOD protein) activity is detected by gel-exclusion chromatography analysis of plasma and no protein is detected by Western blot analysis of blood vessels. EC-SOD activity is not detected in brain. When exposed to >99% oxygen conditions, homozygotes have a shorter survival time than wild-type controls and exhibit a more severe lung edema at death. Homozygotes are more sensitive to induced transient focal cerebral ischemia, which results in greater total infarct volume and more severe hemiparesis. Alloxan-induced diabetes causes increased initial hyperglycemia with delayed recovery of glycemic control. Extracellular superoxide radical concentration is doubled and normal age-related loss of endothelial cells is increased in the cornea. Mutant mice are more susceptible to LPS-induced inflammation of the cornea and lung. Homozygotes exhibit increased vascular nitric oxide consumption, higher levels of vascular superoxide anions, weakened nitric oxide mediated endothelium-derived vasodilation (relaxation) in the brain and aorta and are more sensitive to CNS oxygen toxicity. Hippocampal neurogenesis after ionizing irradiation treatment is improved compared to wildtype controls. Homozygotes are more susceptible to bleomycin-induced pulmonary fibrosis, angiotensin II-induced hypertension, and reperfusion injury in skeletal muscle with delayed and incomplete recovery. Levels of the oxidant stress marker, plasma thiobarbituric acid-reactive substances (TBARS), are elevated. Mutant mice exhibit more severe collagen-induced arthritis (on the DBA/1J background). Response to crocidolite-induced asbestosis is enhanced with increased inflammation and total bronchoalveolar lavage fluid protein with more oxidative damage of lung tissue. Myocardial-infarction (MI)-induced heart failure results in increased ventricular hypertrophy and fibrosis. Serum erythropoietin is increased but without a corresponding increase in hematocrit and reticulocyte counts in response to hypoxia. This mutant mouse strain may be useful in studies of oxidative stress and damage, inflammatory response, hypoxia, ischemia and reperfusion (I/R) injury, and alloxan-induced diabetes.

Development
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt the coding exon. The construct was electroporated into 129P2/OlaHsd derived E14.1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The donating investigator reported that the resulting chimeric male animals were crossed to C57BL/6 females, and then backcrossed to C57BL/6J (see SNP note below) for 10 generations.

A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, 1 of 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a mixed C57BL/6J ; C57BL/6N genetic background.

Control Information

  Control
   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.

Sod3tm1Mrkl/Sod3tm1Mrkl

        involves: 129P2/OlaHsd * C57BL/6
  • mortality/aging
  • increased sensitivity to induced morbidity/mortality
    • when stressed by exposure to hyperoxia (>99% oxygen), mice exhibit significantly reduced survival relative to wild-type controls   (MGI Ref ID J:26851)
  • homeostasis/metabolism phenotype
  • increased susceptibility to injury
    • after exposure to hyperoxia (>99% oxygen for 70 hrs), mice exhibit significantly more severe lung edema than wild-type controls   (MGI Ref ID J:26851)
    • however, mice develop normally and remain healthy until at least 14 months of age when placed under normal physiological conditions; no compensatory induction of other SOD isoenzymes or other antioxidant enzymes is observed   (MGI Ref ID J:26851)

Sod3tm1Mrkl/Sod3tm1Mrkl

        D1.129P2-Sod3tm1Mrkl
  • immune system phenotype
  • arthritis
    • on day 53, the joints of null animals have a 2.2 fold greater mean inflammation score than wild-type, with a pannus score 2.4 fold higher, the cartilage damage score 2.3 fold greater and the bone damage score 2.3 fold greater   (MGI Ref ID J:106273)
    • increased susceptibility to induced arthritis
      • after immunization with collagen II on day 21, clinical disease activity score is higher in knockouts by between days 36 and 53 after the initial injection compared with wild-type   (MGI Ref ID J:106273)
  • increased tumor necrosis factor secretion
    • in culture, LPS-stimulated spleen cells from null mice produce greater levels of TNF than wild-type control cells   (MGI Ref ID J:106273)
  • skeleton phenotype
  • arthritis
    • on day 53, the joints of null animals have a 2.2 fold greater mean inflammation score than wild-type, with a pannus score 2.4 fold higher, the cartilage damage score 2.3 fold greater and the bone damage score 2.3 fold greater   (MGI Ref ID J:106273)
    • increased susceptibility to induced arthritis
      • after immunization with collagen II on day 21, clinical disease activity score is higher in knockouts by between days 36 and 53 after the initial injection compared with wild-type   (MGI Ref ID J:106273)
View Research Applications

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

Cardiovascular Research
Hypertension
Ischemia studies
Other
Vascular Defects

Diabetes and Obesity Research
Hyperglycemia
      alloxan induced

Immunology, Inflammation and Autoimmunity Research
Inflammation
      collagen induced arthritis

Research Tools
Cardiovascular Research
Immunology, Inflammation and Autoimmunity Research
Toxicology Research
      free radical research

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Sod3tm1Mrkl
Allele Name targeted mutation 1, Stefan L Marklund
Allele Type Targeted (Null/Knockout)
Common Name(s) EC-SOD-; ecSOD-;
Mutation Made By LingYi Chang,   Natl Jewish Med & Res Ctr
Strain of Origin129P2/OlaHsd
Gene Symbol and Name Sod3, superoxide dismutase 3, extracellular
Chromosome 5
Gene Common Name(s) AI314465; EC-SOD; ECSODPT; MGC:13799; expressed sequence AI314465;
Molecular Note Sequence encoding the active site of the protein was disrupted by the insertion of a neomycin selection cassette. Superoxide dismutase activity was undetected in plasma obtained from homozygous mutant mice. [MGI Ref ID J:26851]

Genotyping

Genotyping Information

Genotyping Protocols

Sod3tm1Mrkl STD PCR, Melt Curve Analysis
Sod3tm1Mrkl STD PCR, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Carlsson LM; Jonsson J; Edlund T; Marklund SL. 1995. Mice lacking extracellular superoxide dismutase are more sensitive to hyperoxia. Proc Natl Acad Sci U S A 92(14):6264-8. [PubMed: 7603981]  [MGI Ref ID J:26851]

Additional References

Sod3tm1Mrkl related

Andreassen OA; Ferrante RJ; Dedeoglu A; Albers DW; Klivenyi P; Carlson EJ; Epstein CJ; Beal MF. 2001. Mice with a partial deficiency of manganese superoxide dismutase show increased vulnerability to the mitochondrial toxins malonate, 3-nitropropionic acid, and MPTP. Exp Neurol 167(1):189-95. [PubMed: 11161607]  [MGI Ref ID J:118022]

Behndig A. 2008. Corneal endothelial integrity in aging mice lacking superoxide dismutase-1 and/or superoxide dismutase-3. Mol Vis 14:2025-30. [PubMed: 18989385]  [MGI Ref ID J:143187]

Behndig A; Karlsson K; Brannstrom T; Sentman ML; Marklund SL. 2001. Corneal endothelial integrity in mice lacking extracellular superoxide dismutase. Invest Ophthalmol Vis Sci 42(12):2784-8. [PubMed: 11687518]  [MGI Ref ID J:72949]

Bowler RP; Nicks M; Tran K; Tanner G; Chang LY; Young SK; Worthen GS. 2004. Extracellular superoxide dismutase attenuates lipopolysaccharide-induced neutrophilic inflammation. Am J Respir Cell Mol Biol 31(4):432-9. [PubMed: 15256385]  [MGI Ref ID J:103602]

Break TJ; Jun S; Indramohan M; Carr KD; Sieve AN; Dory L; Berg RE. 2012. Extracellular superoxide dismutase inhibits innate immune responses and clearance of an intracellular bacterial infection. J Immunol 188(7):3342-50. [PubMed: 22393157]  [MGI Ref ID J:183085]

Demchenko IT; Oury TD; Crapo JD; Piantadosi CA. 2002. Regulation of the brain's vascular responses to oxygen. Circ Res 91(11):1031-7. [PubMed: 12456489]  [MGI Ref ID J:133980]

Fattman CL; Chang LY; Termin TA; Petersen L; Enghild JJ; Oury TD. 2003. Enhanced bleomycin-induced pulmonary damage in mice lacking extracellular superoxide dismutase. Free Radic Biol Med 35(7):763-71. [PubMed: 14583340]  [MGI Ref ID J:134601]

Fattman CL; Tan RJ; Tobolewski JM; Oury TD. 2006. Increased sensitivity to asbestos-induced lung injury in mice lacking extracellular superoxide dismutase. Free Radic Biol Med 40(4):601-7. [PubMed: 16458190]  [MGI Ref ID J:105870]

Ganguly K; Stoeger T; Wesselkamper SC; Reinhard C; Sartor MA; Medvedovic M; Tomlinson CR; Bolle I; Mason JM; Leikauf GD; Schulz H. 2007. Candidate genes controlling pulmonary function in mice: transcript profiling and predicted protein structure. Physiol Genomics 31(3):410-21. [PubMed: 17804602]  [MGI Ref ID J:128696]

Gao F; Koenitzer JR; Tobolewski JM; Jiang D; Liang J; Noble PW; Oury TD. 2008. Extracellular superoxide dismutase inhibits inflammation by preventing oxidative fragmentation of hyaluronan. J Biol Chem 283(10):6058-66. [PubMed: 18165226]  [MGI Ref ID J:133663]

Gongora MC; Qin Z; Laude K; Kim HW; McCann L; Folz JR; Dikalov S; Fukai T; Harrison DG. 2006. Role of extracellular superoxide dismutase in hypertension. Hypertension 48(3):473-81. [PubMed: 16864745]  [MGI Ref ID J:135874]

Jonsson LM; Rees DD; Edlund T; Marklund SL. 2002. Nitric oxide and blood pressure in mice lacking extracellular-superoxide dismutase. Free Radic Res 36(7):755-8. [PubMed: 12180126]  [MGI Ref ID J:103261]

Jung O; Marklund SL; Geiger H; Pedrazzini T; Busse R; Brandes RP. 2003. Extracellular superoxide dismutase is a major determinant of nitric oxide bioavailability: in vivo and ex vivo evidence from ecSOD-deficient mice. Circ Res 93(7):622-9. [PubMed: 12933702]  [MGI Ref ID J:115686]

Kim HW; Lin A; Guldberg RE; Ushio-Fukai M; Fukai T. 2007. Essential role of extracellular SOD in reparative neovascularization induced by hindlimb ischemia. Circ Res 101(4):409-19. [PubMed: 17601801]  [MGI Ref ID J:140296]

Kliment CR; Englert JM; Gochuico BR; Yu G; Kaminski N; Rosas I; Oury TD. 2009. Oxidative stress alters syndecan-1 distribution in lungs with pulmonary fibrosis. J Biol Chem 284(6):3537-45. [PubMed: 19073610]  [MGI Ref ID J:147596]

Kliment CR; Suliman HB; Tobolewski JM; Reynolds CM; Day BJ; Zhu X; McTiernan CF; McGaffin KR; Piantadosi CA; Oury TD. 2009. Extracellular superoxide dismutase regulates cardiac function and fibrosis. J Mol Cell Cardiol 47(5):730-42. [PubMed: 19695260]  [MGI Ref ID J:155018]

Lee YS; Cheon IS; Kim BH; Kwon MJ; Lee HW; Kim TY. 2013. Loss of extracellular superoxide dismutase induces severe IL-23-mediated skin inflammation in mice. J Invest Dermatol 133(3):732-41. [PubMed: 23223134]  [MGI Ref ID J:196512]

Levin ED; Brady TC; Hochrein EC; Oury TD; Jonsson LM; Marklund SL; Crapo JD. 1998. Molecular manipulations of extracellular superoxide dismutase: functional importance for learning. Behav Genet 28(5):381-90. [PubMed: 9926619]  [MGI Ref ID J:129116]

Lu Z; Xu X; Hu X; Zhu G; Zhang P; van Deel ED; French JP; Fassett JT; Oury TD; Bache RJ; Chen Y. 2008. Extracellular superoxide dismutase deficiency exacerbates pressure overload-induced left ventricular hypertrophy and dysfunction. Hypertension 51(1):19-25. [PubMed: 17998475]  [MGI Ref ID J:147516]

Lund DD; Chu Y; Miller JD; Heistad DD. 2009. Protective effect of extracellular superoxide dismutase on endothelial function during aging. Am J Physiol Heart Circ Physiol 296(6):H1920-5. [PubMed: 19376805]  [MGI Ref ID J:150871]

Manni ML; Epperly MW; Han W; Blackwell TS; Duncan SR; Piganelli JD; Oury TD. 2012. Leukocyte-derived extracellular superoxide dismutase does not contribute to airspace EC-SOD after interstitial pulmonary injury. Am J Physiol Lung Cell Mol Physiol 302(1):L160-6. [PubMed: 22003088]  [MGI Ref ID J:183330]

Manni ML; Tomai LP; Norris CA; Thomas LM; Kelley EE; Salter RD; Crapo JD; Chang LY; Watkins SC; Piganelli JD; Oury TD. 2011. Extracellular superoxide dismutase in macrophages augments bacterial killing by promoting phagocytosis. Am J Pathol 178(6):2752-9. [PubMed: 21641397]  [MGI Ref ID J:173474]

Muller FL; Lustgarten MS; Jang Y; Richardson A; Van Remmen H. 2007. Trends in oxidative aging theories. Free Radic Biol Med 43(4):477-503. [PubMed: 17640558]  [MGI Ref ID J:123504]

Park JW; Qi WN; Cai Y; Zelko I; Liu JQ; Chen LE; Urbaniak JR; Folz RJ. 2005. Skeletal muscle reperfusion injury is enhanced in extracellular superoxide dismutase knockout mouse. Am J Physiol Heart Circ Physiol 289(1):H181-7. [PubMed: 15778274]  [MGI Ref ID J:99889]

Patel M; Li QY; Chang LY; Crapo J; Liang LP. 2005. Activation of NADPH oxidase and extracellular superoxide production in seizure-induced hippocampal damage. J Neurochem 92(1):123-31. [PubMed: 15606902]  [MGI Ref ID J:95450]

Rola R; Zou Y; Huang TT; Fishman K; Baure J; Rosi S; Milliken H; Limoli CL; Fike JR. 2007. Lack of extracellular superoxide dismutase (EC-SOD) in the microenvironment impacts radiation-induced changes in neurogenesis. Free Radic Biol Med 42(8):1133-45; discussion 1131-2. [PubMed: 17382195]  [MGI Ref ID J:121520]

Ross AD; Banda NK; Muggli M; Arend WP. 2004. Enhancement of collagen-induced arthritis in mice genetically deficient in extracellular superoxide dismutase. Arthritis Rheum 50(11):3702-11. [PubMed: 15529385]  [MGI Ref ID J:106273]

Sentman ML; Brannstrom T; Marklund SL. 2002. EC-SOD and the response to inflammatory reactions and aging in mouse lung. Free Radic Biol Med 32(10):975-81. [PubMed: 12008113]  [MGI Ref ID J:77784]

Sentman ML; Brannstrom T; Westerlund S; Laukkanen MO; Yla-Herttuala S; Basu S; Marklund SL. 2001. Extracellular superoxide dismutase deficiency and atherosclerosis in mice. Arterioscler Thromb Vasc Biol 21(9):1477-82. [PubMed: 11557675]  [MGI Ref ID J:103233]

Sentman ML; Granstrom M; Jakobson H; Reaume A; Basu S; Marklund SL. 2006. Phenotypes of mice lacking extracellular superoxide dismutase and copper- and zinc-containing superoxide dismutase. J Biol Chem 281(11):6904-9. [PubMed: 16377630]  [MGI Ref ID J:110486]

Sentman ML; Jonsson LM; Marklund SL. 1999. Enhanced alloxan-induced beta-cell damage and delayed recovery from hyperglycemia in mice lacking extracellular-superoxide dismutase. Free Radic Biol Med 27(7-8):790-6. [PubMed: 10515583]  [MGI Ref ID J:59726]

Sheng H; Brady TC; Pearlstein RD; Crapo JD; Warner DS. 1999. Extracellular superoxide dismutase deficiency worsens outcome from focal cerebral ischemia in the mouse. Neurosci Lett 267(1):13-6. [PubMed: 10400237]  [MGI Ref ID J:107981]

Stepp MW; Folz RJ; Yu J; Zelko IN. 2014. The c10orf10 gene product is a new link between oxidative stress and autophagy. Biochim Biophys Acta 1843(6):1076-88. [PubMed: 24530860]  [MGI Ref ID J:211582]

Sudhahar V; Urao N; Oshikawa J; McKinney RD; Llanos RM; Mercer JF; Ushio-Fukai M; Fukai T. 2013. Copper transporter ATP7A protects against endothelial dysfunction in type 1 diabetic mice by regulating extracellular superoxide dismutase. Diabetes 62(11):3839-50. [PubMed: 23884884]  [MGI Ref ID J:208942]

Suliman HB; Ali M; Piantadosi CA. 2004. Superoxide dismutase-3 promotes full expression of the EPO response to hypoxia. Blood 104(1):43-50. [PubMed: 15016652]  [MGI Ref ID J:90918]

Tan RJ; Lee JS; Manni ML; Fattman CL; Tobolewski JM; Zheng M; Kolls JK; Martin TR; Oury TD. 2006. Inflammatory cells as a source of airspace extracellular superoxide dismutase after pulmonary injury. Am J Respir Cell Mol Biol 34(2):226-32. [PubMed: 16224105]  [MGI Ref ID J:120192]

Welch WJ; Chabrashvili T; Solis G; Chen Y; Gill PS; Aslam S; Wang X; Ji H; Sandberg K; Jose P; Wilcox CS. 2006. Role of extracellular superoxide dismutase in the mouse angiotensin slow pressor response. Hypertension 48(5):934-41. [PubMed: 17015770]  [MGI Ref ID J:135931]

Yao H; Arunachalam G; Hwang JW; Chung S; Sundar IK; Kinnula VL; Crapo JD; Rahman I. 2010. Extracellular superoxide dismutase protects against pulmonary emphysema by attenuating oxidative fragmentation of ECM. Proc Natl Acad Sci U S A 107(35):15571-6. [PubMed: 20713693]  [MGI Ref ID J:163752]

Zelko IN; Folz RJ. 2005. Extracellular superoxide dismutase functions as a major repressor of hypoxia-induced erythropoietin gene expression. Endocrinology 146(1):332-40. [PubMed: 15375030]  [MGI Ref ID J:95879]

Zou Y; Corniola R; Leu D; Khan A; Sahbaie P; Chakraborti A; Clark DJ; Fike JR; Huang TT. 2012. Extracellular superoxide dismutase is important for hippocampal neurogenesis and preservation of cognitive functions after irradiation. Proc Natl Acad Sci U S A 109(52):21522-7. [PubMed: 23236175]  [MGI Ref ID J:193171]

van Deel ED; Lu Z; Xu X; Zhu G; Hu X; Oury TD; Bache RJ; Duncker DJ; Chen Y. 2008. Extracellular superoxide dismutase protects the heart against oxidative stress and hypertrophy after myocardial infarction. Free Radic Biol Med 44(7):1305-13. [PubMed: 18206658]  [MGI Ref ID J:134217]

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 & HusbandryWhen maintaining a live colony, these mice can be bred as homozygotes, but reproductive performance can be inconsistent.

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* $2140.00
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.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • 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* $2782.00
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.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • 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
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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