Strain Name:

FVB.129S2(B6)-Hmox2tm1Poss/J

Stock Number:

008660

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Homozygotes for this Hmox2 (heme oxygenase (decycling) 2) targeted null mutation may be useful in studies of oxidative stress and injury, hyperoxia, iron homeostasis and metabolism, vasodilation regulation, and the physiology of neuroprotection.

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; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Specieslaboratory mouse
GenerationN10pN1
Generation Definitions
 
Donating Investigator Raymond F. Burk,   Vanderbilt University

Description
Homozygotes have reduced total heme oxygenase activity in brain and testes, diminished inflammatory pain response and are more susceptible to hyperoxia with attenuated hypoxic ventilatory response. Cultured neurons from homozygotes exhibit increased neurotoxicity and cell death. Neuronal and endothelial cell damage due to transient focal ischemia and glutamate induced cytotoxicity is increased. Olfactory epithelial neurons have decreased proliferation of neuronal precursors and increased apoptosis. Mutant pulmonary venous myocardium is hypertrophic. After hyperoxic exposure, total lung iron content increased 3.5 fold in homozygotes compared to wild-type. Homozygotes have a slower overall gastrointestinal transit time than wild-type. Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Although homozygous male animals exhibit ejaculatory abnormalities, both male and female homozygotes are fertile. No gene product (mRNA or protein) is detected by Northern or Western blot analysis in lung tissue or brain. This mutant mouse strain may be useful in studies of oxidative stress and injury, hyperoxia, iron homeostasis and metabolism, vasodilation regulation, and the physiology of neuroprotection.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development
A targeting vector containing a PGK-neo selection cassette was used to disrupt exons 4 and 5. The construct was electroporated into 129S2/SvPas derived D3 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting male chimeric animals were crossed to C57BL/6 female mice. Heterozygotes were crossed to generate homozygotes. The mice were then backcrossed to C57BL/6 for an unknown number of generations and then backcrossed to FVB for 10 generations before arriving at The Jackson Laboratory.

Control Information

  Control
   001800 FVB/NJ
 
  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.

Hmox2tm1Poss/Hmox2tm1Poss

        involves: 129S2/SvPas * C57BL/6
  • mortality/aging
  • increased sensitivity to induced morbidity/mortality
    • increased susceptibility to hyperoxia (95% oxygen), died in 8.5 days as opposed to 13.4 days   (MGI Ref ID J:46183)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • brain morphology normal and basal synaptic functions all normal in the hippocampus, long term potentiation normal   (MGI Ref ID J:29523)
    • abnormal nerve fiber response
      • neuronal depolarization abnormalities result in failure of enteric smooth muscle relaxation   (MGI Ref ID J:89562)
  • respiratory system phenotype
  • abnormal respiratory system physiology
    • total glutathione in lungs increased over normal levels   (MGI Ref ID J:46183)
    • glutathione levels decrease 50% after 3 days of 95% hyperoxia   (MGI Ref ID J:46183)
    • 1.3 fold increase in lung protein carbonyls after 3 days of 95% hyperoxia   (MGI Ref ID J:46183)
    • increased Hmox1 levels after 3 days of 95% hyperoxia but not to the extent seen in controls   (MGI Ref ID J:46183)
    • higher levels of nitrotyrosine than in controls, indicating damage induced by NO   (MGI Ref ID J:46183)
  • homeostasis/metabolism phenotype
  • abnormal iron level
    • significantly increased levels of lung hemoproteins after exposure to hyperoxia   (MGI Ref ID J:46183)
    • heavy iron staining of lung endothelium after exposure to hyperoxia   (MGI Ref ID J:46183)
    • less lung ferritin protein protein after exposure to hyperoxia   (MGI Ref ID J:46183)
  • digestive/alimentary phenotype
  • abnormal intestinal transit time
    • longer gastrointestinal transit times due to failure of enteric smooth muscle to relax normally   (MGI Ref ID J:89562)

Hmox2tm1Poss/Hmox2tm1Poss

        B6.129S2-Hmox2tm1Poss
  • respiratory system phenotype
  • abnormal respiration
    • lung architecture and ventilation normal   (MGI Ref ID J:91075)
    • less responsive to acute hypoxia   (MGI Ref ID J:91075)
    • abnormal vital capacity
      • lower tidal volume and minute ventilataion   (MGI Ref ID J:91075)
    • decreased pulmonary respiratory rate
      • lower respiratory frequency   (MGI Ref ID J:91075)
  • homeostasis/metabolism phenotype
  • abnormal circulating protein level
    • reduced blood carboxyhemoglobin   (MGI Ref ID J:91075)
  • hypoxia
    • hypoxemia under ether anaesthesia   (MGI Ref ID J:91075)
  • cardiovascular system phenotype
  • abnormal pulmonary vein morphology
    • thickened walls of pulmonary veins due to hypertrophied pulmonary venous myocardium   (MGI Ref ID J:91075)
    • also overexpression of Hmox1   (MGI Ref ID J:91075)
  • behavior/neurological phenotype
  • abnormal nociception after inflammation
    • lower response to inflammatory pain as determined by formalin injection   (MGI Ref ID J:102990)
    • phase 1 licking time only 26% of controls and phase 2 time 40% of controls   (MGI Ref ID J:102990)
  • integument phenotype
  • abnormal nociception after inflammation
    • lower response to inflammatory pain as determined by formalin injection   (MGI Ref ID J:102990)
    • phase 1 licking time only 26% of controls and phase 2 time 40% of controls   (MGI Ref ID J:102990)

Hmox2tm1Poss/Hmox2tm1Poss

        involves: 129S2/SvPas
  • muscle phenotype
  • abnormal muscle physiology
    • the resting membrane potential of jejunal smooth muscle cells is depolarized about 8 mV compared to wild type cells   (MGI Ref ID J:89581)
    • hyperpolarization and induction of an inhibitory junction potential in response to electrical field stimulation under nonadrenergic noncholinergic conditions in jejunal muscle strips are markedly reduced   (MGI Ref ID J:89581)
    • exposure to 10% CO gas partial restores nonadrenergic noncholinergic inhibitory transmission   (MGI Ref ID J:89581)
    • abnormal muscle relaxation
      • the decrease in muscle contractions in jejunal muscle strips in response to electrical field stimulation is markedly reduced   (MGI Ref ID J:89581)
View Research Applications

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

Immunology, Inflammation and Autoimmunity Research
Inflammation

Internal/Organ Research
Gastrointestinal Defects

Metabolism Research
Iron Metabolism

Neurobiology Research
Neurodegeneration

Research Tools
Apoptosis Research

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Hmox2tm1Poss
Allele Name targeted mutation 1, Kenneth D Poss
Allele Type Targeted (Null/Knockout)
Common Name(s) HO-2-; HO-2delta; HO2-;
Mutation Made By Raymond Burk,   Vanderbilt University
Strain of Origin129S2/SvPas
ES Cell Line NameD3
ES Cell Line Strain129S2/SvPas
Gene Symbol and Name Hmox2, heme oxygenase (decycling) 2
Chromosome 16
Gene Common Name(s) HO-2; HO2;
Molecular Note Approximately 80% of the coding region was replaced with a neomycin selection cassette inserted by homologous recombination. The deleted region included the putative membrane spanning region. Transcript was undetected in homozygous mutant mice by Northern blot analysis of brain tissue. An assay based on bilirubin production indicated complete functional ablation in homozygous mutant mice. [MGI Ref ID J:29523]

Genotyping

Genotyping Information

Genotyping Protocols

Hmox2tm1Poss, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Poss KD; Thomas MJ; Ebralidze AK; O'Dell TJ; Tonegawa S. 1995. Hippocampal long-term potentiation is normal in heme oxygenase-2 mutant mice. Neuron 15(4):867-73. [PubMed: 7576635]  [MGI Ref ID J:29523]

Additional References

Hmox2tm1Poss related

Adachi T; Ishikawa K; Hida W; Matsumoto H; Masuda T; Date F; Ogawa K; Takeda K; Furuyama K; Zhang Y; Kitamuro T; Ogawa H; Maruyama Y; Shibahara S. 2004. Hypoxemia and blunted hypoxic ventilatory responses in mice lacking heme oxygenase-2. Biochem Biophys Res Commun 320(2):514-22. [PubMed: 15219859]  [MGI Ref ID J:91075]

Bellner L; Vitto M; Patil KA; Dunn MW; Regan R; Laniado-Schwartzman M. 2008. Exacerbated corneal inflammation and neovascularization in the HO-2 null mice is ameliorated by biliverdin. Exp Eye Res 87(3):268-78. [PubMed: 18602389]  [MGI Ref ID J:141882]

Burnett AL; Johns DG; Kriegsfeld LJ; Klein SL; Calvin DC; Demas GE; Schramm LP; Tonegawa S; Nelson RJ; Snyder SH; Poss KD. 1998. Ejaculatory abnormalities in mice with targeted disruption of the gene for heme oxygenase-2. Nat Med 4(1):84-7. [PubMed: 9427611]  [MGI Ref ID J:45047]

Chen J; Regan RF. 2004. Heme oxygenase-2 gene deletion increases astrocyte vulnerability to hemin. Biochem Biophys Res Commun 318(1):88-94. [PubMed: 15110757]  [MGI Ref ID J:89356]

Chen J; Tu Y; Moon C; Nagata E; Ronnett GV. 2003. Heme oxygenase-1 and heme oxygenase-2 have distinct roles in the proliferation and survival of olfactory receptor neurons mediated by cGMP and bilirubin, respectively. J Neurochem 85(5):1247-61. [PubMed: 12753084]  [MGI Ref ID J:83633]

Dennery PA; Spitz DR; Yang G; Tatarov A; Lee CS; Shegog ML; Poss KD. 1998. Oxygen toxicity and iron accumulation in the lungs of mice lacking heme oxygenase-2. J Clin Invest 101(5):1001-11. [PubMed: 9486970]  [MGI Ref ID J:46183]

Dennery PA; Visner G; Weng YH; Nguyen X; Lu F; Zander D; Yang G. 2003. Resistance to hyperoxia with heme oxygenase-1 disruption: role of iron. Free Radic Biol Med 34(1):124-33. [PubMed: 12498987]  [MGI Ref ID J:118007]

Dore S; Goto S; Sampei K; Blackshaw S; Hester LD; Ingi T; Sawa A; Traystman RJ; Koehler RC; Snyder SH. 2000. Heme oxygenase-2 acts to prevent neuronal death in brain cultures and following transient cerebral ischemia. Neuroscience 99(4):587-92. [PubMed: 10974422]  [MGI Ref ID J:119168]

Goodman AI; Chander PN; Rezzani R; Schwartzman ML; Regan RF; Rodella L; Turkseven S; Lianos EA; Dennery PA; Abraham NG. 2006. Heme oxygenase-2 deficiency contributes to diabetes-mediated increase in superoxide anion and renal dysfunction. J Am Soc Nephrol 17(4):1073-81. [PubMed: 16524951]  [MGI Ref ID J:135768]

Goto S; Sampei K; Alkayed NJ; Dore S; Koehler RC. 2003. Characterization of a new double-filament model of focal cerebral ischemia in heme oxygenase-2-deficient mice. Am J Physiol Regul Integr Comp Physiol 285(1):R222-30. [PubMed: 12663258]  [MGI Ref ID J:109297]

Han F; Takeda K; Ishikawa K; Ono M; Date F; Yokoyama S; Furuyama K; Shinozawa Y; Urade Y; Shibahara S. 2009. Induction of lipocalin-type prostaglandin D synthase in mouse heart under hypoxemia. Biochem Biophys Res Commun 385(3):449-53. [PubMed: 19470375]  [MGI Ref ID J:150669]

Kang L; Grande JP; Farrugia G; Croatt AJ; Katusic ZS; Nath KA. 2013. Functioning of an arteriovenous fistula requires heme oxygenase-2. Am J Physiol Renal Physiol 305(4):F545-52. [PubMed: 23678042]  [MGI Ref ID J:200857]

Li A; Xi Q; Umstot ES; Bellner L; Schwartzman ML; Jaggar JH; Leffler CW. 2008. Astrocyte-derived CO is a diffusible messenger that mediates glutamate-induced cerebral arteriolar dilation by activating smooth muscle Cell KCa channels. Circ Res 102(2):234-41. [PubMed: 17991880]  [MGI Ref ID J:145594]

Li X; Clark JD. 2000. Heme oxygenase type 2 plays a role in formalin-induced nociception. Pain 86(1-2):75-80. [PubMed: 10779663]  [MGI Ref ID J:102990]

Li X; Clark JD. 2001. Spinal cord nitric oxide synthase and heme oxygenase limit morphine induced analgesia. Brain Res Mol Brain Res 95(1-2):96-102. [PubMed: 11687280]  [MGI Ref ID J:72814]

Liang DY; Li X; Clark JD. 2004. Formalin-induced spinal cord calcium/calmodulin-dependent protein kinase II alpha expression is modulated by heme oxygenase in mice. Neurosci Lett 360(1-2):61-4. [PubMed: 15082179]  [MGI Ref ID J:121026]

Marrazzo G; Bellner L; Halilovic A; Li Volti G; Drago F; Dunn MW; Schwartzman ML. 2011. The role of neutrophils in corneal wound healing in HO-2 null mice. PLoS One 6(6):e21180. [PubMed: 21695050]  [MGI Ref ID J:174790]

Morikawa T; Kajimura M; Nakamura T; Hishiki T; Nakanishi T; Yukutake Y; Nagahata Y; Ishikawa M; Hattori K; Takenouchi T; Takahashi T; Ishii I; Matsubara K; Kabe Y; Uchiyama S; Nagata E; Gadalla MM; Snyder SH; Suematsu M. 2012. Hypoxic regulation of the cerebral microcirculation is mediated by a carbon monoxide-sensitive hydrogen sulfide pathway. Proc Natl Acad Sci U S A :. [PubMed: 22232681]  [MGI Ref ID J:179917]

Ortega-Saenz P; Pascual A; Gomez-Diaz R; Lopez-Barneo J. 2006. Acute oxygen sensing in heme oxygenase-2 null mice. J Gen Physiol 128(4):405-11. [PubMed: 16966473]  [MGI Ref ID J:136743]

Parfenova H; Basuroy S; Bhattacharya S; Tcheranova D; Qu Y; Regan RF; Leffler CW. 2006. Glutamate induces oxidative stress and apoptosis in cerebral vascular endothelial cells: contributions of HO-1 and HO-2 to cytoprotection. Am J Physiol Cell Physiol 290(5):C1399-410. [PubMed: 16371440]  [MGI Ref ID J:115773]

Qin X; Kwansa H; Bucci E; Dore S; Boehning D; Shugar D; Koehler RC. 2008. Role of heme oxygenase-2 in pial arteriolar response to acetylcholine in mice with and without transfusion of cell-free hemoglobin polymers. Am J Physiol Regul Integr Comp Physiol 295(2):R498-504. [PubMed: 18495834]  [MGI Ref ID J:148642]

Rattan S; Regan RF; Patel CA; De Godoy MA. 2005. Nitric oxide not carbon monoxide mediates nonadrenergic noncholinergic relaxation in the murine internal anal sphincter. Gastroenterology 129(6):1954-66. [PubMed: 16344064]  [MGI Ref ID J:124936]

Rogers B; Yakopson V; Teng ZP; Guo Y; Regan RF. 2003. Heme oxygenase-2 knockout neurons are less vulnerable to hemoglobin toxicity. Free Radic Biol Med 35(8):872-81. [PubMed: 14556851]  [MGI Ref ID J:118737]

Roth M; Rupp M; Hofmann S; Mittal M; Fuchs B; Sommer N; Parajuli N; Quanz K; Schubert D; Dony E; Schermuly RT; Ghofrani HA; Sausbier U; Rutschmann K; Wilhelm S; Seeger W; Ruth P; Grimminger F; Sausbier M; Weissmann N. 2009. Heme oxygenase-2 and large-conductance Ca2+-activated K+ channels: lung vascular effects of hypoxia. Am J Respir Crit Care Med 180(4):353-64. [PubMed: 19498059]  [MGI Ref ID J:164956]

Sedlak TW; Saleh M; Higginson DS; Paul BD; Juluri KR; Snyder SH. 2009. Bilirubin and glutathione have complementary antioxidant and cytoprotective roles. Proc Natl Acad Sci U S A 106(13):5171-6. [PubMed: 19286972]  [MGI Ref ID J:147138]

Seta F; Bellner L; Rezzani R; Regan RF; Dunn MW; Abraham NG; Gronert K; Laniado-Schwartzman M. 2006. Heme oxygenase-2 is a critical determinant for execution of an acute inflammatory and reparative response. Am J Pathol 169(5):1612-23. [PubMed: 17071585]  [MGI Ref ID J:114571]

Sha L; Farrugia G; Harmsen WS; Szurszewski JH. 2007. Membrane potential gradient is carbon monoxide-dependent in mouse and human small intestine. Am J Physiol Gastrointest Liver Physiol 293(2):G438-45. [PubMed: 17510199]  [MGI Ref ID J:125239]

Shah ZA; Nada SE; Dore S. 2011. Heme oxygenase 1, beneficial role in permanent ischemic stroke and in Gingko biloba (EGb 761) neuroprotection. Neuroscience 180:248-55. [PubMed: 21334424]  [MGI Ref ID J:173691]

Stec DE; Vera T; Storm MV; McLemore Jr GR; Ryan MJ. 2009. Blood pressure and renal blood flow responses in heme oxygenase-2 knockout mice. Am J Physiol Regul Integr Comp Physiol :. [PubMed: 19846746]  [MGI Ref ID J:154451]

Vanella L; Li Volti G; Guccione S; Rappazzo G; Salvo E; Pappalardo M; Forte S; Schwartzman ML; Abraham NG. 2013. Heme oxygenase-2/adiponectin protein-protein interaction in metabolic syndrome. Biochem Biophys Res Commun 432(4):606-11. [PubMed: 23438433]  [MGI Ref ID J:200798]

Wang J; Zhuang H; Dore S. 2006. Heme oxygenase 2 is neuroprotective against intracerebral hemorrhage. Neurobiol Dis 22(3):473-6. [PubMed: 16459095]  [MGI Ref ID J:111290]

Watkins CC; Boehning D; Kaplin AI; Rao M; Ferris CD; Snyder SH. 2004. Carbon monoxide mediates vasoactive intestinal polypeptide-associated nonadrenergic/noncholinergic neurotransmission. Proc Natl Acad Sci U S A 101(8):2631-5. [PubMed: 14983060]  [MGI Ref ID J:88640]

Xue L; Farrugia G; Miller SM; Ferris CD; Snyder SH; Szurszewski JH. 2000. Carbon monoxide and nitric oxide as coneurotransmitters in the enteric nervous system: evidence from genomic deletion of biosynthetic enzymes. Proc Natl Acad Sci U S A 97(4):1851-5. [PubMed: 10677545]  [MGI Ref ID J:89581]

Zakhary R; Poss KD; Jaffrey SR; Ferris CD; Tonegawa S; Snyder SH. 1997. Targeted gene deletion of heme oxygenase 2 reveals neural role for carbon monoxide. Proc Natl Acad Sci U S A 94(26):14848-53. [PubMed: 9405702]  [MGI Ref ID J:89562]

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.

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.

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* $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.

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
   001800 FVB/NJ
 
  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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