Strain Name:

FVB.129S2(B6)-Hmox1tm1Poss/J

Stock Number:

008311

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Availability:

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Use Restrictions Apply, see Terms of Use
Mice that are homozygous for this Hmox1 (heme oxygenase (decycling) 1) targeted mutation develop anemia with diminished serum iron, increased serum ferritin, iron accumulation in kidney and liver and progressive chronic inflammatory disease. Homozygotes occur at a lower than expected frequency, or are not produced, from heterozygous crosses and have decreased postnatal survival. This mutant mouse strain may be useful in studies of hemochromatosis, inflammation and iron metabolism.

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 Stock; 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
Mice that are homozygous for this targeted mutation are slightly smaller in size than wildtype littermates and exhibit poor grooming and hypoactivity. As early as 20 weeks of age, homozygotes develop anemia with diminished serum iron and increased serum ferritin. Histological analysis reveals iron accumulation in kidney and liver. Elevated oxidized proteins and lipid peroxidation develop in the liver and kidney. Homozygotes develop progressive chronic inflammatory disease, including enlarged spleen and lymph nodes, inflammatory infiltrates, glomerulonephritis, fibrosis. Homozygous male mice have smaller testis than wildtype controls. Homozygotes occur at a lower than expected frequency, or are not produced, from heterozygous crosses and have decreased postnatal survival. An almost undetectable abnormal gene product (mRNA) is detected by Northern blot analysis of total splenic RNA. This mutant mouse strain may be useful in studies of hemochromatosis, inflammation and iron metabolism.

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 PGK-neo cassette was used to disrupt 3.7kb of sequence containing exons 3, 4 and part of exon 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 chimeric animals were crossed to C57BL/6 mice, and then backcrossed to FVB for 10 generations.

Control Information

  Control
   Wild-type from the colony
   001800 FVB/NJ
 
  Considerations for Choosing Controls

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Heme Oxygenase 1 Deficiency; HMOX1D   (HMOX1)
Pulmonary Disease, Chronic Obstructive; COPD   (HMOX1)
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.

Hmox1tm1Poss/Hmox1tm1Poss

        involves: 129S2/SvPas * C57BL/6
  • mortality/aging
  • partial postnatal lethality
    • homozygotes exhibit low postnatal survival, with only 20% of the expected number of homozygotes obtained at 3 weeks; a similar survival % is observed in matings between homozygous and heterozygous mutant mice   (MGI Ref ID J:79254)
    • percentage of surviving homozygotes can be increased to 48% of those expected by in vitro fertilization techniques using gametes from homozygous and heterozygous animals   (MGI Ref ID J:79254)
  • premature death
    • post-weaning survivors commonly die after 25 weeks of age; one homozygote lived up to 22 months   (MGI Ref ID J:79254)
  • hematopoietic system phenotype
  • abnormal leukocyte cell number
    • adult homozygotes exhibit high peripheral white blood cell counts   (MGI Ref ID J:79254)
  • abnormal splenic cell ratio
    • adult homozygotes display high splenic CD4+:CD8+ T-cell ratios with numerous activated CD4+ T cells   (MGI Ref ID J:79254)
  • anisocytosis
    • by 20 weeks of age, homozygotes exhibit variable erythrocyte size on blood smears   (MGI Ref ID J:79254)
  • decreased erythrocyte cell number
    • at 10 (but not at 6) weeks of age, homozygotes start displaying significantly lower red blood cell counts relative to wild-type mice   (MGI Ref ID J:79254)
  • decreased hematocrit
    • at 10 weeks of age, homozygotes start displaying significantly reduced hematocrits relative to wild-type mice   (MGI Ref ID J:79254)
  • decreased hemoglobin content
    • at 10 (but not at 6) weeks of age, homozygotes start displaying significantly reduced blood hemoglobin concentrations relative to wild-type mice   (MGI Ref ID J:79254)
  • decreased mean corpuscular volume
    • at 10 weeks of age, homozygotes start displaying extremely reduced mean corpuscular volumes relative to wild-type mice   (MGI Ref ID J:79254)
  • enlarged spleen
    • adult homozygotes exhibit enlarged spleens due to both extramedullary hematopoiesis and follicular hyperplasia   (MGI Ref ID J:79254)
    • spleen hyperplasia
      • adult homozygotes display spleen follicular hyperplasia   (MGI Ref ID J:79254)
  • extramedullary hematopoiesis
    • adult homozygotes exhibit extramedullary hematopoiesis   (MGI Ref ID J:79254)
  • microcytic anemia
    • at 20-24 weeks of age, homozygotes display normochromic and microcytic anemia which becomes severe by 40-55 weeks of age   (MGI Ref ID J:79254)
  • homeostasis/metabolism phenotype
  • abnormal iron homeostasis
    • by 20 weeks of age, homozygotes exhibit an increased total iron-binding capacity (high serum transferrin levels), resulting in a reduced iron saturation percentage and increased iron deposition relative to wild-type mice   (MGI Ref ID J:79254)
    • by ~50 weeks of age, all homozygotes exhibit pathological iron-loading (nonheme iron deposits) in renal proximal cortical tubules, liver Kupffer cells, hepatocytes, and hepatic vascular tissue (with variable severity) while the spleen remains unaffected   (MGI Ref ID J:79254)
    • decreased circulating iron level
      • by 20 weeks of age, homozygotes display significantly reduced serum iron levels relative to wild-type mice   (MGI Ref ID J:79254)
  • increased blood urea nitrogen level
    • at day 3 after cisplatin administration, homozygotes exhibit significantly increased BUN values, indicating exacerbated renal dysfunction relative to similarly treated wild-type mice; no significant differences in body weight reduction are observed   (MGI Ref ID J:62437)
  • increased circulating ferritin level
    • despite iron deficiency, homozygotes exhibit progressively increasing serum ferritin levels up to ~50 weeks of age   (MGI Ref ID J:79254)
  • immune system phenotype
  • abnormal leukocyte cell number
    • adult homozygotes exhibit high peripheral white blood cell counts   (MGI Ref ID J:79254)
  • abnormal lymph node cell ratio
    • adult homozygotes display high lymph node CD4+:CD8+ T-cell ratios with numerous activated CD4+ T cells   (MGI Ref ID J:79254)
  • abnormal splenic cell ratio
    • adult homozygotes display high splenic CD4+:CD8+ T-cell ratios with numerous activated CD4+ T cells   (MGI Ref ID J:79254)
  • chronic inflammation
    • homozygotes develop a progressive chronic inflammatory disease   (MGI Ref ID J:79254)
  • enlarged lymph nodes   (MGI Ref ID J:79254)
  • enlarged spleen
    • adult homozygotes exhibit enlarged spleens due to both extramedullary hematopoiesis and follicular hyperplasia   (MGI Ref ID J:79254)
    • spleen hyperplasia
      • adult homozygotes display spleen follicular hyperplasia   (MGI Ref ID J:79254)
  • glomerulonephritis
    • at ~50 weeks, homozygotes display glomerulonephritis, caused either by iron toxicity or by deposition of immune complexes   (MGI Ref ID J:79254)
  • liver inflammation
    • at ~50 weeks of age, homozygotes show hepatic inflammatory cell infiltrates, consisting of lymphocytes, plasma cells, neutrophils, and macrophages   (MGI Ref ID J:79254)
    • many infiltrates are periportal while others show a predilection for the portal venous tissue which often contains iron deposits   (MGI Ref ID J:79254)
    • hepatic vascular lesions invlove the proliferation of smooth muscle, the infiltration of neutrophils and lymphocytes into the vessel wall, and adherence of monocytes to the inner vessel wall   (MGI Ref ID J:79254)
  • lung inflammation
    • at ~50 weeks of age, homozygotes occasionally exhibit vascular and perivascular infiltrates in their lungs   (MGI Ref ID J:79254)
  • renal/urinary system phenotype
  • glomerular crescent
    • by ~75 weeks, homozygotes display glomerular crescent formation   (MGI Ref ID J:79254)
  • glomerulonephritis
    • at ~50 weeks, homozygotes display glomerulonephritis, caused either by iron toxicity or by deposition of immune complexes   (MGI Ref ID J:79254)
  • glomerulosclerosis
    • by ~75 weeks, homozygotes display severely damaged glomeruli with membranous proliferation, lobularity, crescent formation, and sclerosis   (MGI Ref ID J:79254)
  • increased renal tubule apoptosis
    • at day 3 after cisplatin administration, homozygotes display a 6.6-fold increase in renal tubular apoptosis whereas wild-type mice show a 3-fold increase over saline-treated mice, respectively   (MGI Ref ID J:62437)
  • kidney failure
    • at day 3 after cisplatin-induced renal injury, homozygotes develop more severe renal failure than wild-type mice   (MGI Ref ID J:62437)
  • proximal convoluted tubule brush border loss
    • at day 3 after cisplatin-induced renal injury, homozygotes display more severe loss of brush border than wild-type mice   (MGI Ref ID J:62437)
  • renal cast
    • at day 3 after cisplatin-induced renal injury, homozygotes display tubular casts   (MGI Ref ID J:62437)
  • renal tubular necrosis
    • at day 3, cisplatin-treated homozygotes exhibit severe changes in acute renal injury, including tubular necrosis, degeneration, loss of brush border, red cell extravasation, tubular casts, and apoptotic bodies in the proximal and distal tubules; in contrast, wild-type mice display only mild changes with loss of brush border and red cell extravasation   (MGI Ref ID J:62437)
  • liver/biliary system phenotype
  • liver fibrosis
    • at ~50 weeks of age, homozygotes display fibrosis within hepatic inflammatory cell infiltrates   (MGI Ref ID J:79254)
    • regenerative nodules indicative of hepatic injury are occasionally observed   (MGI Ref ID J:79254)
  • liver inflammation
    • at ~50 weeks of age, homozygotes show hepatic inflammatory cell infiltrates, consisting of lymphocytes, plasma cells, neutrophils, and macrophages   (MGI Ref ID J:79254)
    • many infiltrates are periportal while others show a predilection for the portal venous tissue which often contains iron deposits   (MGI Ref ID J:79254)
    • hepatic vascular lesions invlove the proliferation of smooth muscle, the infiltration of neutrophils and lymphocytes into the vessel wall, and adherence of monocytes to the inner vessel wall   (MGI Ref ID J:79254)
  • behavior/neurological phenotype
  • hypoactivity
    • as early as 25 weeks of age, most post-weaning survivors appear less active than wild-type mice   (MGI Ref ID J:79254)
  • poor grooming
    • as early as 25 weeks of age, most post-weaning survivors exhibit poor grooming   (MGI Ref ID J:79254)
  • growth/size/body phenotype
  • decreased body size
    • homozygotes are slightly smaller than wild-type or heterozygous littermates from birth to early adulthood   (MGI Ref ID J:79254)
    • cachexia
      • between 20 and 40 weeks of age, most surviving homozygotes exhibit significant weight loss indicative of wasting   (MGI Ref ID J:79254)
  • cellular phenotype
  • increased renal tubule apoptosis
    • at day 3 after cisplatin administration, homozygotes display a 6.6-fold increase in renal tubular apoptosis whereas wild-type mice show a 3-fold increase over saline-treated mice, respectively   (MGI Ref ID J:62437)
  • oxidative stress
    • as a result of iron deposition, livers from 20-24-wk-old homozygotes display increased oxidized proteins and lipid peroxidation values of 51% and 95% while kidneys show increases of 69% and 74% relative to heterozygous values, respectively   (MGI Ref ID J:79254)
    • notably, mutant brains, which have no iron deposition, show no evidence of enhanced oxidative damage   (MGI Ref ID J:79254)
  • reproductive system phenotype
  • infertility
    • as early as 25 weeks of age, most post-weaning survivors breed poorly   (MGI Ref ID J:79254)
    • mating pairs of homozygous mutant mice fail to yield viable litters   (MGI Ref ID J:79254)
  • small testis
    • mature male homozygotes show a ~25% reduction in testicular size relative to similarly sized heterozygotes   (MGI Ref ID J:79254)
  • endocrine/exocrine gland phenotype
  • small testis
    • mature male homozygotes show a ~25% reduction in testicular size relative to similarly sized heterozygotes   (MGI Ref ID J:79254)
  • respiratory system phenotype
  • lung inflammation
    • at ~50 weeks of age, homozygotes occasionally exhibit vascular and perivascular infiltrates in their lungs   (MGI Ref ID J:79254)
View Research Applications

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

Hematological Research
Anemia, Iron Deficiency and Transport Defects
      hemochromatosis

Immunology, Inflammation and Autoimmunity Research
Inflammation

Internal/Organ Research
Liver Defects
      hemochromatosis

Metabolism Research
Hemochromatosis
      iron metabolism defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Hmox1tm1Poss
Allele Name targeted mutation 1, Kenneth D Poss
Allele Type Targeted (knock-out)
Common Name(s) HO-1-; HO1-; Hmox1-;
Mutation Made By Kenneth Poss,   Massachusetts Institute of Technology
Strain of Origin129S2/SvPas
ES Cell Line NameD3
ES Cell Line Strain129S2/SvPas
Gene Symbol and Name Hmox1, heme oxygenase (decycling) 1
Chromosome 8
Gene Common Name(s) D8Wsu38e; DNA segment, Chr 8, Wayne State University 38, expressed; HMOX1D; HO-1; HO1; HSP32; Hmox; bK286B10; heme oxygenase 1; hemoxygenase;
General Note Phenotypic Similarity to Human Syndrome: Iron overload disorders including Hemochromatosis and Anemia of chronic inflammation in homozygous mice (J:79254)
Molecular Note A 3.7 kb fragment encompassing exons 3, 4, and a portion of 5 was replaced with a neomycin selection cassette. The deleted region consisted of approximately 85% of the coding region (226 residues). A low level of aberrantly spliced transcript was identified in homozygous mutant mice by Northern blot analysis of total splenic RNA. [MGI Ref ID J:79254]

Genotyping

Genotyping Information

Genotyping Protocols

Hmox1tm1Poss,

MELT


Hmox1tm1Poss, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Poss KD; Tonegawa S. 1997. Heme oxygenase 1 is required for mammalian iron reutilization. Proc Natl Acad Sci U S A 94(20):10919-24. [PubMed: 9380735]  [MGI Ref ID J:79254]

Additional References

Hmox1tm1Poss related

Ahmad AS; Zhuang H; Dore S. 2006. Heme oxygenase-1 protects brain from acute excitotoxicity. Neuroscience 141(4):1703-8. [PubMed: 16828975]  [MGI Ref ID J:113162]

Brines R; Maicas N; Ferrandiz ML; Loboda A; Jozkowicz A; Dulak J; Alcaraz MJ. 2012. Heme oxygenase-1 regulates the progression of K/BxN serum transfer arthritis. PLoS One 7(12):e52435. [PubMed: 23285041]  [MGI Ref ID J:195761]

Cao YA; Wagers AJ; Karsunky H; Zhao H; Reeves R; Wong RJ; Stevenson DK; Weissman IL; Contag CH. 2008. Heme oxygenase-1 deficiency leads to disrupted response to acute stress in stem cells and progenitors. Blood 112(12):4494-502. [PubMed: 18509090]  [MGI Ref ID J:141811]

Chen B; Guo L; Fan C; Bolisetty S; Joseph R; Wright MM; Agarwal A; George JF. 2009. Carbon monoxide rescues heme oxygenase-1-deficient mice from arterial thrombosis in allogeneic aortic transplantation. Am J Pathol 175(1):422-9. [PubMed: 19498004]  [MGI Ref ID J:150057]

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]

Deshane J; Chen S; Caballero S; Grochot-Przeczek A; Was H; Li Calzi S; Lach R; Hock TD; Chen B; Hill-Kapturczak N; Siegal GP; Dulak J; Jozkowicz A; Grant MB; Agarwal A. 2007. Stromal cell-derived factor 1 promotes angiogenesis via a heme oxygenase 1-dependent mechanism. J Exp Med 204(3):605-18. [PubMed: 17339405]  [MGI Ref ID J:125359]

Ferris CD; Jaffrey SR; Sawa A; Takahashi M; Brady SD; Barrow RK; Tysoe SA; Wolosker H; Baranano DE; Dore S; Poss KD; Snyder SH. 1999. Haem oxygenase-1 prevents cell death by regulating cellular iron. Nat Cell Biol 1(3):152-7. [PubMed: 10559901]  [MGI Ref ID J:59677]

Fortes GB; Alves LS; de Oliveira R; Dutra FF; Rodrigues D; Fernandez PL; Souto-Padron T; De Rosa MJ; Kelliher M; Golenbock D; Chan FK; Bozza MT. 2012. Heme induces programmed necrosis on macrophages through autocrine TNF and ROS production. Blood 119(10):2368-75. [PubMed: 22262768]  [MGI Ref ID J:182541]

George JF; Braun A; Brusko TM; Joseph R; Bolisetty S; Wasserfall CH; Atkinson MA; Agarwal A; Kapturczak MH. 2008. Suppression by CD4+CD25+ regulatory T cells is dependent on expression of heme oxygenase-1 in antigen-presenting cells. Am J Pathol 173(1):154-60. [PubMed: 18511516]  [MGI Ref ID J:137311]

Innamorato NG; Jazwa A; Rojo AI; Garcia C; Fernandez-Ruiz J; Grochot-Przeczek A; Stachurska A; Jozkowicz A; Dulak J; Cuadrado A. 2010. Different susceptibility to the Parkinson's toxin MPTP in mice lacking the redox master regulator Nrf2 or its target gene heme oxygenase-1. PLoS One 5(7):e11838. [PubMed: 20676377]  [MGI Ref ID J:163073]

Juncos JP; Tracz MJ; Croatt AJ; Grande JP; Ackerman AW; Katusic ZS; Nath KA. 2008. Genetic deficiency of heme oxygenase-1 impairs functionality and form of an arteriovenous fistula in the mouse. Kidney Int 74(1):47-51. [PubMed: 18368029]  [MGI Ref ID J:152953]

Kang L; Yamada S; Hernandez MC; Croatt AJ; Grande JP; Juncos JP; Vercellotti GM; Hebbel RP; Katusic ZS; Terzic A; Nath KA. 2011. Regional and systemic hemodynamic responses following the creation of a murine arteriovenous fistula. Am J Physiol Renal Physiol 301(4):F845-51. [PubMed: 21697243]  [MGI Ref ID J:176199]

Kapturczak MH; Wasserfall C; Brusko T; Campbell-Thompson M; Ellis TM; Atkinson MA; Agarwal A. 2004. Heme oxygenase-1 modulates early inflammatory responses: evidence from the heme oxygenase-1-deficient mouse. Am J Pathol 165(3):1045-53. [PubMed: 15331427]  [MGI Ref ID J:92399]

Kovtunovych G; Eckhaus MA; Ghosh MC; Ollivierre-Wilson H; Rouault TA. 2010. Dysfunction of the heme recycling system in heme oxygenase 1-deficient mice: effects on macrophage viability and tissue iron distribution. Blood 116(26):6054-62. [PubMed: 20844238]  [MGI Ref ID J:167405]

Nath KA; Haggard JJ; Croatt AJ; Grande JP; Poss KD; Alam J. 2000. The indispensability of heme oxygenase-1 in protecting against acute heme protein-induced toxicity in vivo. Am J Pathol 156(5):1527-35. [PubMed: 10793064]  [MGI Ref ID J:108237]

Nath KA; d'Uscio LV; Juncos JP; Croatt AJ; Manriquez MC; Pittock ST; Katusic ZS. 2007. An analysis of the DOCA-salt model of hypertension in HO-1-/- mice and the Gunn rat. Am J Physiol Heart Circ Physiol 293(1):H333-42. [PubMed: 17351069]  [MGI Ref ID J:126038]

Orozco LD; Kapturczak MH; Barajas B; Wang X; Weinstein MM; Wong J; Deshane J; Bolisetty S; Shaposhnik Z; Shih DM; Agarwal A; Lusis AJ; Araujo JA. 2007. Heme oxygenase-1 expression in macrophages plays a beneficial role in atherosclerosis. Circ Res 100(12):1703-11. [PubMed: 17495224]  [MGI Ref ID J:137771]

Park DJ; Agarwal A; George JF. 2010. Heme oxygenase-1 expression in murine dendritic cell subpopulations: effect on CD8+ dendritic cell differentiation in vivo. Am J Pathol 176(6):2831-9. [PubMed: 20395442]  [MGI Ref ID J:161159]

Pittock ST; Norby SM; Grande JP; Croatt AJ; Bren GD; Badley AD; Caplice NM; Griffin MD; Nath KA. 2005. MCP-1 is up-regulated in unstressed and stressed HO-1 knockout mice: Pathophysiologic correlates. Kidney Int 68(2):611-22. [PubMed: 16014038]  [MGI Ref ID J:114303]

Regev D; Surolia R; Karki S; Zolak J; Montes-Worboys A; Oliva O; Guroji P; Saini V; Steyn AJ; Agarwal A; Antony VB. 2012. Heme oxygenase-1 promotes granuloma development and protects against dissemination of mycobacteria. Lab Invest 92(11):1541-52. [PubMed: 22964851]  [MGI Ref ID J:190134]

Schulz S; Wong RJ; Jang KY; Kalish F; Chisholm KM; Zhao H; Vreman HJ; Sylvester KG; Stevenson DK. 2013. Heme oxygenase-1 deficiency promotes the development of necrotizing enterocolitis-like intestinal injury in a newborn mouse model. Am J Physiol Gastrointest Liver Physiol 304(11):G991-G1001. [PubMed: 23578787]  [MGI Ref ID J:201203]

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]

Shiraishi F; Curtis LM; Truong L; Poss K; Visner GA; Madsen K; Nick HS; Agarwal A. 2000. Heme oxygenase-1 gene ablation or expression modulates cisplatin-induced renal tubular apoptosis Am J Physiol Renal Physiol 278(5):F726-36. [PubMed: 10807584]  [MGI Ref ID J:62437]

So AY; Garcia-Flores Y; Minisandram A; Martin A; Taganov K; Boldin M; Baltimore D. 2012. Regulation of APC development, immune response, and autoimmunity by Bach1/HO-1 pathway in mice. Blood 120(12):2428-37. [PubMed: 22791292]  [MGI Ref ID J:189161]

Starzynski RR; Canonne-Hergaux F; Lenartowicz M; Krzeptowski W; Willemetz A; Stys A; Bierla J; Pietrzak P; Dziaman T; Lipinski P. 2013. Ferroportin expression in haem oxygenase 1-deficient mice. Biochem J 449(1):69-78. [PubMed: 22992020]  [MGI Ref ID J:192884]

Tracz MJ; Juncos JP; Croatt AJ; Ackerman AW; Grande JP; Knutson KL; Kane GC; Terzic A; Griffin MD; Nath KA. 2007. Deficiency of heme oxygenase-1 impairs renal hemodynamics and exaggerates systemic inflammatory responses to renal ischemia. Kidney Int 72(9):1073-80. [PubMed: 17728706]  [MGI Ref ID J:147529]

Tracz MJ; Juncos JP; Grande JP; Croatt AJ; Ackerman AW; Katusic ZS; Nath KA. 2008. Induction of heme oxygenase-1 is a beneficial response in a murine model of venous thrombosis. Am J Pathol 173(6):1882-90. [PubMed: 18988794]  [MGI Ref ID J:141442]

Tracz MJ; Juncos JP; Grande JP; Croatt AJ; Ackerman AW; Rajagopalan G; Knutson KL; Badley AD; Griffin MD; Alam J; Nath KA. 2007. Renal hemodynamic, inflammatory, and apoptotic responses to lipopolysaccharide in HO-1-/- Mice. Am J Pathol 170(6):1820-30. [PubMed: 17525251]  [MGI Ref ID J:122077]

Tsuchihashi S; Livhits M; Zhai Y; Busuttil RW; Araujo JA; Kupiec-Weglinski JW. 2006. Basal rather than induced heme oxygenase-1 levels are crucial in the antioxidant cytoprotection. J Immunol 177(7):4749-57. [PubMed: 16982915]  [MGI Ref ID J:139311]

Wang J; Dore S. 2008. Heme oxygenase 2 deficiency increases brain swelling and inflammation after intracerebral hemorrhage. Neuroscience 155(4):1133-41. [PubMed: 18674596]  [MGI Ref ID J:140981]

Was H; Sokolowska M; Sierpniowska A; Dominik P; Skrzypek K; Lackowska B; Pratnicki A; Grochot-Przeczek A; Taha H; Kotlinowski J; Kozakowska M; Mazan A; Nowak W; Muchova L; Vitek L; Ratajska A; Dulak J; Jozkowicz A. 2011. Effects of heme oxygenase-1 on induction and development of chemically induced squamous cell carcinoma in mice. Free Radic Biol Med 51(9):1717-26. [PubMed: 21867749]  [MGI Ref ID J:178237]

Zelenay S; Chora A; Soares MP; Demengeot J. 2007. Heme oxygenase-1 is not required for mouse regulatory T cell development and function. Int Immunol 19(1):11-8. [PubMed: 17082514]  [MGI Ref ID J:118121]

Zeynalov E; Shah ZA; Li RC; Dore S. 2009. Heme oxygenase 1 is associated with ischemic preconditioning-induced protection against brain ischemia. Neurobiol Dis 35(2):264-9. [PubMed: 19465127]  [MGI Ref ID J:150431]

Zhao H; Azuma J; Kalish F; Wong RJ; Stevenson DK. 2011. Maternal heme oxygenase 1 regulates placental vasculature development via angiogenic factors in mice. Biol Reprod 85(5):1005-12. [PubMed: 21778140]  [MGI Ref ID J:182790]

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 heterozygotes. Fewer than expected or no homozygotes are produced from heterozygote crosses.

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* $2085.00
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 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* $2710.50
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 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
   Wild-type from the colony
   001800 FVB/NJ
 
  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


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

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.


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