Strain Name:

B6;129S-Sod1tm1Leb/J

Stock Number:

002972

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Availability:

Repository- Live

Homozygous SOD1m1BCM knock-out mice mice are characterized by abnormal retinal and cochlear ganglions, and they have age-related defects in hearing, vasculature, and muscle. These mice may be useful in studying retinal dysfunction, autoimmunity, female reproductive development/function, glaucoma, hearing loss, Alzheimer's Disease, familial amyotrophic lateral sclerosis (ALS), and other age-related disorders.

Description

Strain Information

Former Names B6;129S7-Sod1tm1Leb/J    (Changed: 05-OCT-12 )
Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Mating SystemHeterozygote x Heterozygote         (Female x Male)   01-MAR-06
Specieslaboratory mouse
Generation{F?+8p}N2F11 (13-JAN-09)
Generation Definitions
 
Donating InvestigatorDr. Russell Lebovitz,   SUMA Partners

Appearance
black
Related Genotype: a/a

Description
The SOD1m1BCM knock-out allele disrupts exons 1 and 2 of the targeted gene. No protein expression from the targeted locus is detected in brain tissues. Heterozygous mice are viable and fertile. While homozygous males reproduce normally, homozygous females are infertile. Homozygous mice have abnormalities of the retinal ganglion, cochlear ganglion, and female reproductive development/function. Homozygous mice also exhibit age-related deafness, accelerated vascular aging and age-related skeletal muscle defects. These mutant mice may be useful in studying retinal dysfunction, autoimmunity, glaucoma, hearing loss, Alzheimer's Disease, familial amyotrophic lateral sclerosis (ALS), and other age-related disorders.

Development
A targeting construct was designed to delete exons 1 and 2 of the targeted gene with a PGK-HPRT expression cassette. This construct was electroporated into 129S7/SvEvBrd-Hprtb-m2-derived AB2.1 embryonic stem (ES) cells. The resulting mutant mice (SOD1m1BCM) were on a mixed C57BL/6;129SvEv genetic background when they arrived at The Jackson Laboratory Repository in 1997. Upon arrival, mutant mice were bred together, and then to B6129SF1/J (Stock No. 101043) for one generation. After this, heterozygous mice were bred together to maintain the colony.

Control Information

  Control
   Wild-type from the colony
   101043 B6129SF1/J (approximate)
   101045 B6129SF2/J (approximate)
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Sod1tm1Leb allele
003881   B6.129S7-Sod1tm1Leb/DnJ
View Strains carrying   Sod1tm1Leb     (1 strain)

Strains carrying other alleles of Sod1
004140   B6.SOD1-Sod1c/CjeDnJ
005110   FVB-Tg(Sod1*G86R)M1Jwg/J
View Strains carrying other alleles of Sod1     (2 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
Glaucoma, Normal Tension, Susceptibility to
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Amyotrophic Lateral Sclerosis 1; ALS1   (SOD1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Sod1tm1Leb/Sod1+

        B6;129S-Sod1tm1Leb/J
  • nervous system phenotype
  • cochlear ganglion degeneration
    • contrary to previous findings, heterozygotes display no significant differences in ABR thresholds relative to wild-type mice at any age or any frequency tested   (MGI Ref ID J:102419)
    • no degenerative changes are noted in the heterozygous stria vascularis even at 18 months of age   (MGI Ref ID J:102419)
    • however, unlike wild-type mice, aging heterozygotes show a decrease in ganglion cell density at 15 months   (MGI Ref ID J:102419)

Sod1tm1Leb/Sod1tm1Leb

        B6;129S-Sod1tm1Leb/J
  • hearing/vestibular/ear phenotype
  • deafness
    • at 12 and 15 months, homozygotes exhibit an earlier and significantly greater hearing loss than age-matched C57BL/6, wild-type or heterozygous mice   (MGI Ref ID J:102419)
  • increased or absent threshold for auditory brainstem response
    • at 12 and 15 months, homozygotes exhibit significantly increased ABR thresholds for clicks and tone pip stimuli at 8, 16 and 32 kHz relative to C57BL/6, wild-type or heterozygous mice; however, no differences are noted at 7-9 months   (MGI Ref ID J:102419)
    • at 12 months, homozygotes show an ~20 dB elevation in ABR thresholds at 32 kHz relative to C57BL/6 control mice; the latter have ABR thresholds that are ~10 dB higher than those in wild-type or heterozygous mice   (MGI Ref ID J:102419)
  • thin stria vascularis
    • at 15 months, homozygotes display a significantly thinner stria vascularis in the apical turn relative to heterozygous or wild-type mice   (MGI Ref ID J:102419)
    • however, no differences in stria vascularis thickness are noted in the apical turn at 7-9 months   (MGI Ref ID J:102419)
  • nervous system phenotype
  • cochlear ganglion degeneration
    • starting at 7-9 months, homozygotes display severe progressive degeneration of spiral ganglion cells in all cochlear turns   (MGI Ref ID J:102419)
    • in homozygotes, the magnitude of ganglion cell loss is greater than that of C57BL/6 control mice, esp. above the basal turn   (MGI Ref ID J:102419)
  • decreased retinal ganglion cell number
    • number of cells in the retinal ganglion cell layer is reduced in 24 week old mutants but not at 8 weeks of age, indicating a progressive reduction   (MGI Ref ID J:181434)
    • however, photoreceptor cell death is not seen at 24 weeks of age   (MGI Ref ID J:181434)
  • vision/eye phenotype
  • abnormal eye electrophysiology
    • the amplitude of pattern electroretinogram (ERG) is reduced in 24 week old mutants, although dark-adapted and cone ERGs show no impairment, indicating impaired function of retinal ganglion cells   (MGI Ref ID J:181434)
    • however, the intraocular pressure is normal   (MGI Ref ID J:181434)
  • abnormal retinal ganglion layer morphology
    • level of reactive oxygen species (ROS) in the retinal ganglion cell layer is higher in 24-week old mutants than in wild-type mice   (MGI Ref ID J:181434)
    • decreased retinal ganglion cell number
      • number of cells in the retinal ganglion cell layer is reduced in 24 week old mutants but not at 8 weeks of age, indicating a progressive reduction   (MGI Ref ID J:181434)
      • however, photoreceptor cell death is not seen at 24 weeks of age   (MGI Ref ID J:181434)
  • abnormal retinal nerve fiber layer morphology
    • 24 week old mutants exhibit thinning of the nerve fiber layer   (MGI Ref ID J:181434)

Sod1tm1Leb/Sod1tm1Leb

        involves: 129S7/SvEvBrd * C57BL/6
  • reproductive system phenotype
  • abnormal ovary morphology
    • at 12 weeks of age, increased stromal cell proliferation is noted in the center of the mutant ovary   (MGI Ref ID J:64299)
    • decreased corpora lutea number   (MGI Ref ID J:64299)
    • decreased mature ovarian follicle number
      • while normal-appearing primary follicles and some small antral follicles are present, only a few large antral follicles and corpora lutea are observed   (MGI Ref ID J:64299)
    • impaired ovarian folliculogenesis
      • at 6-12 weeks of age, female homozygotes show limited follicular development beyond the early antral follicle stage   (MGI Ref ID J:64299)
    • small ovary
      • homozygous mutant ovaries are often smaller than wild-type ovaries   (MGI Ref ID J:64299)
  • decreased litter size
    • over a 2-6 month period, female homozygotes produced a significantly decreased average litter size relative to female heterozygotes (2.7 vs 8.6 offspring/litter, respectively)   (MGI Ref ID J:64299)
  • female infertility
    • 5 of 16 female homozygotes failed to become pregnant over a 2-6 month period   (MGI Ref ID J:64299)
  • reduced female fertility
    • female homozygotes survive to adulthood and appear to show normal sexual differentiation but are subfertile   (MGI Ref ID J:64299)
    • whereas breeding of 5 female heterozygotes with male heterozygotes over a 6 month period produced an average of 1.0 litter/month, only 11 of 16 female homozygotes became pregnant over a 2-6 month period averaging 0.23 litters/month   (MGI Ref ID J:64299)
    • however, mutant and control females were shown to produce a similar number of eggs upon pharmacological superovulation   (MGI Ref ID J:64299)
    • in contrast to females, male homozygotes are fertile with normal testicular morphology   (MGI Ref ID J:64299)
  • endocrine/exocrine gland phenotype
  • abnormal ovary morphology
    • at 12 weeks of age, increased stromal cell proliferation is noted in the center of the mutant ovary   (MGI Ref ID J:64299)
    • decreased corpora lutea number   (MGI Ref ID J:64299)
    • decreased mature ovarian follicle number
      • while normal-appearing primary follicles and some small antral follicles are present, only a few large antral follicles and corpora lutea are observed   (MGI Ref ID J:64299)
    • impaired ovarian folliculogenesis
      • at 6-12 weeks of age, female homozygotes show limited follicular development beyond the early antral follicle stage   (MGI Ref ID J:64299)
    • small ovary
      • homozygous mutant ovaries are often smaller than wild-type ovaries   (MGI Ref ID J:64299)
  • homeostasis/metabolism phenotype
  • decreased circulating luteinizing hormone level
    • adult female homozygotes exhibit suppressed serum LH levels relative to control females (17.4 +/- 3.0 ng/ml vs 57.8 +/- 17.7 ng/ml, respectively), as shown by RIA analysis   (MGI Ref ID J:64299)
  • suppressed circulating follicle stimulating hormone level
    • adult female homozygotes exhibit suppressed serum FSH levels relative to control females (38.5 +/- 3.1 ng/ml vs 105.0 +/- 17.3 ng/ml, respectively), as shown by RIA analysis   (MGI Ref ID J:64299)
View Research Applications

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

Sensorineural Research
Eye Defects
      hereditary glaucoma

Sod1tm1Leb related

Metabolism Research

Neurobiology Research
Metabolic Defects
Neurodegeneration

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Sod1tm1Leb
Allele Name targeted mutation 1, Russell M Lebovitz
Allele Type Targeted (Null/Knockout)
Common Name(s) Cu,Zn-SOD-; CuZnSOD-; SOD1-; SOD1m1BCM;
Mutation Made ByDr. Russell Lebovitz,   SUMA Partners
Strain of Origin129S7/SvEvBrd-Hprt
ES Cell Line NameAB2.1
ES Cell Line Strain129S7/SvEvBrd-Hprt
Gene Symbol and Name Sod1, superoxide dismutase 1, soluble
Chromosome 16
Gene Common Name(s) ALS; ALS1; B430204E11Rik; Cu(2+)-Zn2+ superoxide dismutase; Cu/Zn-SOD; CuZnSOD; HEL-S-44; IPOA; Ipo-1; Ipo1; RIKEN cDNA B430204E11 gene; SOD; SODC; Sod-1; hSod1; homodimer; indophenol oxidase;
Molecular Note Replacement of exons 1 and 2 with a PGK-hprt expression cassette. Protein was not detected in brain of homozygous mutant mice. [MGI Ref ID J:64299]

Genotyping

Genotyping Information

Genotyping Protocols

Sod1tm1Leb, Melt Curve Analysis


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Matzuk MM; Dionne L; Guo Q; Kumar TR; Lebovitz RM. 1998. Ovarian function in superoxide dismutase 1 and 2 knockout mice. Endocrinology 139(9):4008-11. [PubMed: 9724058]  [MGI Ref ID J:64299]

Additional References

Morikawa K; Shimokawa H; Matoba T; Kubota H; Akaike T; Talukder MA; Hatanaka M; Fujiki T; Maeda H; Takahashi S; Takeshita A. 2003. Pivotal role of Cu,Zn-superoxide dismutase in endothelium-dependent hyperpolarization. J Clin Invest 112(12):1871-9. [PubMed: 14679182]  [MGI Ref ID J:86950]

Sod1tm1Leb related

Akhtar S; Grizenkova J; Wenborn A; Hummerich H; Fernandez de Marco M; Brandner S; Collinge J; Lloyd SE. 2013. Sod1 deficiency reduces incubation time in mouse models of prion disease. PLoS One 8(1):e54454. [PubMed: 23349894]  [MGI Ref ID J:195841]

Asimakis GK; Lick S; Patterson C. 2002. Postischemic recovery of contractile function is impaired in SOD2(+/-) but not SOD1(+/-) mouse hearts. Circulation 105(8):981-6. [PubMed: 11864929]  [MGI Ref ID J:103317]

Baumbach GL; Didion SP; Faraci FM. 2006. Hypertrophy of cerebral arterioles in mice deficient in expression of the gene for CuZn superoxide dismutase. Stroke 37(7):1850-5. [PubMed: 16763183]  [MGI Ref ID J:136409]

Carlstrom M; Brown RD; Sallstrom J; Larsson E; Zilmer M; Zabihi S; Eriksson UJ; Persson AE. 2009. SOD1 deficiency causes salt sensitivity and aggravates hypertension in hydronephrosis. Am J Physiol Regul Integr Comp Physiol 297(1):R82-92. [PubMed: 19403858]  [MGI Ref ID J:150216]

Cooke CL; Davidge ST. 2003. Endothelial-dependent vasodilation is reduced in mesenteric arteries from superoxide dismutase knockout mice. Cardiovasc Res 60(3):635-42. [PubMed: 14659809]  [MGI Ref ID J:162746]

Didion SP; Kinzenbaw DA; Faraci FM. 2005. Critical role for CuZn-superoxide dismutase in preventing angiotensin II-induced endothelial dysfunction. Hypertension 46(5):1147-53. [PubMed: 16216984]  [MGI Ref ID J:135455]

Didion SP; Ryan MJ; Didion LA; Fegan PE; Sigmund CD; Faraci FM. 2002. Increased superoxide and vascular dysfunction in CuZnSOD-deficient mice. Circ Res 91(10):938-44. [PubMed: 12433839]  [MGI Ref ID J:109001]

Groleau J; Dussault S; Haddad P; Turgeon J; Menard C; Chan JS; Rivard A. 2010. Essential role of copper-zinc superoxide dismutase for ischemia-induced neovascularization via modulation of bone marrow-derived endothelial progenitor cells. Arterioscler Thromb Vasc Biol 30(11):2173-81. [PubMed: 20724700]  [MGI Ref ID J:182101]

Groleau J; Dussault S; Turgeon J; Haddad P; Rivard A. 2011. Accelerated vascular aging in CuZnSOD-deficient mice: impact on EPC function and reparative neovascularization. PLoS One 6(8):e23308. [PubMed: 21858065]  [MGI Ref ID J:176492]

Harraz MM; Marden JJ; Zhou W; Zhang Y; Williams A; Sharov VS; Nelson K; Luo M; Paulson H; Schoneich C; Engelhardt JF. 2008. SOD1 mutations disrupt redox-sensitive Rac regulation of NADPH oxidase in a familial ALS model. J Clin Invest 118(2):659-70. [PubMed: 18219391]  [MGI Ref ID J:131850]

Hashizume K; Hirasawa M; Imamura Y; Noda S; Shimizu T; Shinoda K; Kurihara T; Noda K; Ozawa Y; Ishida S; Miyake Y; Shirasawa T; Tsubota K. 2008. Retinal dysfunction and progressive retinal cell death in SOD1-deficient mice. Am J Pathol 172(5):1325-31. [PubMed: 18372426]  [MGI Ref ID J:134267]

He C; Ryan AJ; Murthy S; Carter AB. 2013. Accelerated development of pulmonary fibrosis via Cu,Zn-superoxide dismutase-induced alternative activation of macrophages. J Biol Chem 288(28):20745-57. [PubMed: 23720777]  [MGI Ref ID J:201791]

Imamura Y; Noda S; Hashizume K; Shinoda K; Yamaguchi M; Uchiyama S; Shimizu T; Mizushima Y; Shirasawa T; Tsubota K. 2006. Drusen, choroidal neovascularization, and retinal pigment epithelium dysfunction in SOD1-deficient mice: a model of age-related macular degeneration. Proc Natl Acad Sci U S A 103(30):11282-7. [PubMed: 16844785]  [MGI Ref ID J:111796]

Ishii T; Matsuki S; Iuchi Y; Okada F; Toyosaki S; Tomita Y; Ikeda Y; Fujii J. 2005. Accelerated impairment of spermatogenic cells in SOD1-knockout mice under heat stress. Free Radic Res 39(7):697-705. [PubMed: 16036348]  [MGI Ref ID J:114348]

Iuchi Y; Kibe N; Tsunoda S; Suzuki S; Mikami T; Okada F; Uchida K; Fujii J. 2010. Implication of oxidative stress as a cause of autoimmune hemolytic anemia in NZB mice. Free Radic Biol Med 48(7):935-44. [PubMed: 20079426]  [MGI Ref ID J:158021]

Iuchi Y; Okada F; Onuma K; Onoda T; Asao H; Kobayashi M; Fujii J. 2007. Elevated oxidative stress in erythrocytes due to a SOD1 deficiency causes anaemia and triggers autoantibody production. Biochem J 402(2):219-27. [PubMed: 17059387]  [MGI Ref ID J:118550]

Iuchi Y; Okada F; Takamiya R; Kibe N; Tsunoda S; Nakajima O; Toyoda K; Nagae R; Suematsu M; Soga T; Uchida K; Fujii J. 2009. Rescue of anaemia and autoimmune responses in SOD1-deficient mice by transgenic expression of human SOD1 in erythrocytes. Biochem J 422(2):313-20. [PubMed: 19515016]  [MGI Ref ID J:154894]

Johnson KR; Yu H; Ding D; Jiang H; Gagnon LH; Salvi RJ. 2010. Separate and combined effects of Sod1 and Cdh23 mutations on age-related hearing loss and cochlear pathology in C57BL/6J mice. Hear Res 268(1-2):85-92. [PubMed: 20470874]  [MGI Ref ID J:163035]

Keithley EM; Canto C; Zheng QY; Wang X; Fischel-Ghodsian N; Johnson KR. 2005. Cu/Zn superoxide dismutase and age-related hearing loss. Hear Res 209(1-2):76-85. [PubMed: 16055286]  [MGI Ref ID J:102419]

Kessova IG; Cederbaum AI. 2007. Mitochondrial alterations in livers of Sod1-/- mice fed alcohol. Free Radic Biol Med 42(10):1470-80. [PubMed: 17448893]  [MGI Ref ID J:121616]

Kostrominova TY. 2010. Advanced age-related denervation and fiber-type grouping in skeletal muscle of SOD1 knockout mice. Free Radic Biol Med 49(10):1582-93. [PubMed: 20800676]  [MGI Ref ID J:165857]

Kubota M; Shimmura S; Kubota S; Miyashita H; Kato N; Noda K; Ozawa Y; Usui T; Ishida S; Umezawa K; Kurihara T; Tsubota K. 2011. Hydrogen and N-acetyl-L-cysteine rescue oxidative stress-induced angiogenesis in a mouse corneal alkali-burn model. Invest Ophthalmol Vis Sci 52(1):427-33. [PubMed: 20847117]  [MGI Ref ID J:171558]

Kurahashi T; Konno T; Otsuki N; Kwon M; Tsunoda S; Ito J; Fujii J. 2012. A malfunction in triglyceride transfer from the intracellular lipid pool to apoB in enterocytes of SOD1-deficient mice. FEBS Lett 586(24):4289-95. [PubMed: 23098755]  [MGI Ref ID J:191746]

Meissner F; Molawi K; Zychlinsky A. 2008. Superoxide dismutase 1 regulates caspase-1 and endotoxic shock. Nat Immunol 9(8):866-72. [PubMed: 18604212]  [MGI Ref ID J:137865]

Morikawa K; Shimokawa H; Matoba T; Kubota H; Akaike T; Talukder MA; Hatanaka M; Fujiki T; Maeda H; Takahashi S; Takeshita A. 2003. Pivotal role of Cu,Zn-superoxide dismutase in endothelium-dependent hyperpolarization. J Clin Invest 112(12):1871-9. [PubMed: 14679182]  [MGI Ref ID J:86950]

Murakami K; Inagaki J; Saito M; Ikeda Y; Tsuda C; Noda Y; Kawakami S; Shirasawa T; Shimizu T. 2009. Skin atrophy in cytoplasmic SOD-deficient mice and its complete recovery using a vitamin C derivative. Biochem Biophys Res Commun 382(2):457-61. [PubMed: 19289104]  [MGI Ref ID J:148029]

Murakami K; Murata N; Noda Y; Tahara S; Kaneko T; Kinoshita N; Hatsuta H; Murayama S; Barnham KJ; Irie K; Shirasawa T; Shimizu T. 2011. SOD1 (Copper/Zinc Superoxide Dismutase) Deficiency Drives Amyloid beta Protein Oligomerization and Memory Loss in Mouse Model of Alzheimer Disease. J Biol Chem 286(52):44557-68. [PubMed: 22072713]  [MGI Ref ID J:178835]

Noda Y; Ota K; Shirasawa T; Shimizu T. 2012. Copper/zinc superoxide dismutase insufficiency impairs progesterone secretion and fertility in female mice. Biol Reprod 86(1):1-8. [PubMed: 21900685]  [MGI Ref ID J:185784]

Ramiro-Diaz JM; Nitta CH; Maston LD; Codianni S; Giermakowska W; Resta TC; Bosc LV. 2013. NFAT is required for spontaneous pulmonary hypertension in superoxide dismutase 1 knockout mice. Am J Physiol Lung Cell Mol Physiol 304(9):L613-25. [PubMed: 23475768]  [MGI Ref ID J:196362]

Starzynski RR; Canonne-Hergaux F; Willemetz A; Gralak MA; Wolinski J; Stys A; Olszak J; Lipinski P. 2009. Haemolytic anaemia and alterations in hepatic iron metabolism in aged mice lacking Cu,Zn-superoxide dismutase. Biochem J 420(3):383-90. [PubMed: 19296829]  [MGI Ref ID J:151021]

Starzynski RR; Lipinski P; Drapier JC; Diet A; Smuda E; Bartlomiejczyk T; Gralak MA; Kruszewski M. 2005. Down-regulation of iron regulatory protein 1 activities and expression in superoxide dismutase 1 knock-out mice is not associated with alterations in iron metabolism. J Biol Chem 280(6):4207-12. [PubMed: 15557328]  [MGI Ref ID J:96864]

Tsunoda S; Kawano N; Miyado K; Kimura N; Fujii J. 2012. Impaired fertilizing ability of superoxide dismutase 1-deficient mouse sperm during in vitro fertilization. Biol Reprod 87(5):121. [PubMed: 22933517]  [MGI Ref ID J:192481]

Tsunoda S; Kibe N; Kurahashi T; Fujii J. 2013. Differential responses of SOD1-deficient mouse embryonic fibroblasts to oxygen concentrations. Arch Biochem Biophys 537(1):5-11. [PubMed: 23811199]  [MGI Ref ID J:206690]

Usui S; Oveson BC; Iwase T; Lu L; Lee SY; Jo YJ; Wu Z; Choi EY; Samulski RJ; Campochiaro PA. 2011. Overexpression of SOD in retina: Need for increase in H(2)O(2)-detoxifying enzyme in same cellular compartment. Free Radic Biol Med 51(7):1347-54. [PubMed: 21736939]  [MGI Ref ID J:175696]

Yada T; Shimokawa H; Morikawa K; Takaki A; Shinozaki Y; Mori H; Goto M; Ogasawara Y; Kajiya F. 2008. Role of Cu,Zn-SOD in the synthesis of endogenous vasodilator hydrogen peroxide during reactive hyperemia in mouse mesenteric microcirculation in vivo. Am J Physiol Heart Circ Physiol 294(1):H441-8. [PubMed: 18024543]  [MGI Ref ID J:132306]

Yuki K; Ozawa Y; Yoshida T; Kurihara T; Hirasawa M; Ozeki N; Shiba D; Noda K; Ishida S; Tsubota K. 2011. Retinal ganglion cell loss in superoxide dismutase 1 deficiency. Invest Ophthalmol Vis Sci 52(7):4143-50. [PubMed: 21421868]  [MGI Ref ID J:181434]

Yuki K; Yoshida T; Miyake S; Tsubota K; Ozawa Y. 2013. Neuroprotective role of superoxide dismutase 1 in retinal ganglion cells and inner nuclear layer cells against N-methyl-d-aspartate-induced cytotoxicity. Exp Eye Res 115:230-8. [PubMed: 23856406]  [MGI Ref ID J:210406]

Ziv S; Brenner O; Amariglio N; Smorodinsky NI; Galron R; Carrion DV; Zhang W; Sharma GG; Pandita RK; Agarwal M; Elkon R; Katzin N; Bar-Am I; Pandita TK; Kucherlapati R; Rechavi G; Shiloh Y; Barzilai A. 2005. Impaired genomic stability and increased oxidative stress exacerbate different features of Ataxia-telangiectasia. Hum Mol Genet 14(19):2929-43. [PubMed: 16150740]  [MGI Ref ID J:101745]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX11

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, heterozygous mice are bred together, or heterozygous females are bred to homozygous males. Female homozygous mice are infertile, though male homozygous mice reproduce normally. Average litter size is observed. Expected coat color from breeding is white bellied agouti or black.
Mating SystemHeterozygote x Heterozygote         (Female x Male)   01-MAR-06
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $239.00Female or MaleHeterozygous for Sod1tm1Leb  
$239.00Female or MaleHomozygous for Sod1tm1Leb  
Price per Pair (US dollars $)Pair Genotype
$478.00Heterozygous for Sod1tm1Leb x Heterozygous for Sod1tm1Leb  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $310.70Female or MaleHeterozygous for Sod1tm1Leb  
$310.70Female or MaleHomozygous for Sod1tm1Leb  
Price per Pair (US dollars $)Pair Genotype
$621.40Heterozygous for Sod1tm1Leb x Heterozygous for Sod1tm1Leb  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Control Information

  Control
   Wild-type from the colony
   101043 B6129SF1/J (approximate)
   101045 B6129SF2/J (approximate)
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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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.
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Terms of Use


General Terms and Conditions


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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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