Strain Name:

B6.129X1-Baxtm1Sjk/J

Stock Number:

002994

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Homozygous Baxtm1Sjk mice display aberrant apoptosis with hyperplasia displayed in various tissues, including thymocytes, B cells, and cells of the reproductive organs.

Description

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Mating SystemHeterozygote x Heterozygote         (Female x Male)   01-MAR-06
Specieslaboratory mouse
Background Strain C57BL/6
Donor Strain 129X1 RW-4 ES cell line
GenerationN21+F9N1F3 (12-NOV-08)
Generation Definitions
 
Donating InvestigatorDr. Stanley J. Korsmeyer,   Dana-Farber Cancer Institute

Description
Mice homozygous for the Baxtm1Sjk mutation are viable but display lineage-specific aberrations in cell death. Thymocytes and B cells from homozygous mutant mice display hyperplasia. Ovaries contain unusual atretic follicles with excess granulosa cells while Bax-deficient males are infertile. There is an accumulation of atypical premeiotic germ cells and no mature haploid sperm found in seminiferous tubules. Multinucleated giant cells and dysplastic cells accompany massive cell death.

Used in conjunction with strain B6.129-Bak1tm1Thsn/J (see Stock No. 004183), to generate the double knock-out Bak/Bax, a model for demonstrating severe defects in the regulation of apoptosis during development and tissue homeostasis.


Coat color of Baxtm1Sjk mice
The coat color loci tyrosinase (Tyr) and pink-eyed dilution (p) are linked to the Bcl2-associated X protein (Bax) gene. According to backcross data from the Mouse Genome Database, Bax is at 23.00 cM, p is at 28.00 cM, and Tyr is at 44.00 cM on chromosome 7. The targeted disruption of the Bax gene was performed in a 129-derived RW-4 ES cell line (Aw/Aw p Tyrc-ch/p Tyrc) and has been backcrossed 8 generations to C57BL/6 (a/a +p +Tyr-c/+p +Tyr-c; nonagouti black). Statistically, C57BL/6J-Baxtm1Sjk mice (Stock No. 002994) should be 99.6% C57BL/6-like at all loci not linked to the Bax gene. At the present time The Jackson Laboratory's colony of C57BL/6J-Baxtm1Sjkmice are stillsegregating at the Tyr locus and retain the p allele from the 129 ES cell line. Thus, matings of Bax heterozygous (+/-) mice may produce progeny of varying coat color including black, white, chinchilla, light chinchilla, or grey, with all but the black mice having pink eyes. Because the potential for crossover between the p and Bax loci is small (roughly 5%), progeny that are grey in color and have pink eyes most likely are homozygous for the targeted Bax gene (-/-). However, we strongly recommend that you confirm the genotype of the mice prior to using them for research purposes. The Jackson Laboratory is continuing to backcross the Bax targeted mutation to C57BL/6J to try to eliminate the recessive 129 alleles of Tyr and p. However, in an effort to make these mice available to the research community as soon as possible we will begin distribution of the current colony. To summarize, the C57BL/6J-Baxtm1Sjkmice (Stock No. 002994) have been backcrossed 8 generations to the C57BL/6J inbred strain. However, because of coat color genes linked to the Bax mutation breeder pairs supplied by The Jackson Laboratory may produce progeny of varying coat color.

Development
A Bax targeting vector substituted PGK-Neo for exons 2 through 5, deleting BH1 and BH2 and the capacity for a functional protein.

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Bax
006329   B6;129-Baxtm2Sjk Bak1tm1Thsn/J
View Strains carrying other alleles of Bax     (1 strain)

Additional Web Information

Bax Bulletin

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Baxtm1Sjk/Baxtm1Sjk

        B6.129X1-Baxtm1Sjk/J
  • reproductive system phenotype
  • abnormal seminiferous tubule morphology
    • some tubules have an accumulation of early germ cells while others have fewer germ cells than normal   (MGI Ref ID J:103605)
    • the spermatogonia layer is thicker than in wild-type being up to 3 cell layers thick   (MGI Ref ID J:103605)
  • abnormal spermatogenesis
    • at P15 the number of germ cells in the testis is increased and these are mostly c-Kit+ early germ cells, but in adult males the number of germ cells is decreased by up to 10-fold compared to wild-type   (MGI Ref ID J:103605)
    • arrest of male meiosis
      • arrests before the completion of meiosis in the preleptotene spermatocyte stage   (MGI Ref ID J:103605)
    • azoospermia   (MGI Ref ID J:103605)
  • decreased testis weight
    • in adults testes weigh about 60% that of wild-type   (MGI Ref ID J:103605)
  • male infertility
    • males but not females are sterile   (MGI Ref ID J:103605)
  • growth/size/body phenotype
  • decreased body weight
    • seen in about 50% of mice   (MGI Ref ID J:103605)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • cultured enteric neurons from Bax-deficient embryos that are GDNF-deprived show no significant differences in survival relative to enteric neurons from conditionally-inactivated Gfra1-null mice   (MGI Ref ID J:122607)
  • endocrine/exocrine gland phenotype
  • abnormal seminiferous tubule morphology
    • some tubules have an accumulation of early germ cells while others have fewer germ cells than normal   (MGI Ref ID J:103605)
    • the spermatogonia layer is thicker than in wild-type being up to 3 cell layers thick   (MGI Ref ID J:103605)
  • decreased testis weight
    • in adults testes weigh about 60% that of wild-type   (MGI Ref ID J:103605)

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Baxtm1Sjk/Bax+

        involves: 129X1/SvJ
  • nervous system phenotype
  • abnormal sympathetic neuron morphology
    • cultures of sympathetic neurons grown in the presence of NGF before being deprived of NGF, die with slower kinetics than wild-type, such that after 8 days, 14% of neurons remain viable compared to none in controls   (MGI Ref ID J:35372)
  • increased motor neuron number
    • modest 13% increase in the total number of facial motor neurons at 4 weeks of age relative to wild-type   (MGI Ref ID J:35372)

Baxtm1Sjk/Baxtm1Sjk

        involves: 129X1/SvJ
  • endocrine/exocrine gland phenotype
  • abnormal ovarian follicle morphology
    • atretic follicles with excess granulosa cells   (MGI Ref ID J:29253)
  • abnormal seminiferous tubule morphology
    • disordered   (MGI Ref ID J:29253)
  • hematopoietic system phenotype
  • enlarged spleen   (MGI Ref ID J:29253)
  • increased B cell number   (MGI Ref ID J:29253)
  • increased thymocyte number
    • 1.6 fold increase in thymocyte number relative to wild-type   (MGI Ref ID J:29253)
    • normal distribution of maturational subsets (CD4-CD8-, CD4+CD8+, CD4+, CD8+ cells)   (MGI Ref ID J:29253)
  • immune system phenotype
  • enlarged spleen   (MGI Ref ID J:29253)
  • increased B cell number   (MGI Ref ID J:29253)
  • increased thymocyte number
    • 1.6 fold increase in thymocyte number relative to wild-type   (MGI Ref ID J:29253)
    • normal distribution of maturational subsets (CD4-CD8-, CD4+CD8+, CD4+, CD8+ cells)   (MGI Ref ID J:29253)
  • reproductive system phenotype
  • abnormal male germ cell apoptosis
    • increased male germ cell apoptosis   (MGI Ref ID J:29253)
  • abnormal ovarian follicle morphology
    • atretic follicles with excess granulosa cells   (MGI Ref ID J:29253)
  • abnormal seminiferous tubule morphology
    • disordered   (MGI Ref ID J:29253)
  • arrest of spermatogenesis
    • accumulation of premeiotic germ cells   (MGI Ref ID J:29253)
  • azoospermia
    • absence of sperm in the epididymis and vas deferens   (MGI Ref ID J:29253)
  • male infertility   (MGI Ref ID J:29253)
  • nervous system phenotype
  • abnormal facial motor nucleus morphology
    • mutants exhibit a large reduction in motor neuron death in the facial nucleus following neonatal axotomy compared to wild-type   (MGI Ref ID J:35372)
  • abnormal phrenic nerve morphology
    • the phrenic nerve is thicker in mutants, however neuromuscular synapses were normal   (MGI Ref ID J:91066)
  • abnormal proprioceptive neuron morphology
    • about 30% of pSNs in the rostral lumbar DRG have cell body diameters in the wild-type range, with 70% having smaller somatic diameters   (MGI Ref ID J:197913)
  • abnormal superior cervical ganglion morphology
    • superior cervical ganglion of neonates contains 2.5 and 1.8 times more neurons than wild-type and heterozygous ganglia, respectively   (MGI Ref ID J:35372)
  • abnormal sympathetic neuron morphology
    • sympathetic neurons from superior cervical ganglion show a dramatic reduction of death after trophic factor (NGF) deprivation   (MGI Ref ID J:35372)
  • decreased neuron apoptosis
    • developmental sympathetic and motor neuronal death is reduced   (MGI Ref ID J:35372)
  • increased motor neuron number
    • contralateral nonaxotomized facial nucleus shows a 51% increase in neuronal number relative to wild-type at 4 weeks of age   (MGI Ref ID J:35372)
    • mutants display an increase in the number of small- to medium-sized motor neurons   (MGI Ref ID J:35372)
  • increased sensory neuron number
    • number of proprioceptive sensory neurons (pSNs) is increased by 2-fold compared to wild-type controls   (MGI Ref ID J:197913)
  • cellular phenotype
  • abnormal male germ cell apoptosis
    • increased male germ cell apoptosis   (MGI Ref ID J:29253)
  • decreased neuron apoptosis
    • developmental sympathetic and motor neuronal death is reduced   (MGI Ref ID J:35372)

Baxtm1Sjk/Baxtm1Sjk

        involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6
  • nervous system phenotype
  • abnormal axon extension
    • neurite outgrowth is significantly less than that of Isl1tm1(cre)Cos Mapttm1(Ewsr1/Etv4)Arbr heterozygotes with or without treatment with neurotrphin-3   (MGI Ref ID J:100886)
  • abnormal dorsal root ganglion morphology
    • dorsal root ganglia neurons survive without neurotrophic factors   (MGI Ref ID J:100886)
  • increased sensory neuron number
    • apoptosis rates are decreased resulting in increased number of neurons in the lumbar dorsal root ganglia (170% of wild-type numbers)   (MGI Ref ID J:100886)
  • cellular phenotype
  • abnormal axon extension
    • neurite outgrowth is significantly less than that of Isl1tm1(cre)Cos Mapttm1(Ewsr1/Etv4)Arbr heterozygotes with or without treatment with neurotrphin-3   (MGI Ref ID J:100886)

Baxtm1Sjk/Baxtm1Sjk

        involves: 129X1/SvJ * C57BL/6
  • endocrine/exocrine gland phenotype
  • abnormal ovarian folliculogenesis
    • reduced incidence of atresia of primordial and primary follicles relative to wild-type   (MGI Ref ID J:52574)
    • increased number of follicles observed at 42 days   (MGI Ref ID J:52574)
    • follicles persisted in aged females (20 to 22 months old)   (MGI Ref ID J:52574)
  • increased mature ovarian follicle number
    • increased number of follicles observed at 42 days of age   (MGI Ref ID J:52574)
    • persistence of hundreds of follicles of all developmental stages in aged females (20 to 22 months old)   (MGI Ref ID J:52574)
  • nervous system phenotype
  • abnormal dorsal root ganglion morphology
    • the number of dorsal root ganglia neurons in L4 is increased relative to in wild-type mice   (MGI Ref ID J:83461)
  • reproductive system phenotype
  • abnormal ovarian folliculogenesis
    • reduced incidence of atresia of primordial and primary follicles relative to wild-type   (MGI Ref ID J:52574)
    • increased number of follicles observed at 42 days   (MGI Ref ID J:52574)
    • follicles persisted in aged females (20 to 22 months old)   (MGI Ref ID J:52574)
  • increased mature ovarian follicle number
    • increased number of follicles observed at 42 days of age   (MGI Ref ID J:52574)
    • persistence of hundreds of follicles of all developmental stages in aged females (20 to 22 months old)   (MGI Ref ID J:52574)
  • uterus hypertrophy
    • ovarian steroid-driven uternine hypertrophy is observed in aged females (20 to 22 months old)   (MGI Ref ID J:52574)

The following phenotype relates to a compound genotype created using this strain.
Contact JAX® Services jaxservices@jax.org for customized breeding options.

Bak1tm1Thsn/Bak1tm1Thsn Baxtm1Sjk/Baxtm1Sjk

        involves: 129S1/Sv * 129S1/SvImJ * 129X1/SvJ * C57BL/6
  • mortality/aging
  • partial neonatal lethality
    • majority die within 48 hours of birth, although some survive to adulthood   (MGI Ref ID J:66872)
  • limbs/digits/tail phenotype
  • interdigital webbing
    • mutants retain interdigital webs on both fore and rear paws   (MGI Ref ID J:66872)
  • reproductive system phenotype
  • vagina atresia
    • seen in all adult females   (MGI Ref ID J:66872)
  • behavior/neurological phenotype
  • circling
    • display circling behavior when exposed to external stress   (MGI Ref ID J:66872)
  • seizures
    • stress-induced seizure activity   (MGI Ref ID J:66872)
  • hearing/vestibular/ear phenotype
  • abnormal hearing physiology
    • unresponsive to auditory stimuli   (MGI Ref ID J:66872)
  • hematopoietic system phenotype
  • abnormal hematopoiesis
    • hematopoietic colony assays show an increase in the number of myeloid colony forming units and a mild increase in erythroid and megakaryocyte colony forming units   (MGI Ref ID J:66872)
    • abnormal B cell morphology
      • B220+ B cells present in the lymph node and spleen are skewed toward a B220brightIgD- phenotype, indicating an increase in the number of class-switched or memory B cells   (MGI Ref ID J:66872)
    • abnormal T cell morphology
      • T cells that accumulate in mutants are skewed toward a memory cell phenotype   (MGI Ref ID J:66872)
    • anemia
      • mild anemia   (MGI Ref ID J:66872)
    • decreased platelet cell number   (MGI Ref ID J:66872)
    • increased leukocyte cell number   (MGI Ref ID J:66872)
      • increased lymphocyte cell number
        • increases within the circulation and the peripheral lymphoid organs   (MGI Ref ID J:66872)
        • lymphocytic infiltration is seen in parenchymal organs, liver, and kidney   (MGI Ref ID J:66872)
  • abnormal splenocyte physiology
    • isolated splenocytes cultured in suspension show enhanced survival   (MGI Ref ID J:66872)
  • enlarged spleen   (MGI Ref ID J:66872)
  • increased spleen red pulp amount
    • expanded red pulp contains a large increase in the number of plasma cells and histiocytes   (MGI Ref ID J:66872)
  • increased spleen white pulp amount
    • pronounced hyperplasia   (MGI Ref ID J:66872)
  • immune system phenotype
  • abnormal B cell morphology
    • B220+ B cells present in the lymph node and spleen are skewed toward a B220brightIgD- phenotype, indicating an increase in the number of class-switched or memory B cells   (MGI Ref ID J:66872)
  • abnormal T cell morphology
    • T cells that accumulate in mutants are skewed toward a memory cell phenotype   (MGI Ref ID J:66872)
  • abnormal splenocyte physiology
    • isolated splenocytes cultured in suspension show enhanced survival   (MGI Ref ID J:66872)
  • enlarged lymph nodes   (MGI Ref ID J:66872)
  • enlarged spleen   (MGI Ref ID J:66872)
  • increased leukocyte cell number   (MGI Ref ID J:66872)
    • increased lymphocyte cell number
      • increases within the circulation and the peripheral lymphoid organs   (MGI Ref ID J:66872)
      • lymphocytic infiltration is seen in parenchymal organs, liver, and kidney   (MGI Ref ID J:66872)
  • increased spleen red pulp amount
    • expanded red pulp contains a large increase in the number of plasma cells and histiocytes   (MGI Ref ID J:66872)
  • increased spleen white pulp amount
    • pronounced hyperplasia   (MGI Ref ID J:66872)
  • nervous system phenotype
  • abnormal brain morphology
    • increase in the number of neurons in multiple regions of the brain   (MGI Ref ID J:66872)
    • large accumulation of small neuronal cells (neural stem cells) with dense chromatin staining in the periventricular region   (MGI Ref ID J:66872)
    • increased brain size   (MGI Ref ID J:66872)
  • increased neuron number
    • in multiple regions of the brain   (MGI Ref ID J:66872)
  • seizures
    • stress-induced seizure activity   (MGI Ref ID J:66872)
  • cellular phenotype
  • decreased cellular sensitivity to gamma-irradiation
    • thymocytes show enhanced survival compared to wild-type when exposed to gamma irradiation   (MGI Ref ID J:66872)
  • homeostasis/metabolism phenotype
  • decreased physiological sensitivity to xenobiotic
    • thymocytes are resistant to treatment with etoposide, a chemotherapeutic agent that normally induces cell death   (MGI Ref ID J:66872)
View Research Applications

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

Baxtm1Sjk related

Apoptosis Research
Endogenous Regulators

Cancer Research
Genes Regulating Growth and Proliferation

Developmental Biology Research
Internal/Organ Defects
      gonads

Immunology, Inflammation and Autoimmunity Research
Intracellular Signaling Molecules

Reproductive Biology Research
Developmental Defects Affecting Gonads
Fertility Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Baxtm1Sjk
Allele Name targeted mutation 1, Stanley J Korsmeyer
Allele Type Targeted (knock-out)
Common Name(s) Bax-; Bax1;
Mutation Made ByDr. Stanley Korsmeyer,   Dana-Farber Cancer Institute
Strain of Origin129X1/SvJ
ES Cell Line NameRW-4
ES Cell Line Strain129X1/SvJ
Gene Symbol and Name Bax, BCL2-associated X protein
Chromosome 7
Gene Common Name(s) BCL2L4;
Molecular Note A neomycin selection cassette replaced exons 2 through 4 and part of exon 5, which encode sequences that correspond to the two BCL2 homology domains BH1 and BH2. Immunoblots did not detect the endcoded protein in tissue lysates derived from homozygous mice. [MGI Ref ID J:29253]

Genotyping

Genotyping Information

Genotyping Protocols

Baxtm1Sjk, Melt Curve Analysis
Baxtm1Sjk, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Knudson CM; Tung KS; Tourtellotte WG; Brown GA; Korsmeyer SJ. 1995. Bax-deficient mice with lymphoid hyperplasia and male germ cell death. Science 270(5233):96-9. [PubMed: 7569956]  [MGI Ref ID J:29253]

Additional References

Forger NG; Rosen GJ; Waters EM; Jacob D; Simerly RB; de Vries GJ. 2004. Deletion of Bax eliminates sex differences in the mouse forebrain. Proc Natl Acad Sci U S A 101(37):13666-71. [PubMed: 15342910]  [MGI Ref ID J:92614]

Khaled AR; Li WQ; Huang J; Fry TJ; Khaled AS; Mackall CL; Muegge K; Young HA; Durum SK. 2002. Bax deficiency partially corrects interleukin-7 receptor alpha deficiency. Immunity 17(5):561-73. [PubMed: 12433363]  [MGI Ref ID J:93139]

Knudson CM; Korsmeyer SJ. 1997. Bcl-2 and Bax function independently to regulate cell death. Nat Genet 16(4):358-63. [PubMed: 9241272]  [MGI Ref ID J:42051]

Lu YP; Lou YR; Peng QY; Xie JG; Conney AH. 2004. Stimulatory effect of topical application of caffeine on UVB-induced apoptosis in the epidermis of p53 and Bax knockout mice. Cancer Res 64(14):5020-7. [PubMed: 15256477]  [MGI Ref ID J:91506]

Yin C; Knudson CM; Korsmeyer SJ; Van Dyke T. 1997. Bax suppresses tumorigenesis and stimulates apoptosis in vivo. Nature 385(6617):637-40. [PubMed: 9024662]  [MGI Ref ID J:38331]

Baxtm1Sjk related

Abdo H; Li L; Lallemend F; Bachy I; Xu XJ; Rice FL; Ernfors P. 2011. Dependence on the transcription factor Shox2 for specification of sensory neurons conveying discriminative touch. Eur J Neurosci 34(10):1529-41. [PubMed: 22103411]  [MGI Ref ID J:184160]

Alton M; Taketo T. 2007. Switch from BAX-dependent to BAX-independent germ cell loss during the development of fetal mouse ovaries. J Cell Sci 120(Pt 3):417-24. [PubMed: 17213335]  [MGI Ref ID J:120767]

Armstrong A; Ryu YK; Chieco D; Kuruvilla R. 2011. Frizzled3 Is Required for Neurogenesis and Target Innervation during Sympathetic Nervous System Development. J Neurosci 31(7):2371-81. [PubMed: 21325504]  [MGI Ref ID J:169444]

Bailey DP; Kashyap M; Bouton LA; Murray PJ; Ryan JJ. 2006. Interleukin-10 induces apoptosis in developing mast cells and macrophages. J Leukoc Biol 80(3):581-9. [PubMed: 16829633]  [MGI Ref ID J:112579]

Baines CP; Kaiser RA; Sheiko T; Craigen WJ; Molkentin JD. 2007. Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death. Nat Cell Biol 9(5):550-5. [PubMed: 17417626]  [MGI Ref ID J:129616]

Barone MC; Desouza LA; Freeman RS. 2008. Pin1 promotes cell death in NGF-dependent neurons through a mechanism requiring c-Jun activity. J Neurochem 106(2):734-45. [PubMed: 18419764]  [MGI Ref ID J:139389]

Ben-Zvi A; Manor O; Schachner M; Yaron A; Tessier-Lavigne M; Behar O. 2008. The Semaphorin receptor PlexinA3 mediates neuronal apoptosis during dorsal root ganglia development. J Neurosci 28(47):12427-32. [PubMed: 19020035]  [MGI Ref ID J:142362]

Ben-Zvi A; Sweetat S; Behar O. 2013. Elimination of aberrant DRG circuitries in Sema3A mutant mice leads to extensive neuronal deficits. PLoS One 8(7):e70085. [PubMed: 23922915]  [MGI Ref ID J:204365]

Berens HM; Tyler KL. 2011. The pro-apoptotic Bcl-2 protein Bax plays an important role in the pathogenesis of reovirus encephalitis. J Virol :. [PubMed: 21307199]  [MGI Ref ID J:168899]

Bernal NP; Stehr W; Coyle R; Erwin CR; Warner BW. 2006. Epidermal growth factor receptor signaling regulates Bax and Bcl-w expression and apoptotic responses during intestinal adaptation in mice. Gastroenterology 130(2):412-23. [PubMed: 16472596]  [MGI Ref ID J:124922]

Bruckheimer EM; Cho S; Brisbay S; Johnson DJ; Gingrich JR; Greenberg N; McDonnell TJ. 2000. The impact of bcl-2 expression and bax deficiency on prostate homeostasis in vivo. Oncogene 19(20):2404-12. [PubMed: 10828882]  [MGI Ref ID J:62297]

Buss RR; Gould TW; Ma J; Vinsant S; Prevette D; Winseck A; Toops KA; Hammarback JA; Smith TL; Oppenheim RW. 2006. Neuromuscular development in the absence of programmed cell death: phenotypic alteration of motoneurons and muscle. J Neurosci 26(52):13413-27. [PubMed: 17192424]  [MGI Ref ID J:117220]

Chang MY; Sun W; Ochiai W; Nakashima K; Kim SY; Park CH; Kang JS; Shim JW; Jo AY; Kang CS; Lee YS; Kim JS; Lee SH. 2007. Bcl-XL/Bax proteins direct the fate of embryonic cortical precursor cells. Mol Cell Biol 27(12):4293-305. [PubMed: 17438128]  [MGI Ref ID J:122346]

Chao JR; Parganas E; Boyd K; Hong CY; Opferman JT; Ihle JN. 2008. Hax1-mediated processing of HtrA2 by Parl allows survival of lymphocytes and neurons. Nature 452(7183):98-102. [PubMed: 18288109]  [MGI Ref ID J:132627]

Chavez-Reyes A; Parant JM; Amelse LL; de Oca Luna RM; Korsmeyer SJ; Lozano G. 2003. Switching mechanisms of cell death in mdm2- and mdm4-null mice by deletion of p53 downstream targets. Cancer Res 63(24):8664-9. [PubMed: 14695178]  [MGI Ref ID J:87065]

Chen L; Faire M; Kissner MD; Laird DJ. 2013. Primordial germ cells and gastrointestinal stromal tumors respond distinctly to a cKit overactivating allele. Hum Mol Genet 22(2):313-27. [PubMed: 23077213]  [MGI Ref ID J:191131]

Chen WV; Alvarez FJ; Lefebvre JL; Friedman B; Nwakeze C; Geiman E; Smith C; Thu CA; Tapia JC; Tasic B; Sanes JR; Maniatis T. 2012. Functional significance of isoform diversification in the protocadherin gamma gene cluster. Neuron 75(3):402-9. [PubMed: 22884324]  [MGI Ref ID J:188341]

Cheung EC; Melanson-Drapeau L; Cregan SP; Vanderluit JL; Ferguson KL; McIntosh WC; Park DS; Bennett SA; Slack RS. 2005. Apoptosis-inducing factor is a key factor in neuronal cell death propagated by BAX-dependent and BAX-independent mechanisms. J Neurosci 25(6):1324-34. [PubMed: 15703386]  [MGI Ref ID J:98103]

Chi MM; Pingsterhaus J; Carayannopoulos M; Moley KH. 2000. Decreased glucose transporter expression triggers BAX-dependent apoptosis in the murine blastocyst J Biol Chem 275(51):40252-7. [PubMed: 10995754]  [MGI Ref ID J:66414]

Chi MM; Schlein AL; Moley KH. 2000. High insulin-like growth factor 1 (IGF-1) and insulin concentrations trigger apoptosis in the mouse blastocyst via down-regulation of the IGF-1 receptor. Endocrinology 141(12):4784-92. [PubMed: 11108294]  [MGI Ref ID J:115385]

Chong MJ; Murray MR; Gosink EC; Russell HR; Srinivasan A; Kapsetaki M; Korsmeyer SJ; McKinnon PJ. 2000. Atm and Bax cooperate in ionizing radiation-induced apoptosis in the central nervous system. Proc Natl Acad Sci U S A 97(2):889-94. [PubMed: 10639175]  [MGI Ref ID J:59934]

Cleland MM; Norris KL; Karbowski M; Wang C; Suen DF; Jiao S; George NM; Luo X; Li Z; Youle RJ. 2011. Bcl-2 family interaction with the mitochondrial morphogenesis machinery. Cell Death Differ 18(2):235-47. [PubMed: 20671748]  [MGI Ref ID J:186336]

Clemente EJ; Furlong RA; Loveland KL; Affara NA. 2006. Gene expression study in the juvenile mouse testis: identification of stage-specific molecular pathways during spermatogenesis. Mamm Genome 17(9):956-75. [PubMed: 16964443]  [MGI Ref ID J:112872]

Cook MS; Coveney D; Batchvarov I; Nadeau JH; Capel B. 2009. BAX-mediated cell death affects early germ cell loss and incidence of testicular teratomas in Dnd1(Ter/Ter) mice. Dev Biol 328(2):377-83. [PubMed: 19389346]  [MGI Ref ID J:149469]

Cook MS; Munger SC; Nadeau JH; Capel B. 2011. Regulation of male germ cell cycle arrest and differentiation by DND1 is modulated by genetic background. Development 138(1):23-32. [PubMed: 21115610]  [MGI Ref ID J:167041]

Coulpier M; Messiaen S; Hamel R; Fernandez de Marco M; Lilin T; Eloit M. 2006. Bax deletion does not protect neurons from BSE-induced death. Neurobiol Dis 23(3):603-11. [PubMed: 16854590]  [MGI Ref ID J:147030]

Coultas L; Bouillet P; Loveland KL; Meachem S; Perlman H; Adams JM; Strasser A. 2005. Concomitant loss of proapoptotic BH3-only Bcl-2 antagonists Bik and Bim arrests spermatogenesis. EMBO J 24(22):3963-73. [PubMed: 16270031]  [MGI Ref ID J:103605]

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Southwell DG; Paredes MF; Galvao RP; Jones DL; Froemke RC; Sebe JY; Alfaro-Cervello C; Tang Y; Garcia-Verdugo JM; Rubenstein JL; Baraban SC; Alvarez-Buylla A. 2012. Intrinsically determined cell death of developing cortical interneurons. Nature 491(7422):109-13. [PubMed: 23041929]  [MGI Ref ID J:189225]

Speiran K; Bailey DP; Fernando J; Macey M; Barnstein B; Kolawole M; Curley D; Watowich SS; Murray PJ; Oskeritzian C; Ryan JJ. 2009. Endogenous suppression of mast cell development and survival by IL-4 and IL-10. J Leukoc Biol 85(5):826-36. [PubMed: 19228815]  [MGI Ref ID J:149777]

Stallock J; Molyneaux K; Schaible K; Knudson CM; Wylie C. 2003. The pro-apoptotic gene Bax is required for the death of ectopic primordial germ cells during their migration in the mouse embryo. Development 130(26):6589-97. [PubMed: 14660547]  [MGI Ref ID J:86513]

Steckley D; Karajgikar M; Dale LB; Fuerth B; Swan P; Drummond-Main C; Poulter MO; Ferguson SS; Strasser A; Cregan SP. 2007. Puma is a dominant regulator of oxidative stress induced Bax activation and neuronal apoptosis. J Neurosci 27(47):12989-99. [PubMed: 18032672]  [MGI Ref ID J:127640]

Steele AD; King OD; Jackson WS; Hetz CA; Borkowski AW; Thielen P; Wollmann R; Lindquist S. 2007. Diminishing apoptosis by deletion of Bax or overexpression of Bcl-2 does not protect against infectious prion toxicity in vivo. J Neurosci 27(47):13022-7. [PubMed: 18032675]  [MGI Ref ID J:141553]

Steimer DA; Boyd K; Takeuchi O; Fisher JK; Zambetti GP; Opferman JT. 2009. Selective roles for antiapoptotic MCL-1 during granulocyte development and macrophage effector function. Blood 113(12):2805-15. [PubMed: 19064728]  [MGI Ref ID J:146310]

Su H; Marcheva B; Meng S; Liang FA; Kohsaka A; Kobayashi Y; Xu AW; Bass J; Wang X. 2010. Gamma-protocadherins regulate the functional integrity of hypothalamic feeding circuitry in mice. Dev Biol 339(1):38-50. [PubMed: 20025866]  [MGI Ref ID J:157958]

Sun W; Gould TW; Vinsant S; Prevette D; Oppenheim RW. 2003. Neuromuscular development after the prevention of naturally occurring neuronal death by Bax deletion. J Neurosci 23(19):7298-310. [PubMed: 12917363]  [MGI Ref ID J:88191]

Sun W; Oppenheim RW. 2003. Response of motoneurons to neonatal sciatic nerve axotomy in Bax-knockout mice. Mol Cell Neurosci 24(4):875-86. [PubMed: 14697655]  [MGI Ref ID J:87200]

Sun W; Winseck A; Vinsant S; Park OH; Kim H; Oppenheim RW. 2004. Programmed cell death of adult-generated hippocampal neurons is mediated by the proapoptotic gene Bax. J Neurosci 24(49):11205-13. [PubMed: 15590937]  [MGI Ref ID J:96804]

Suzuki A; Igarashi K; Aisaki K; Kanno J; Saga Y. 2010. NANOS2 interacts with the CCR4-NOT deadenylation complex and leads to suppression of specific RNAs. Proc Natl Acad Sci U S A 107(8):3594-9. [PubMed: 20133598]  [MGI Ref ID J:157579]

Suzuki A; Saga Y. 2008. Nanos2 suppresses meiosis and promotes male germ cell differentiation. Genes Dev 22(4):430-5. [PubMed: 18281459]  [MGI Ref ID J:132711]

Suzuki H; Aoyama Y; Senzaki K; Vincler M; Wittenauer S; Yoshikawa M; Ozaki S; Oppenheim RW; Shiga T. 2010. Characterization of sensory neurons in the dorsal root ganglia of Bax-deficient mice. Brain Res 1362:23-31. [PubMed: 20846512]  [MGI Ref ID J:166957]

Suzuki H; Tsuda M; Kiso M; Saga Y. 2008. Nanos3 maintains the germ cell lineage in the mouse by suppressing both Bax-dependent and -independent apoptotic pathways. Dev Biol 318(1):133-42. [PubMed: 18436203]  [MGI Ref ID J:136687]

Takeuchi O; Fisher J; Suh H; Harada H; Malynn BA; Korsmeyer SJ. 2005. Essential role of BAX,BAK in B cell homeostasis and prevention of autoimmune disease. Proc Natl Acad Sci U S A 102(32):11272-7. [PubMed: 16055554]  [MGI Ref ID J:100463]

Tesfaigzi Y; Fischer MJ; Daheshia M; Green FH; De Sanctis GT; Wilder JA. 2002. Bax is crucial for IFN-gamma-induced resolution of allergen-induced mucus cell metaplasia. J Immunol 169(10):5919-25. [PubMed: 12421976]  [MGI Ref ID J:80074]

Tessner TG; Muhale F; Riehl TE; Anant S; Stenson WF. 2004. Prostaglandin E2 reduces radiation-induced epithelial apoptosis through a mechanism involving AKT activation and bax translocation. J Clin Invest 114(11):1676-85. [PubMed: 15578100]  [MGI Ref ID J:94433]

Tian H; Ma M. 2008. Activity plays a role in eliminating olfactory sensory neurons expressing multiple odorant receptors in the mouse septal organ. Mol Cell Neurosci 38(4):484-8. [PubMed: 18538580]  [MGI Ref ID J:141795]

Uesaka T; Enomoto H. 2010. Neural precursor death is central to the pathogenesis of intestinal aganglionosis in Ret hypomorphic mice. J Neurosci 30(15):5211-8. [PubMed: 20392943]  [MGI Ref ID J:159854]

Uesaka T; Jain S; Yonemura S; Uchiyama Y; Milbrandt J; Enomoto H. 2007. Conditional ablation of GFRalpha1 in postmigratory enteric neurons triggers unconventional neuronal death in the colon and causes a Hirschsprung's disease phenotype. Development 134(11):2171-81. [PubMed: 17507417]  [MGI Ref ID J:122607]

Uo T; Kinoshita Y; Morrison RS. 2007. Apoptotic actions of p53 require transcriptional activation of PUMA and do not involve a direct mitochondrial/cytoplasmic site of action in postnatal cortical neurons. J Neurosci 27(45):12198-210. [PubMed: 17989286]  [MGI Ref ID J:127443]

Upton JP; Austgen K; Nishino M; Coakley KM; Hagen A; Han D; Papa FR; Oakes SA. 2008. Caspase-2 cleavage of BID is a critical apoptotic signal downstream of endoplasmic reticulum stress. Mol Cell Biol 28(12):3943-51. [PubMed: 18426910]  [MGI Ref ID J:137299]

Vaughn AE; Deshmukh M. 2007. Essential postmitochondrial function of p53 uncovered in DNA damage-induced apoptosis in neurons. Cell Death Differ 14(5):973-81. [PubMed: 17218959]  [MGI Ref ID J:139242]

Vila M; Jackson-Lewis V; Vukosavic S; Djaldetti R; Liberatore G; Offen D; Korsmeyer SJ; Przedborski S. 2001. Bax ablation prevents dopaminergic neurodegeneration in the 1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease. Proc Natl Acad Sci U S A 98(5):2837-42. [PubMed: 11226327]  [MGI Ref ID J:67861]

Villunger A; Scott C; Bouillet P; Strasser A. 2003. Essential role for the BH3-only protein Bim but redundant roles for Bax, Bcl-2, and Bcl-w in the control of granulocyte survival. Blood 101(6):2393-400. [PubMed: 12433687]  [MGI Ref ID J:82641]

Vince JE; Wong WW; Gentle I; Lawlor KE; Allam R; O'Reilly L; Mason K; Gross O; Ma S; Guarda G; Anderton H; Castillo R; Hacker G; Silke J; Tschopp J. 2012. Inhibitor of Apoptosis Proteins Limit RIP3 Kinase-Dependent Interleukin-1 Activation. Immunity 36(2):215-27. [PubMed: 22365665]  [MGI Ref ID J:181625]

Wang X; Eno CO; Altman BJ; Zhu Y; Zhao G; Olberding KE; Rathmell JC; Li C. 2011. ER stress modulates cellular metabolism. Biochem J 435(1):285-96. [PubMed: 21241252]  [MGI Ref ID J:170628]

Weiner JA; Wang X; Tapia JC; Sanes JR. 2005. Gamma protocadherins are required for synaptic development in the spinal cord. Proc Natl Acad Sci U S A 102(1):8-14. [PubMed: 15574493]  [MGI Ref ID J:95826]

Weinlich R; Oberst A; Dillon CP; Janke LJ; Milasta S; Lukens JR; Rodriguez DA; Gurung P; Savage C; Kanneganti TD; Green DR. 2013. Protective roles for caspase-8 and cFLIP in adult homeostasis. Cell Rep 5(2):340-8. [PubMed: 24095739]  [MGI Ref ID J:203778]

Werth JL; Deshmukh M; Cocabo J; Johnson EM Jr; Rothman SM. 2000. Reversible physiological alterations in sympathetic neurons deprived of NGF but protected from apoptosis by caspase inhibition or Bax deletion. Exp Neurol 161(1):203-11. [PubMed: 10683286]  [MGI Ref ID J:115320]

White FA; Keller-Peck CR; Knudson CM; Korsmeyer SJ; Snider WD. 1998. Widespread elimination of naturally occurring neuronal death in Bax-deficient mice. J Neurosci 18(4):1428-39. [PubMed: 9454852]  [MGI Ref ID J:45764]

White MJ; Schoenwaelder SM; Josefsson EC; Jarman KE; Henley KJ; James C; Debrincat MA; Jackson SP; Huang DC; Kile BT. 2012. Caspase-9 mediates the apoptotic death of megakaryocytes and platelets, but is dispensable for their generation and function. Blood 119(18):4283-90. [PubMed: 22294729]  [MGI Ref ID J:185011]

Whitney IE; Raven MA; Ciobanu DC; Williams RW; Reese BE. 2009. Multiple genes on chromosome 7 regulate dopaminergic amacrine cell number in the mouse retina. Invest Ophthalmol Vis Sci 50(5):1996-2003. [PubMed: 19168892]  [MGI Ref ID J:149703]

Wickramasinghe SR; Alvania RS; Ramanan N; Wood JN; Mandai K; Ginty DD. 2008. Serum response factor mediates NGF-dependent target innervation by embryonic DRG sensory neurons. Neuron 58(4):532-45. [PubMed: 18498735]  [MGI Ref ID J:145293]

Winseck AK; Oppenheim RW. 2006. An in vivo analysis of Schwann cell programmed cell death in embryonic mice: the role of axons, glial growth factor, and the pro-apoptotic gene Bax. Eur J Neurosci 24(8):2105-17. [PubMed: 17042795]  [MGI Ref ID J:116994]

Wolpaw AJ; Shimada K; Skouta R; Welsch ME; Akavia UD; Pe'er D; Shaik F; Bulinski JC; Stockwell BR. 2011. Modulatory profiling identifies mechanisms of small molecule-induced cell death. Proc Natl Acad Sci U S A 108(39):E771-80. [PubMed: 21896738]  [MGI Ref ID J:176584]

Xiang C; Zhang KH; Yin J; Arends JJ; Erzurumlu RS; Jacquin MF; Chen ZF. 2010. The transcription factor, Lmx1b, is necessary for the development of the principal trigeminal nucleus-based lemniscal pathway. Mol Cell Neurosci 44(4):394-403. [PubMed: 20621716]  [MGI Ref ID J:164254]

Xiang CX; Zhang KH; Johnson RL; Jacquin MF; Chen ZF. 2012. The transcription factor, Lmx1b, promotes a neuronal glutamate phenotype and suppresses a GABA one in the embryonic trigeminal brainstem complex. Somatosens Mot Res 29(1):1-12. [PubMed: 22397680]  [MGI Ref ID J:200736]

Xiang J; Rir-Sim-Ah J; Tesfaigzi Y. 2008. IL-9 and IL-13 induce mucous cell metaplasia that is reduced by IFN-gamma in a Bax-mediated pathway. Am J Respir Cell Mol Biol 38(3):310-7. [PubMed: 17901408]  [MGI Ref ID J:146356]

Xu X; Qiao W; Linke SP; Cao L; Li WM; Furth PA; Harris CC; Deng CX. 2001. Genetic interactions between tumor suppressors Brca1 and p53 in apoptosis, cell cycle and tumorigenesis. Nat Genet 28(3):266-71. [PubMed: 11431698]  [MGI Ref ID J:70271]

Yamauchi J; Kumar A; Duarte L; Mehuron T; Girgenrath M. 2013. Triggering regeneration and tackling apoptosis: a combinatorial approach to treating congenital muscular dystrophy type 1 A. Hum Mol Genet 22(21):4306-17. [PubMed: 23773998]  [MGI Ref ID J:202292]

Yang L; Bula D; Arroyo JG; Chen DF. 2004. Preventing retinal detachment-associated photoreceptor cell loss in Bax-deficient mice. Invest Ophthalmol Vis Sci 45(2):648-54. [PubMed: 14744910]  [MGI Ref ID J:109756]

Yee KS; Wilkinson S; James J; Ryan KM; Vousden KH. 2009. PUMA- and Bax-induced autophagy contributes to apoptosis. Cell Death Differ 16(8):1135-45. [PubMed: 19300452]  [MGI Ref ID J:164186]

Yin C; Knudson CM; Korsmeyer SJ; Van Dyke T. 1997. Bax suppresses tumorigenesis and stimulates apoptosis in vivo. Nature 385(6617):637-40. [PubMed: 9024662]  [MGI Ref ID J:38331]

Zaman F; Chrysis D; Huntjens K; Fadeel B; Savendahl L. 2012. Ablation of the pro-apoptotic protein Bax protects mice from glucocorticoid-induced bone growth impairment. PLoS One 7(3):e33168. [PubMed: 22442678]  [MGI Ref ID J:187038]

Zeng Q; Kwan A; Oakley B. 2000. Gustatory innervation and bax-dependent caspase-2: participants in the life and death pathways of mouse taste receptor cells. J Comp Neurol 424(4):640-50. [PubMed: 10931486]  [MGI Ref ID J:63729]

Zhao Y; Li S; Childs EE; Kuharsky DK; Yin XM. 2001. Activation of pro-death bcl-2 family proteins and mitochondria apoptosis pathway in tumor necrosis factor-alpha -induced liver injury. J Biol Chem 276(29):27432-40. [PubMed: 11369777]  [MGI Ref ID J:70549]

Zhu X; Libby RT; de Vries WN; Smith RS; Wright DL; Bronson RT; Seburn KL; John SW. 2012. Mutations in a P-type ATPase gene cause axonal degeneration. PLoS Genet 8(8):e1002853. [PubMed: 22912588]  [MGI Ref ID J:188127]

Zhu Y; Liu X; Hildeman D; Peyerl FW; White J; Kushnir E; Kappler J; Marrack P. 2006. Bax does not have to adopt its final form to drive T cell death. J Exp Med 203(5):1147-52. [PubMed: 16651384]  [MGI Ref ID J:124139]

Zong WX; Ditsworth D; Bauer DE; Wang ZQ; Thompson CB. 2004. Alkylating DNA damage stimulates a regulated form of necrotic cell death. Genes Dev 18(11):1272-82. [PubMed: 15145826]  [MGI Ref ID J:118568]

de Nooij JC; Doobar S; Jessell TM. 2013. Etv1 inactivation reveals proprioceptor subclasses that reflect the level of NT3 expression in muscle targets. Neuron 77(6):1055-68. [PubMed: 23522042]  [MGI Ref ID J:197913]

de Rivero Vaccari JC; Casey GP; Aleem S; Park WM; Corriveau RA. 2006. NMDA receptors promote survival in somatosensory relay nuclei by inhibiting Bax-dependent developmental cell death. Proc Natl Acad Sci U S A 103(45):16971-6. [PubMed: 17077143]  [MGI Ref ID J:117103]

de Vries GJ; Jardon M; Reza M; Rosen GJ; Immerman E; Forger NG. 2008. Sexual differentiation of vasopressin innervation of the brain: cell death versus phenotypic differentiation. Endocrinology 149(9):4632-7. [PubMed: 18499746]  [MGI Ref ID J:145504]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX11

Colony Maintenance

Breeding & HusbandryThe strain is maintained through heterozygous matings. BAX-deficient males are infertile and females are extremely poor breeders. Expected coat color from breeding:Black,Beige,Albino,Gray
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 $232.00Female or MaleHeterozygous for Baxtm1Sjk  
$232.00Female or MaleHomozygous for Baxtm1Sjk  
Price per Pair (US dollars $)Pair Genotype
$464.00Heterozygous for Baxtm1Sjk x Heterozygous for Baxtm1Sjk  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $301.60Female or MaleHeterozygous for Baxtm1Sjk  
$301.60Female or MaleHomozygous for Baxtm1Sjk  
Price per Pair (US dollars $)Pair Genotype
$603.20Heterozygous for Baxtm1Sjk x Heterozygous for Baxtm1Sjk  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  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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JAX® Mice
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Terms of Use

Terms of Use


General Terms and Conditions


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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.

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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.

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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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