Strain Name:

B6.129S4-Vdrtm1Mbd/J

Stock Number:

006133

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Availability:

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These Vdr knockout mutants exhibit a phenotype similar to that seen in patients with hereditary vitamin D-dependent rickets type II. They display a range of traits including hypocalcemia, hypophosphatemia, hyperparathyroidism, increased serum parathyroid hormone, abnormal blood mineral levels, and growth retardation.

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)   16-MAY-07
Specieslaboratory mouse
GenerationN8+N1+F15 (11-DEC-13)
Generation Definitions
 
Donating Investigator Marie Demay,   Massachusetts General Hospital

Description
Heterozygous mice are phenotypically indistinguishable from wildtype siblings. As originally characterized on a mixed B6;129 genetic background, homozygous mice are viable and fertile with normal survival until approximately 14 months. RNA isolated from the intestine and kidney show a truncated deletion of the second zinc finger coding region followed by a premature termination codon, resulting in the absence of receptor protein. Homozygous mice exhibit an identical phenotype as the human disease hereditary vitamin D-dependent rickets type II (HVDDR). As early as 21 days of age, mutant mice demonstrate hypocalcemia, hypophosphatemia, hyperparathyroidism, increased serum parathyroid hormone, abnormal blood mineral levels, and growth retardation. In addition, renin and plasma angiotensin II levels are increased. Homozygous mice are hypertensive and exhibit cardiachypertrophy. At 4 weeks of age, homozygous mice exhibit perioral and periorbital alopecia that progresses over the entire body by 4 months of age. Rickets and osteomalacia develop by 35 days. Homozygous mice have increased bone fragility and other skeletal abnormalities. Introducing a diet enriched for calcium, phosphorus, and lactose, to young homozygous mice prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia. Lymphocytes isolated from homozygous mice have an inflammatory phenotype. Null mice have increased susceptibility to induced inflammatory bowel disease. Mutant mice may be useful in studies of rickets, alopecia, skeletal homeostasis, intestinal absorption, and inflammatory bowel disease.

( Note: It has been the experience of The Jackson Laboratory that homozygotes on the C57BL/6 congenic background survive to only 2 months of age.)

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. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development
A targeting vector containing a mouse phosphoglycerate kinase promoter driven neomycin resistance gene was used to replace exon 3 of the endogenous gene. The construct was electroporated into the 129S4/SvJae-derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. The resulting chimeric mice were bred to C57BL/6 to generate mutant colonies. The donating investigator stated that heterozygotes were mated to C57BL/6 mice (see SNP note below) for more than 8 generations before arriving at The Jackson Laboratory.

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

Control Information

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

Related Strains

Strains carrying other alleles of Vdr
006956   NOD.Cg-Vdrtm1Ska/CmatJ
View Strains carrying other alleles of Vdr     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Vitamin D-Dependent Rickets, Type 2A; VDDR2A
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Osteoporosis   (VDR)
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.

Vdrtm1Mbd/Vdr+

        involves: 129S4/SvJae * C57BL/6
  • cardiovascular system phenotype
  • *normal* cardiovascular system phenotype
    • plasma levels of angiotensin II or aldosterone are not different from wild-type   (MGI Ref ID J:120353)
    • ECG analysis does not reveal any significant differences from wild-type at 3, 6, or 9 months   (MGI Ref ID J:120353)
    • increased heart weight
      • heart weight to body weight ratio is increased 14% relative to wild-type   (MGI Ref ID J:120353)

Vdrtm1Mbd/Vdr+

        involves: 129S4/SvJae
  • skeleton phenotype
  • increased bone mass
    • without overt rachitic abnormalities   (MGI Ref ID J:196471)
  • increased bone mineral density
  • increased trabecular bone volume   (MGI Ref ID J:196471)

Vdrtm1Mbd/Vdrtm1Mbd

        involves: 129S4/SvJae
  • endocrine/exocrine gland phenotype
  • enlarged parathyroid gland
    • more than 10-fold increase in parathyroid gland size of 70-day-old mice   (MGI Ref ID J:42815)
  • growth/size/body phenotype
  • decreased body weight
    • weigh 10% less than controls by 91 days of age; weight is normal at birth   (MGI Ref ID J:42815)
  • postnatal growth retardation
    • from 24 days of age, fail to grow as rapidly as controls   (MGI Ref ID J:42815)
  • homeostasis/metabolism phenotype
  • decreased circulating calcium level
    • become progressively hypocalcemic after day 21, maintaining ionized calcium levels about 25% lower than controls   (MGI Ref ID J:42815)
    • blood ionized calcium levels are decreased by 30%   (MGI Ref ID J:78067)
    • treatment with HCa-Lac (calcium, phosphorus, lactose) diet for 5 weeks normalizes calcium levels   (MGI Ref ID J:78067)
  • increased circulating angiotensinogen level
    • plasma angiotensinogen II levels are increased more than 2.5 fold compared to wildtype, however, expression of angiotensinogen is the same as wildtype   (MGI Ref ID J:78067)
    • on a high salt (8%) diet, plasma angiotensinogen II levels are significantly increased over treated control   (MGI Ref ID J:78067)
    • plasma angiotensinogen II levels are increased following 24 hour dehydration, however, levels for treated control exhibit a comparatively higher increase   (MGI Ref ID J:78067)
  • increased circulating parathyroid hormone level   (MGI Ref ID J:63291)
    • starting on day 21, exhibit a progressive increase in parathyroid hormone levels   (MGI Ref ID J:42815)
    • serum PTH concentration is increased 150-fold by 3 months of age   (MGI Ref ID J:78067)
    • treatment with HCa-Lac (calcium, phosphorus, lactose) diet for 5 weeks lowers PTH concentration to 7-fold higher than control   (MGI Ref ID J:78067)
  • increased circulating renin level
    • renin is increased in the afferent glomerular arterioles as determined by immunoreactivity   (MGI Ref ID J:78067)
  • increased renin activity
    • circulating levels of angiotensin II are higher but liver levels of the angiotensinogen precursor are normal suggesting increased rennin activity   (MGI Ref ID J:78067)
  • increased urine potassium level
    • mice excrete 19% more potassium in urine, however, blood potassium concentration is normal   (MGI Ref ID J:78067)
  • increased urine sodium level
    • mice excrete 37% more sodium in urine, however, blood sodium concentration is normal   (MGI Ref ID J:78067)
  • skeleton phenotype
  • abnormal bone mineralization
    • decreased bone mineralization in 35 day old mice but not 15 day old mice   (MGI Ref ID J:42815)
  • abnormal tibia morphology
    • decreased cortical width along the diaphysis and expansion and flaring of the growth plate at 35 days of age   (MGI Ref ID J:42815)
    • short tibia
      • tibias are about 15% shorter   (MGI Ref ID J:42815)
  • disorganized long bone epiphyseal plate
    • 35 day old growth plate is disorganized with an increase in vascularity and matrix   (MGI Ref ID J:42815)
  • increased width of hypertrophic chondrocyte zone
    • 15% increase in the number of hypertrophic chondrocytes per column in the tibia and vertebra of 15 day old mice and increased hypertrophic chondrocyte zone in 35 day old growth plate   (MGI Ref ID J:42815)
  • short femur
    • femurs are about 15% shorter   (MGI Ref ID J:42815)
  • limbs/digits/tail phenotype
  • abnormal tibia morphology
    • decreased cortical width along the diaphysis and expansion and flaring of the growth plate at 35 days of age   (MGI Ref ID J:42815)
    • short tibia
      • tibias are about 15% shorter   (MGI Ref ID J:42815)
  • short femur
    • femurs are about 15% shorter   (MGI Ref ID J:42815)
  • behavior/neurological phenotype
  • increased fluid intake
    • mice drink approximately twice as much water as controls, however, glucose and insulin levels are normal   (MGI Ref ID J:78067)
  • cardiovascular system phenotype
  • hypertension
    • mice are hypertensive with high systolic and the diastolic blood pressures caused in part by high circulating levels of renin and angiotensin II   (MGI Ref ID J:78067)
  • increased heart weight
    • heart weight to body weight ratio is significantly higher than control   (MGI Ref ID J:78067)
  • increased systemic arterial diastolic blood pressure
    • diastolic blood pressure is significantly higher (>20 mmHg) than those of wild-type littermates   (MGI Ref ID J:78067)
  • increased systemic arterial systolic blood pressure
    • systolic blood pressure is significantly higher (>20 mmHg) than those of wild-type littermates   (MGI Ref ID J:78067)
  • renal/urinary system phenotype
  • increased urine potassium level
    • mice excrete 19% more potassium in urine, however, blood potassium concentration is normal   (MGI Ref ID J:78067)
  • increased urine sodium level
    • mice excrete 37% more sodium in urine, however, blood sodium concentration is normal   (MGI Ref ID J:78067)
  • polyuria   (MGI Ref ID J:78067)
  • integument phenotype
  • abnormal hair follicle morphology
    • dilation of the hair follicles   (MGI Ref ID J:42815)
  • alopecia
    • at 4 weeks of age, begin to develop perioral and periorbital alopecia   (MGI Ref ID J:42815)
    • hair loss progresses to the entire body over the next 3 months, with more rapid progression in females than males   (MGI Ref ID J:42815)
  • dermal cysts   (MGI Ref ID J:42815)

Vdrtm1Mbd/Vdrtm1Mbd

        involves: 129S4/SvJae * C57BL/6J
  • homeostasis/metabolism phenotype
  • abnormal mineral homeostasis   (MGI Ref ID J:99866)
    • decreased circulating phosphate level   (MGI Ref ID J:99866)
  • skeleton phenotype
  • abnormal chondrocyte morphology
    • impaired hypertrophic chondrocyte apoptosis   (MGI Ref ID J:99866)
    • a 'rescue diet' of high-calcium/low-phosphate restores the normal level of apoptosis and the growth plate phenotype   (MGI Ref ID J:99866)
  • increased width of hypertrophic chondrocyte zone
    • expansion of the growth plate is associated with impaired apoptosis of late hypertrophic chondrocytes   (MGI Ref ID J:99866)
  • rickets
    • mutants develop rickets secondary to impaired apoptosis of late hypertrophic chondrocytes   (MGI Ref ID J:99866)

Vdrtm1Mbd/Vdrtm1Mbd

        involves: 129S4/SvJae * C57BL/6
  • mortality/aging
  • increased sensitivity to xenobiotic induced morbidity/mortality
    • up to 70% of mutants treated with DSS to induce colitis die within 2 weeks, compared to no mortality in treated wild-type   (MGI Ref ID J:130511)
  • growth/size/body phenotype
  • weight loss
    • mice treated with 2.5% DSS lose up to 15% of body weight within 8 days after treatment, compared to almost no weight loss in treated wild-type   (MGI Ref ID J:130511)
  • digestive/alimentary phenotype
  • abnormal intestinal epithelium morphology
    • severely distrupted and opened tight junctions and desmosomes are seen in colonic epithelia of DSS-treated mutants; in treated wild-type, epithelia appear normal   (MGI Ref ID J:130511)
    • abnormal intestinal mucosa morphology
      • erosions of mucosa of colon are observed on day 3 with 2.5% DSS treatment and substantial ulcerations are seen by day 7, while wild-type mice show no or some focal damage to mucosa on day 3 and day 7   (MGI Ref ID J:130511)
      • in mice treated with 2% DSS for 2 or 3 days, transepithelial electrical resistance (TER) is significantly reduced even in absence of clinical symptoms of colitis, compared to controls, indicating impaired mucosal barrier integrity   (MGI Ref ID J:130511)
      • abnormal large intestine crypts of Lieberkuhn morphology
        • in some colon segments, ulceration is so severe that entire crypt structure is lost   (MGI Ref ID J:130511)
        • no new crypts form around ulcers in mutants   (MGI Ref ID J:130511)
      • intestinal ulcer
        • severe ulceration is seen on day 7 of treatment for 7 days   (MGI Ref ID J:130511)
        • by day 10, some epithelial cells appear to cover ulcerations, but very little cell proliferation or healing is seen compared to wild-type mice which show healing and reepithelization of ulcers with new crypts forming around ulcers at equivalent time point   (MGI Ref ID J:130511)
  • intestinal inflammation
    • spontaneous inflammatory bowel disease (IBD) develops   (MGI Ref ID J:107077)
    • increased susceptibility to induced colitis
      • mice treated with 2.5% dextran sodium sulfate (DSS) for 1 week show more severe colitis development than treated wild-type   (MGI Ref ID J:130511)
  • immune system phenotype
  • *normal* immune system phenotype
    • at 5 weeks, thymi are not different than in wild-type   (MGI Ref ID J:107077)
    • abnormal interleukin level
      • Il-1beta is expressed in the colon; older mutants (>9 months) display 10-fold higher levels than younger mice, whereas wild-type controls do not express any cytokines in the colon at any age   (MGI Ref ID J:107077)
    • abnormal tumor necrosis factor level
      • low levels of expression are detected in colons of young animals, and levels are 20-fold higher in older mice (>9 months)   (MGI Ref ID J:107077)
    • increased thymus weight
      • increases with time and IBD   (MGI Ref ID J:107077)
    • intestinal inflammation
      • spontaneous inflammatory bowel disease (IBD) develops   (MGI Ref ID J:107077)
      • increased susceptibility to induced colitis
        • mice treated with 2.5% dextran sodium sulfate (DSS) for 1 week show more severe colitis development than treated wild-type   (MGI Ref ID J:130511)
    • thymus hyperplasia
      • increases with time and IBD   (MGI Ref ID J:107077)
  • hematopoietic system phenotype
  • increased thymus weight
    • increases with time and IBD   (MGI Ref ID J:107077)
  • thymus hyperplasia
    • increases with time and IBD   (MGI Ref ID J:107077)
  • cardiovascular system phenotype
  • *normal* cardiovascular system phenotype
    • plasma levels of angiotensin II or aldosterone are not different from wild-type   (MGI Ref ID J:120353)
    • ECG analysis does not reveal any significant differences from wild-type at 3, 6, or 9 months   (MGI Ref ID J:120353)
    • abnormal myocardial fiber physiology   (MGI Ref ID J:131143)
    • cardiac fibrosis
      • heart tissue displays increased collagen deposition primarily in the extracellular matrix   (MGI Ref ID J:120340)
    • cardiac hypertrophy
      • heart tissue displays increased cell size   (MGI Ref ID J:120340)
    • decreased systemic arterial systolic blood pressure
      • at 9 months, pressure is significantly lower than in wild-type   (MGI Ref ID J:120353)
    • increased heart weight
      • heart weight to body weight ratio is increased 41% relative to wild-type   (MGI Ref ID J:120353)
      • heart weight to body weight ratio is increased to 6.9 from 4.9 in wild-type at 12 months   (MGI Ref ID J:120340)
  • endocrine/exocrine gland phenotype
  • abnormal large intestine crypts of Lieberkuhn morphology
    • in some colon segments, ulceration is so severe that entire crypt structure is lost   (MGI Ref ID J:130511)
    • no new crypts form around ulcers in mutants   (MGI Ref ID J:130511)
  • increased thymus weight
    • increases with time and IBD   (MGI Ref ID J:107077)
  • thymus hyperplasia
    • increases with time and IBD   (MGI Ref ID J:107077)
  • homeostasis/metabolism phenotype
  • abnormal enzyme/coenzyme activity
    • matrix metalloproteinase-2 and -9 activities in heart tissue (ventricular) are increased relative to wild-type   (MGI Ref ID J:120340)
    • abnormal renin activity
      • plasma renin activity is increased by 50% but difference from wild-type activity is not significant   (MGI Ref ID J:120353)
  • abnormal interleukin level
    • Il-1beta is expressed in the colon; older mutants (>9 months) display 10-fold higher levels than younger mice, whereas wild-type controls do not express any cytokines in the colon at any age   (MGI Ref ID J:107077)
  • abnormal tumor necrosis factor level
    • low levels of expression are detected in colons of young animals, and levels are 20-fold higher in older mice (>9 months)   (MGI Ref ID J:107077)
  • increased sensitivity to xenobiotic induced morbidity/mortality
    • up to 70% of mutants treated with DSS to induce colitis die within 2 weeks, compared to no mortality in treated wild-type   (MGI Ref ID J:130511)
View Research Applications

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

Cardiovascular Research
Other

Dermatology Research
Skin and Hair Texture Defects

Endocrine Deficiency Research
Bone/Bone Marrow Defects
Gastrointestinal Defects
Skin Defects

Immunology, Inflammation and Autoimmunity Research
Growth Factors/Receptors/Cytokines
Immunodeficiency
      Inflammatory bowel disease
Inflammation
      Inflammatory bowel disease

Internal/Organ Research
Gastrointestinal Defects
      colitis
Kidney Defects

Vdrtm1Mbd related

Cardiovascular Research
Other

Dermatology Research
Skin and Hair Texture Defects

Endocrine Deficiency Research
Bone/Bone Marrow Defects
Gastrointestinal Defects
Skin Defects

Immunology, Inflammation and Autoimmunity Research
Growth Factors/Receptors/Cytokines
Immunodeficiency
      Inflammatory bowel disease
Inflammation
      Inflammatory bowel disease

Internal/Organ Research
Gastrointestinal Defects
      colitis
Kidney Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Vdrtm1Mbd
Allele Name targeted mutation 1, Marie B Demay
Allele Type Targeted (Null/Knockout)
Common Name(s) VDR -; VDR-KO; VDRKO;
Mutation Made By Marie Demay,   Massachusetts General Hospital
Strain of Origin129S4/SvJae
ES Cell Line NameJ1
ES Cell Line Strain129S4/SvJae
Gene Symbol and Name Vdr, vitamin D receptor
Chromosome 15
Gene Common Name(s) NR1I1; PPP1R163;
Molecular Note A 5 kb region of the gene encompassing exon 3 was replaced with a PGK-neo cassette via homologous recombination resulting in deletion of the second zinc finger of the DNA-binding domain. RT-PCR analysis of intestines and kidneys from homozygous mutant animals detected a mutant transcript. Sequence analysis revealed a 131 bp deletion corresponding to the second zinc finger and results in a frameshift and nonsense codon 12 bp downstream. [MGI Ref ID J:42815]

Genotyping

Genotyping Information

Genotyping Protocols

Vdrsuptm1Mbd/sup, High Resolution Melting
Vdrtm1Mbd, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Vdrtm1Mbd related

Amling M; Priemel M; Holzmann T; Chapin K; Rueger JM; Baron R; Demay MB. 1999. Rescue of the skeletal phenotype of vitamin D receptor-ablated mice in the setting of normal mineral ion homeostasis: formal histomorphometric and biomechanical analyses. Endocrinology 140(11):4982-7. [PubMed: 10537122]  [MGI Ref ID J:114167]

Bolt MJ; Liu W; Qiao G; Kong J; Zheng W; Krausz T; Cs-Szabo G; Sitrin MD; Li YC. 2004. Critical role of vitamin D in sulfate homeostasis: regulation of the sodium-sulfate cotransporter by 1,25-dihydroxyvitamin D3. Am J Physiol Endocrinol Metab 287(4):E744-9. [PubMed: 15165995]  [MGI Ref ID J:95405]

Brown AJ; Zhang F; Ritter CS. 2012. The vitamin D analog ED-71 is a potent regulator of intestinal phosphate absorption and NaPi-IIb. Endocrinology 153(11):5150-6. [PubMed: 22948213]  [MGI Ref ID J:192912]

Bruce D; Whitcomb JP; August A; McDowell MA; Cantorna MT. 2009. Elevated non-specific immunity and normal Listeria clearance in young and old vitamin D receptor knockout mice. Int Immunol 21(2):113-22. [PubMed: 19088060]  [MGI Ref ID J:144532]

Chen CH; Sakai Y; Demay MB. 2001. Targeting expression of the human vitamin D receptor to the keratinocytes of vitamin D receptor null mice prevents alopecia. Endocrinology 142(12):5386-9. [PubMed: 11713240]  [MGI Ref ID J:108797]

Chen Y; Liu W; Sun T; Huang Y; Wang Y; Deb DK; Yoon D; Kong J; Thadhani R; Li YC. 2013. 1,25-Dihydroxyvitamin D Promotes Negative Feedback Regulation of TLR Signaling via Targeting MicroRNA-155-SOCS1 in Macrophages. J Immunol 190(7):3687-95. [PubMed: 23436936]  [MGI Ref ID J:194743]

Cheng Q; Li YC; Boucher BJ; Leung PS. 2011. A novel role for vitamin D: modulation of expression and function of the local renin-angiotensin system in mouse pancreatic islets. Diabetologia :. [PubMed: 21424540]  [MGI Ref ID J:170444]

Christakos S; Dhawan P; Ajibade D; Benn BS; Feng J; Joshi SS. 2010. Mechanisms involved in vitamin D mediated intestinal calcium absorption and in non-classical actions of vitamin D. J Steroid Biochem Mol Biol 121(1-2):183-7. [PubMed: 20214989]  [MGI Ref ID J:165468]

Chung I; Han G; Seshadri M; Gillard BM; Yu WD; Foster BA; Trump DL; Johnson CS. 2009. Role of vitamin D receptor in the antiproliferative effects of calcitriol in tumor-derived endothelial cells and tumor angiogenesis in vivo. Cancer Res 69(3):967-75. [PubMed: 19141646]  [MGI Ref ID J:144997]

Demay MB. 2012. The hair cycle and Vitamin D receptor. Arch Biochem Biophys 523(1):19-21. [PubMed: 22008469]  [MGI Ref ID J:191412]

Demay MB; MacDonald PN; Skorija K; Dowd DR; Cianferotti L; Cox M. 2007. Role of the vitamin D receptor in hair follicle biology. J Steroid Biochem Mol Biol 103(3-5):344-6. [PubMed: 17223342]  [MGI Ref ID J:120248]

Ding N; Yu RT; Subramaniam N; Sherman MH; Wilson C; Rao R; Leblanc M; Coulter S; He M; Scott C; Lau SL; Atkins AR; Barish GD; Gunton JE; Liddle C; Downes M; Evans RM. 2013. A vitamin D receptor/SMAD genomic circuit gates hepatic fibrotic response. Cell 153(3):601-13. [PubMed: 23622244]  [MGI Ref ID J:198440]

Ellison TI; Smith MK; Gilliam AC; MacDonald PN. 2008. Inactivation of the vitamin D receptor enhances susceptibility of murine skin to UV-induced tumorigenesis. J Invest Dermatol 128(10):2508-17. [PubMed: 18509362]  [MGI Ref ID J:141809]

Froicu M; Zhu Y; Cantorna MT. 2006. Vitamin D receptor is required to control gastrointestinal immunity in IL-10 knockout mice. Immunology 117(3):310-8. [PubMed: 16476050]  [MGI Ref ID J:107077]

Fudge NJ; Kovacs CS. 2010. Pregnancy up-regulates intestinal calcium absorption and skeletal mineralization independently of the vitamin D receptor. Endocrinology 151(3):886-95. [PubMed: 20051486]  [MGI Ref ID J:168524]

Goltzman D. 2007. Use of genetically modified mice to examine the skeletal anabolic activity of vitamin D. J Steroid Biochem Mol Biol 103(3-5):587-91. [PubMed: 17254773]  [MGI Ref ID J:120278]

Gunther T; Chen ZF; Kim J; Priemel M; Rueger JM; Amling M; Moseley JM; Martin TJ; Anderson DJ; Karsenty G. 2000. Genetic ablation of parathyroid glands reveals another source of parathyroid hormone. Nature 406(6792):199-203. [PubMed: 10910362]  [MGI Ref ID J:63291]

Guzey M; Jukic D; Arlotti J; Acquafondata M; Dhir R; Getzenberg RH. 2004. Increased apoptosis of periprostatic adipose tissue in VDR null mice. J Cell Biochem 93(1):133-41. [PubMed: 15352170]  [MGI Ref ID J:92877]

He Q; Ananaba GA; Patrickson J; Pitts S; Yi Y; Yan F; Eko FO; Lyn D; Black CM; Igietseme JU; Thierry-Palmer M. 2013. Chlamydial infection in vitamin D receptor knockout mice is more intense and prolonged than in wild-type mice. J Steroid Biochem Mol Biol 135:7-14. [PubMed: 23201171]  [MGI Ref ID J:196794]

Jeanson NT; Scadden DT. 2010. Vitamin D receptor deletion leads to increased hematopoietic stem and progenitor cells residing in the spleen. Blood 116(20):4126-9. [PubMed: 20664059]  [MGI Ref ID J:166469]

Kong J; Grando SA; Li YC. 2006. Regulation of IL-1 family cytokines IL-1alpha, IL-1 receptor antagonist, and IL-18 by 1,25-dihydroxyvitamin D3 in primary keratinocytes. J Immunol 176(6):3780-7. [PubMed: 16517748]  [MGI Ref ID J:129534]

Kong J; Qiao G; Zhang Z; Liu SQ; Li YC. 2008. Targeted vitamin D receptor expression in juxtaglomerular cells suppresses renin expression independent of parathyroid hormone and calcium. Kidney Int 74(12):1577-81. [PubMed: 19034301]  [MGI Ref ID J:162709]

Kong J; Zhang Z; Musch MW; Ning G; Sun J; Hart J; Bissonnette M; Li YC. 2008. Novel role of the vitamin D receptor in maintaining the integrity of the intestinal mucosal barrier. Am J Physiol Gastrointest Liver Physiol 294(1):G208-16. [PubMed: 17962355]  [MGI Ref ID J:130511]

Kong J; Zhu X; Shi Y; Liu T; Chen Y; Bhan I; Zhao Q; Thadhani R; Li YC. 2013. VDR attenuates acute lung injury by blocking Ang-2-Tie-2 pathway and renin-angiotensin system. Mol Endocrinol 27(12):2116-25. [PubMed: 24196349]  [MGI Ref ID J:211899]

Kovacs CS; Woodland ML; Fudge NJ; Friel JK. 2005. The vitamin D receptor is not required for fetal mineral homeostasis or for the regulation of placental calcium transfer in mice. Am J Physiol Endocrinol Metab 289(1):E133-44. [PubMed: 15741244]  [MGI Ref ID J:99514]

Larriba MJ; Ordonez-Moran P; Chicote I; Martin-Fernandez G; Puig I; Munoz A; Palmer HG. 2011. Vitamin D receptor deficiency enhances Wnt/beta-catenin signaling and tumor burden in colon cancer. PLoS One 6(8):e23524. [PubMed: 21858154]  [MGI Ref ID J:178127]

Lee CS; Chen J; Wang Y; Williams JK; Ranly DM; Schwartz Z; Boyan BD. 2011. Coordinated tether formation in anatomically distinct mice growth centers is dependent on a functional vitamin D receptor and is tightly linked to three-dimensional tissue morphology. Bone 49(3):419-27. [PubMed: 21601024]  [MGI Ref ID J:175399]

Li YC; Amling M; Pirro AE; Priemel M; Meuse J; Baron R; Delling G; Demay MB. 1998. Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice. Endocrinology 139(10):4391-6. [PubMed: 9751523]  [MGI Ref ID J:148679]

Li YC; Bolt MJ; Cao LP; Sitrin MD. 2001. Effects of vitamin D receptor inactivation on the expression of calbindins and calcium metabolism. Am J Physiol Endocrinol Metab 281(3):E558-64. [PubMed: 11500311]  [MGI Ref ID J:107742]

Li YC; Kong J; Wei M; Chen ZF; Liu SQ; Cao LP. 2002. 1,25-Dihydroxyvitamin D(3) is a negative endocrine regulator of the renin-angiotensin system. J Clin Invest 110(2):229-38. [PubMed: 12122115]  [MGI Ref ID J:78067]

Li YC; Pirro AE; Amling M; Delling G; Baron R; Bronson R; Demay MB. 1997. Targeted ablation of the vitamin D receptor: an animal model of vitamin D-dependent rickets type II with alopecia. Proc Natl Acad Sci U S A 94(18):9831-5. [PubMed: 9275211]  [MGI Ref ID J:42815]

Li YC; Pirro AE; Demay MB. 1998. Analysis of vitamin D-dependent calcium-binding protein messenger ribonucleic acid expression in mice lacking the vitamin D receptor. Endocrinology 139(3):847-51. [PubMed: 9492012]  [MGI Ref ID J:114263]

Liu NQ; Kaplan AT; Lagishetty V; Ouyang YB; Ouyang Y; Simmons CF; Equils O; Hewison M. 2011. Vitamin D and the regulation of placental inflammation. J Immunol 186(10):5968-74. [PubMed: 21482732]  [MGI Ref ID J:173088]

Liu W; Chen Y; Golan MA; Annunziata ML; Du J; Dougherty U; Kong J; Musch M; Huang Y; Pekow J; Zheng C; Bissonnette M; Hanauer SB; Li YC. 2013. Intestinal epithelial vitamin D receptor signaling inhibits experimental colitis. J Clin Invest 123(9):3983-96. [PubMed: 23945234]  [MGI Ref ID J:201599]

Luderer HF; Gori F; Demay MB. 2011. Lymphoid enhancer-binding factor-1 (LEF1) interacts with the DNA-binding domain of the vitamin D receptor. J Biol Chem 286(21):18444-51. [PubMed: 21471213]  [MGI Ref ID J:173782]

Luderer HF; Nazarian RM; Zhu ED; Demay MB. 2013. Ligand-dependent actions of the vitamin D receptor are required for activation of TGF-beta signaling during the inflammatory response to cutaneous injury. Endocrinology 154(1):16-24. [PubMed: 23132743]  [MGI Ref ID J:192827]

Ma Y; Samaraweera M; Cooke-Hubley S; Kirby BJ; Karaplis AC; Lanske B; Kovacs CS. 2014. Neither absence nor excess of FGF23 disturbs murine fetal-placental phosphorus homeostasis or prenatal skeletal development and mineralization. Endocrinology 155(5):1596-605. [PubMed: 24601885]  [MGI Ref ID J:210730]

Marks HD; Fleet JC; Peleg S. 2007. Transgenic expression of the human Vitamin D receptor (hVDR) in the duodenum of VDR-null mice attenuates the age-dependent decline in calcium absorption. J Steroid Biochem Mol Biol 103(3-5):513-6. [PubMed: 17207992]  [MGI Ref ID J:120281]

Narvaez CJ; Matthews D; Broun E; Chan M; Welsh J. 2009. Lean phenotype and resistance to diet-induced obesity in vitamin D receptor knockout mice correlates with induction of uncoupling protein-1 in white adipose tissue. Endocrinology 150(2):651-61. [PubMed: 18845643]  [MGI Ref ID J:158102]

Panda DK; Miao D; Bolivar I; Li J; Huo R; Hendy GN; Goltzman D. 2004. Inactivation of the 25-hydroxyvitamin D 1alpha-hydroxylase and vitamin D receptor demonstrates independent and interdependent effects of calcium and vitamin D on skeletal and mineral homeostasis. J Biol Chem 279(16):16754-66. [PubMed: 14739296]  [MGI Ref ID J:89533]

Rahman A; Hershey S; Ahmed S; Nibbelink K; Simpson RU. 2007. Heart extracellular matrix gene expression profile in the vitamin D receptor knockout mice. J Steroid Biochem Mol Biol 103(3-5):416-9. [PubMed: 17275288]  [MGI Ref ID J:120340]

Sabbagh Y; Carpenter TO; Demay MB. 2005. Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes. Proc Natl Acad Sci U S A 102(27):9637-42. [PubMed: 15976027]  [MGI Ref ID J:99866]

Sakai Y; Demay MB. 2000. Evaluation of keratinocyte proliferation and differentiation in vitamin D receptor knockout mice. Endocrinology 141(6):2043-9. [PubMed: 10830288]  [MGI Ref ID J:108817]

Sakai Y; Kishimoto J; Demay MB. 2001. Metabolic and cellular analysis of alopecia in vitamin D receptor knockout mice. J Clin Invest 107(8):961-6. [PubMed: 11306599]  [MGI Ref ID J:68883]

Salehi-Tabar R; Nguyen-Yamamoto L; Tavera-Mendoza LE; Quail T; Dimitrov V; An BS; Glass L; Goltzman D; White JH. 2012. Vitamin D receptor as a master regulator of the c-MYC/MXD1 network. Proc Natl Acad Sci U S A 109(46):18827-32. [PubMed: 23112173]  [MGI Ref ID J:191735]

Schwarz A; Navid F; Sparwasser T; Clausen BE; Schwarz T. 2012. 1,25-dihydroxyvitamin D exerts similar immunosuppressive effects as UVR but is dispensable for local UVR-induced immunosuppression. J Invest Dermatol 132(12):2762-9. [PubMed: 22854622]  [MGI Ref ID J:191596]

Simpson RU; Hershey SH; Nibbelink KA. 2007. Characterization of heart size and blood pressure in the vitamin D receptor knockout mouse. J Steroid Biochem Mol Biol 103(3-5):521-4. [PubMed: 17275289]  [MGI Ref ID J:120353]

Skorija K; Cox M; Sisk JM; Dowd DR; Macdonald PN; Thompson CC; Demay MB. 2005. Ligand-independent actions of the vitamin d receptor maintain hair follicle homeostasis. Mol Endocrinol 19(4):855-62. [PubMed: 15591533]  [MGI Ref ID J:96966]

St-Arnaud R; Arabian A; Travers R; Barletta F; Raval-Pandya M; Chapin K; Depovere J; Mathieu C; Christakos S; Demay MB; Glorieux FH. 2000. Deficient mineralization of intramembranous bone in vitamin D-24-hydroxylase-ablated mice is due to elevated 1,25-dihydroxyvitamin D and not to the absence of 24,25-dihydroxyvitamin D. Endocrinology 141(7):2658-66. [PubMed: 10875271]  [MGI Ref ID J:63457]

Sundar IK; Hwang JW; Wu S; Sun J; Rahman I. 2011. Deletion of vitamin D receptor leads to premature emphysema/COPD by increased matrix metalloproteinases and lymphoid aggregates formation. Biochem Biophys Res Commun 406(1):127-33. [PubMed: 21300024]  [MGI Ref ID J:170919]

Tishkoff DX; Nibbelink KA; Holmberg KH; Dandu L; Simpson RU. 2008. Functional vitamin D receptor (VDR) in the t-tubules of cardiac myocytes: VDR knockout cardiomyocyte contractility. Endocrinology 149(2):558-64. [PubMed: 17974622]  [MGI Ref ID J:131143]

Waisberg M; Vickers BK; Yager SB; Lin CK; Pierce SK. 2012. Testing in mice the hypothesis that melanin is protective in malaria infections. PLoS One 7(1):e29493. [PubMed: 22242171]  [MGI Ref ID J:184147]

Wang Y; Becklund BR; DeLuca HF. 2010. Identification of a highly specific and versatile vitamin D receptor antibody. Arch Biochem Biophys 494(2):166-77. [PubMed: 19951695]  [MGI Ref ID J:158462]

Wang Y; Marling SJ; Zhu JG; Severson KS; Deluca HF. 2012. Development of experimental autoimmune encephalomyelitis (EAE) in mice requires vitamin D and the vitamin D receptor. Proc Natl Acad Sci U S A 109(22):8501-4. [PubMed: 22592802]  [MGI Ref ID J:184751]

Welsh J; Wietzke JA; Zinser GM; Smyczek S; Romu S; Tribble E; Welsh JC; Byrne B; Narvaez CJ. 2003. Impact of the Vitamin D3 receptor on growth-regulatory pathways in mammary gland and breast cancer. J Steroid Biochem Mol Biol 83(1-5):85-92. [PubMed: 12650704]  [MGI Ref ID J:82977]

Welsh J; Zinser LN; Mianecki-Morton L; Martin J; Waltz SE; James H; Zinser GM. 2011. Age-related changes in the epithelial and stromal compartments of the mammary gland in normocalcemic mice lacking the vitamin D3 receptor. PLoS One 6(1):e16479. [PubMed: 21298063]  [MGI Ref ID J:180942]

Wong KE; Szeto FL; Zhang W; Ye H; Kong J; Zhang Z; Sun XJ; Li YC. 2009. Involvement of the vitamin D receptor in energy metabolism: regulation of uncoupling proteins. Am J Physiol Endocrinol Metab 296(4):E820-8. [PubMed: 19176352]  [MGI Ref ID J:148131]

Wu S; Liao AP; Xia Y; Li YC; Li JD; Sartor RB; Sun J. 2010. Vitamin D receptor negatively regulates bacterial-stimulated NF-kappaB activity in intestine. Am J Pathol 177(2):686-97. [PubMed: 20566739]  [MGI Ref ID J:163398]

Xiang W; Kong J; Chen S; Cao LP; Qiao G; Zheng W; Liu W; Li X; Gardner DG; Li YC. 2005. Cardiac hypertrophy in vitamin D receptor knockout mice: role of the systemic and cardiac renin-angiotensin systems. Am J Physiol Endocrinol Metab 288(1):E125-32. [PubMed: 15367398]  [MGI Ref ID J:96045]

Yamamoto Y; Yoshizawa T; Fukuda T; Shirode-Fukuda Y; Yu T; Sekine K; Sato T; Kawano H; Aihara K; Nakamichi Y; Watanabe T; Shindo M; Inoue K; Inoue E; Tsuji N; Hoshino M; Karsenty G; Metzger D; Chambon P; Kato S; Imai Y. 2013. Vitamin D receptor in osteoblasts is a negative regulator of bone mass control. Endocrinology 154(3):1008-20. [PubMed: 23389957]  [MGI Ref ID J:196471]

Yu S; Cantorna MT. 2008. The vitamin D receptor is required for iNKT cell development. Proc Natl Acad Sci U S A 105(13):5207-12. [PubMed: 18364394]  [MGI Ref ID J:133570]

Yu X; Sabbagh Y; Davis SI; Demay MB; White KE. 2005. Genetic dissection of phosphate- and vitamin D-mediated regulation of circulating Fgf23 concentrations. Bone 36(6):971-7. [PubMed: 15869926]  [MGI Ref ID J:123814]

Zhang C; Tang W; Li Y; Yang F; Dowd DR; MacDonald PN. 2011. Osteoblast-specific transcription factor Osterix increases vitamin D receptor gene expression in osteoblasts. PLoS One 6(10):e26504. [PubMed: 22028889]  [MGI Ref ID J:178091]

Zhang Z; Sun L; Wang Y; Ning G; Minto AW; Kong J; Quigg RJ; Li YC. 2008. Renoprotective role of the vitamin D receptor in diabetic nephropathy. Kidney Int 73(2):163-71. [PubMed: 17928826]  [MGI Ref ID J:152885]

Zheng W; Wong KE; Zhang Z; Dougherty U; Mustafi R; Kong J; Deb DK; Zheng H; Bissonnette M; Li YC. 2012. Inactivation of the vitamin D receptor in APC(min/+) mice reveals a critical role for the vitamin D receptor in intestinal tumor growth. Int J Cancer 130(1):10-9. [PubMed: 21328347]  [MGI Ref ID J:178583]

Zheng W; Xie Y; Li G; Kong J; Feng JQ; Li YC. 2004. Critical role of calbindin-D28k in calcium homeostasis revealed by mice lacking both vitamin D receptor and calbindin-D28k. J Biol Chem 279(50):52406-13. [PubMed: 15456794]  [MGI Ref ID J:95170]

Zhu Y; Mahon BD; Froicu M; Cantorna MT. 2005. Calcium and 1 alpha,25-dihydroxyvitamin D3 target the TNF-alpha pathway to suppress experimental inflammatory bowel disease. Eur J Immunol 35(1):217-24. [PubMed: 15593122]  [MGI Ref ID J:95228]

Zinser G; Packman K; Welsh J. 2002. Vitamin D(3) receptor ablation alters mammary gland morphogenesis. Development 129(13):3067-76. [PubMed: 12070083]  [MGI Ref ID J:110843]

Zinser GM; Suckow M; Welsh J. 2005. Vitamin D receptor (VDR) ablation alters carcinogen-induced tumorigenesis in mammary gland, epidermis and lymphoid tissues. J Steroid Biochem Mol Biol 97(1-2):153-64. [PubMed: 16111884]  [MGI Ref ID J:102891]

Zinser GM; Sundberg JP; Welsh J. 2002. Vitamin D(3) receptor ablation sensitizes skin to chemically induced tumorigenesis. Carcinogenesis 23(12):2103-9. [PubMed: 12507934]  [MGI Ref ID J:81031]

Zinser GM; Welsh J. 2004. Accelerated Mammary Gland Development during Pregnancy and Delayed Postlactational Involution in Vitamin D3 Receptor Null Mice. Mol Endocrinol 18(9):2208-23. [PubMed: 15178742]  [MGI Ref ID J:92080]

Zinser GM; Welsh J. 2004. Vitamin D receptor status alters mammary gland morphology and tumorigenesis in MMTV-neu mice. Carcinogenesis 25(12):2361-72. [PubMed: 15333467]  [MGI Ref ID J:94402]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX10

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony on a C57BL/6 background, mutant mice can be bred as heterozygotes.
Mating SystemHeterozygote x Heterozygote         (Female x Male)   16-MAY-07
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 Vdrtm1Mbd  
$232.00Female or MaleHomozygous for Vdrtm1Mbd  
Price per Pair (US dollars $)Pair Genotype
$464.00Heterozygous for Vdrtm1Mbd x Heterozygous for Vdrtm1Mbd  

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 $301.60Female or MaleHeterozygous for Vdrtm1Mbd  
$301.60Female or MaleHomozygous for Vdrtm1Mbd  
Price per Pair (US dollars $)Pair Genotype
$603.20Heterozygous for Vdrtm1Mbd x Heterozygous for Vdrtm1Mbd  

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

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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.
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JAX® Mice
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JAX® Services
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Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
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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.

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General inquiries regarding Terms of Use

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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.

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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