Strain Name:

B6;129-Ahrtm1Bra/J

Stock Number:

002727

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Availability:

Cryopreserved - Ready for recovery

Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Specieslaboratory mouse
 
Donating InvestigatorDr. Christopher Bradfield,   University of Wisconsin Medical School

Appearance
black
Related Genotype: a/a

Description
Mice homozygous for the Ahrtm1Bra targeted mutation are viable and fertile. Homozygotes do not respond to aryl-hydrocarbon receptor agonists. They show reduced liver weight (25% decrease) delayed extramedullary hematopoiesis, and transient hepatic microvesicular steatosis.

Development
The strain was developed using a construct that replaced exon 2 of the endogenous gene with the neomycin gene. The construct was electroporated into both (129X1/SvJ x 129S1/Sv)F1-derived R1 embryonic stem (ES) cells and CCE-derived 129S6/SvEvTac ES cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts and transfered into pseudopregnant CD1 foster mothers. Chimeric males were bred to C57BL/6 females. Heterozygous mice were bred to generate homozygotes.

Control Information

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

Related Strains

Strains carrying   Ahrtm1Bra allele
002831   B6.129-Ahrtm1Bra/J
View Strains carrying   Ahrtm1Bra     (1 strain)

Strains carrying other alleles of Ahr
000690   129P3/J
000645   A/HeJ
000646   A/J
000648   AKR/J
002920   B6(D2N).Spretus-Ahrb-3/J
000130   B6.C-H17c/(HW14)ByJ
000136   B6.C-H34c/(HW22)ByJ
000370   B6.C-H38c/(HW119)ByJ
008599   B6.Cg-Del(9Cyp1a2-Cyp1a1)1Dwn Ahrd Tg(CYP1A1,CYP1A2)1Dwn/DwnJ
002921   B6.D2N-Ahrd/J
001026   BALB/cByJ
000652   BDP/J
000653   BUB/BnJ
000659   C3H/HeJ
000663   C57BL/6By
001139   C57BL/6ByJ
000664   C57BL/6J
000662   C57BLKS/J
000667   C57BR/cdJ
000668   C57L/J
000669   C58/J
000926   CAROLI/EiJ
000928   CAST/EiJ
000656   CBA/J
000657   CE/J
000351   CXB1/ByJ
000352   CXB2/ByJ
000353   CXB3/ByJ
000354   CXB4/ByJ
000355   CXB5/ByJ
000356   CXB6/ByJ
000357   CXB7/ByJ
002937   D2.B6-Ahrb-1/J
000671   DBA/2J
000673   HRS/J
000674   I/LnJ
000675   LG/J
000676   LP/J
000677   MA/MyJ
000550   MOLF/EiJ
000684   NZB/BlNJ
000679   P/J
000930   PERA/EiJ
000726   RBF/DnJ
000682   RF/J
000644   SEA/GnJ
000280   SF/CamEiJ
000686   SJL/J
001146   SPRET/EiJ
000688   ST/bJ
006203   STOCK Ahrtm3.1Bra/J
000689   SWR/J
000693   WC/ReJ KitlSl/J
000933   YBR/EiJ
View Strains carrying other alleles of Ahr     (54 strains)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Ahrtm1Bra/Ahrtm1Bra

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6
  • homeostasis/metabolism phenotype
  • decreased physiological sensitivity to xenobiotic
    • resistance to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced toxicity; mutants do not exhibit hepatomegaly, thymic involution or cleft palate formation in response to TCDD administration   (MGI Ref ID J:83597)
  • cardiovascular system phenotype
  • patent ductus venosus   (MGI Ref ID J:83597)
  • growth/size/body phenotype
  • decreased body weight   (MGI Ref ID J:33827)
  • postnatal growth retardation   (MGI Ref ID J:33827)
  • immune system phenotype
  • abnormal Langerhans cell morphology
    • expression analysis indicates impaired maturation after 3 days in culture   (MGI Ref ID J:148870)
    • immature cells are slightly smaller and remain of lower granularity after maturation compared to controls   (MGI Ref ID J:148870)
  • abnormal Langerhans cell physiology
    • expression of CD24a is reduced on immature and mature Langerhans cells   (MGI Ref ID J:148870)
    • after 45, but not after 90, minutes in culture phagocytic activity is increased   (MGI Ref ID J:148870)
  • abnormal cytokine secretion
    • secretion of granulocyte macrophage colony stimulating factor (CSF2) is reduced in cultured epidermal cells (about 90% keratinocytes)   (MGI Ref ID J:148870)
  • decreased spleen germinal center size
    • smaller germinal centers   (MGI Ref ID J:33827)
  • decreased susceptibility to type IV hypersensitivity reaction
    • the increase in ear thickness following exposure to fluorescein isothiocyanate (FITC) is decreased compared to similarly treated controls   (MGI Ref ID J:148870)
  • enlarged spleen
    • exhibited by ~50% at 6 weeks of age   (MGI Ref ID J:33827)
    • increased erythroid component   (MGI Ref ID J:33827)
    • ~50% increase in mononuclear cell numbers at 6 weeks of age, but not at 2 or 3 weeks of age   (MGI Ref ID J:33827)
  • liver/biliary system phenotype
  • hepatic steatosis
    • extensive microvesicular fatty metamorphosis that was neither consistently pericentral or periportal   (MGI Ref ID J:33827)
    • evidence of fatty metamorphosis dissipated by 3 weeks of age   (MGI Ref ID J:33827)
  • liver hyperplasia
    • hypercellularity with thickening and fibrosis in portal regions by 2 weeks of age   (MGI Ref ID J:33827)
  • pale liver
    • evident prior to 2 weeks of age   (MGI Ref ID J:33827)
  • small liver   (MGI Ref ID J:33827)
    • decreased liver weight
      • reduced liver weight (28% less than wild-type)   (MGI Ref ID J:83597)
  • reproductive system phenotype
  • abnormal primordial ovarian follicle morphology
    • at P4 the number of primordial follicles is increased about 2 fold compared to littermate controls   (MGI Ref ID J:59155)
  • endocrine/exocrine gland phenotype
  • abnormal primordial ovarian follicle morphology
    • at P4 the number of primordial follicles is increased about 2 fold compared to littermate controls   (MGI Ref ID J:59155)
  • hematopoietic system phenotype
  • abnormal Langerhans cell morphology
    • expression analysis indicates impaired maturation after 3 days in culture   (MGI Ref ID J:148870)
    • immature cells are slightly smaller and remain of lower granularity after maturation compared to controls   (MGI Ref ID J:148870)
  • decreased spleen germinal center size
    • smaller germinal centers   (MGI Ref ID J:33827)
  • enlarged spleen
    • exhibited by ~50% at 6 weeks of age   (MGI Ref ID J:33827)
    • increased erythroid component   (MGI Ref ID J:33827)
    • ~50% increase in mononuclear cell numbers at 6 weeks of age, but not at 2 or 3 weeks of age   (MGI Ref ID J:33827)
  • extramedullary hematopoiesis
    • occuring in postnatal livers   (MGI Ref ID J:33827)
    • varying penetrance, tending to be milder in livers with more severe fatty metamorphosis   (MGI Ref ID J:33827)
  • integument phenotype
  • abnormal keratinocyte physiology
    • secretion of granulocyte macrophage colony stimulating factor (CSF2) is reduced in cultured epidermal cells (about 90% keratinocytes)   (MGI Ref ID J:148870)
  • cellular phenotype
  • patent ductus venosus   (MGI Ref ID J:83597)

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

Ahrtm1Bra/Ahrtm1Bra

        involves: 129S1/Sv * 129X1/SvJ
  • cardiovascular system phenotype
  • patent ductus venosus
    • a patent ductus venosus (shunting blood around the liver) was seen in all mutants   (MGI Ref ID J:94465)
    • exposure to non-teratogenic concentration of dioxin on E18.5 did not result in closure of the ductus venosus in any mutants unlike in Ahrtm3Bra homozygotes   (MGI Ref ID J:94465)
    • in all mice   (MGI Ref ID J:166864)
  • reproductive system phenotype
  • abnormal ovarian folliculogenesis
    • reduced numbers preantral and antral follicles   (MGI Ref ID J:82983)
    • no increase in atresia relative to wild-type   (MGI Ref ID J:82983)
    • increased number of primordial follicles relative to wild-type at 2 to 3 days of age, similar numbers were observed in both mutant and wild-type ovaries between 8 and 53 days of age   (MGI Ref ID J:83527)
    • reduced numbers preantral and antral follicles at 53 days of age   (MGI Ref ID J:83527)
  • abnormal ovary physiology
    • following treatment with a low dose equine chorionic gonadotropin (eCG) fewer corpora lutea are present compared to similarly treated controls   (MGI Ref ID J:124374)
  • abnormal ovulation
    • fewer corpora lutea by 45 days of age   (MGI Ref ID J:82983)
    • abnormal superovulation
      • following treatment with low doses of exogenous gonadotropins fewer oocytes are collected compared to similarly treated controls   (MGI Ref ID J:124374)
      • however, ovulation in response to higher doses of exogenous gonadotropins is similar to controls   (MGI Ref ID J:124374)
  • decreased corpora lutea number
    • fewer corpora lutea by 45 days of age   (MGI Ref ID J:83527)
  • decreased germ cell number
    • similar number of germ cells as wild-type at E18   (MGI Ref ID J:83527)
    • 70% reduction in the number of ovarian germ cells at 2 days of age   (MGI Ref ID J:83527)
  • small ovary   (MGI Ref ID J:82983)
    • decreased ovary weight
      • following treatment with a low dose equine chorionic gonadotropin (eCG) ovarian weights are significantly less than similarly treated controls   (MGI Ref ID J:124374)
      • however, in the absence of treatment or after treatment with a high dose of eCG ovarian weights are similar to controls   (MGI Ref ID J:124374)
  • endocrine/exocrine gland phenotype
  • abnormal branching of the mammary ductal tree
    • the number of terminal end buds is reduced by about 50% compared to littermate controls most ducts appear to be blunt ended or narrowed at the tip   (MGI Ref ID J:51158)
  • abnormal ovarian folliculogenesis
    • reduced numbers preantral and antral follicles   (MGI Ref ID J:82983)
    • no increase in atresia relative to wild-type   (MGI Ref ID J:82983)
    • increased number of primordial follicles relative to wild-type at 2 to 3 days of age, similar numbers were observed in both mutant and wild-type ovaries between 8 and 53 days of age   (MGI Ref ID J:83527)
    • reduced numbers preantral and antral follicles at 53 days of age   (MGI Ref ID J:83527)
  • abnormal ovary physiology
    • following treatment with a low dose equine chorionic gonadotropin (eCG) fewer corpora lutea are present compared to similarly treated controls   (MGI Ref ID J:124374)
  • decreased corpora lutea number
    • fewer corpora lutea by 45 days of age   (MGI Ref ID J:83527)
  • small ovary   (MGI Ref ID J:82983)
    • decreased ovary weight
      • following treatment with a low dose equine chorionic gonadotropin (eCG) ovarian weights are significantly less than similarly treated controls   (MGI Ref ID J:124374)
      • however, in the absence of treatment or after treatment with a high dose of eCG ovarian weights are similar to controls   (MGI Ref ID J:124374)
  • integument phenotype
  • abnormal branching of the mammary ductal tree
    • the number of terminal end buds is reduced by about 50% compared to littermate controls most ducts appear to be blunt ended or narrowed at the tip   (MGI Ref ID J:51158)
  • cellular phenotype
  • patent ductus venosus
    • a patent ductus venosus (shunting blood around the liver) was seen in all mutants   (MGI Ref ID J:94465)
    • exposure to non-teratogenic concentration of dioxin on E18.5 did not result in closure of the ductus venosus in any mutants unlike in Ahrtm3Bra homozygotes   (MGI Ref ID J:94465)
    • in all mice   (MGI Ref ID J:166864)

Ahrtm1Bra/Ahrtm1Bra

        B6.129-Ahrtm1Bra/J
  • homeostasis/metabolism phenotype
  • abnormal cytokine level
    • levels of proinflammatory cytokines are increased in bronchoalveolar lavage (BAL) fluid   (MGI Ref ID J:118646)
    • abnormal chemokine level
      • levels of proinflammatory chemokines are increased in bronchoalveolar lavage (BAL) fluid   (MGI Ref ID J:118646)
      • basal and 4 h post cigarette smoke exposure levels of CXCL2 and PGE2 are increased in BAL fluid relative to similarly treated controls   (MGI Ref ID J:118646)
    • abnormal interleukin level
      • increased levels of IL6 in BAL fluid   (MGI Ref ID J:118646)
    • abnormal tumor necrosis factor level
      • both basal levels and expression 4 h after cigarette smoke exposure are increased in BAL fluid relative to similarly treated controls   (MGI Ref ID J:118646)
  • abnormal enzyme/coenzyme activity
    • basal pulmonary ethoxyresorufin O-deethylase (EROD) activity is reduced and exposure to hyperoxia fails to increase pulmonary or hepatic EROD activity   (MGI Ref ID J:100359)
    • basal hepatic methoxyresorufin O-demethylase (MROD) activity is reduced   (MGI Ref ID J:100359)
    • however, hyperoxia still induces an increase in MROD activity   (MGI Ref ID J:100359)
  • increased physiological sensitivity to xenobiotic
    • following cigarette smoke exposure neutrophil influx into and beta-glucuronidase activity in the lungs are increased compared to similarly exposed wild-type controls   (MGI Ref ID J:118646)
    • following cigarette smoke exposure perivascular infiltrates are more pronounced in the lungs   (MGI Ref ID J:118646)
  • increased susceptibility to injury
    • mice are more susceptible to hyperoxia induced lung injury with severe alveolar flooding, pulmonary edema, and increased lung inflammation   (MGI Ref ID J:100359)
  • pulmonary edema
    • severe edema is seen after exposure to hyperoxia   (MGI Ref ID J:100359)
    • pulmonary alveolar edema
      • severe alveolar flooding after exposure to hyperoxia   (MGI Ref ID J:100359)
  • reproductive system phenotype
  • abnormal ovary physiology
    • cultured fetal ovaries show a decrease in the number of apoptotic germ cells   (MGI Ref ID J:59155)
  • abnormal primordial ovarian follicle morphology
    • at P4 the number of primordial follicles is increased about 2 fold compared to littermate controls   (MGI Ref ID J:59155)
  • immune system phenotype
  • abnormal cytokine level
    • levels of proinflammatory cytokines are increased in bronchoalveolar lavage (BAL) fluid   (MGI Ref ID J:118646)
    • abnormal chemokine level
      • levels of proinflammatory chemokines are increased in bronchoalveolar lavage (BAL) fluid   (MGI Ref ID J:118646)
      • basal and 4 h post cigarette smoke exposure levels of CXCL2 and PGE2 are increased in BAL fluid relative to similarly treated controls   (MGI Ref ID J:118646)
    • abnormal interleukin level
      • increased levels of IL6 in BAL fluid   (MGI Ref ID J:118646)
    • abnormal tumor necrosis factor level
      • both basal levels and expression 4 h after cigarette smoke exposure are increased in BAL fluid relative to similarly treated controls   (MGI Ref ID J:118646)
  • abnormal macrophage physiology
    • macrophages from BAL fluid exposed to LPS in vitro produce more IL6 and TNF   (MGI Ref ID J:118646)
    • exposure to an NFKB inhibitor (helenalin or SN50) blocks LPS induced IL6 and TNF expression in both mutant and wild-type mice   (MGI Ref ID J:118646)
  • increased susceptibility to bacterial infection
    • inflammatory response in the lungs following aerosol exposure to LPS is increased compared to similarly treated controls   (MGI Ref ID J:118646)
    • macrophages from BAL fluid exposed to LPS in vitro produce more IL6 and TNF   (MGI Ref ID J:118646)
  • lung inflammation
    • lung inflammation after exposure to hyperoxia is increased compared to wild-type controls   (MGI Ref ID J:100359)
    • following cigarette smoke exposure neutrophil influx into and beta-glucuronidase activity in the lungs are increased compared to similarly exposed wild-type controls   (MGI Ref ID J:118646)
    • following cigarette smoke exposure perivascular infiltrates are more pronounced   (MGI Ref ID J:118646)
    • inflammatory response in the lungs following aerosol exposure to LPS is increased compared to similarly treated controls   (MGI Ref ID J:118646)
  • endocrine/exocrine gland phenotype
  • abnormal ovary physiology
    • cultured fetal ovaries show a decrease in the number of apoptotic germ cells   (MGI Ref ID J:59155)
  • abnormal primordial ovarian follicle morphology
    • at P4 the number of primordial follicles is increased about 2 fold compared to littermate controls   (MGI Ref ID J:59155)
  • respiratory system phenotype
  • lung inflammation
    • lung inflammation after exposure to hyperoxia is increased compared to wild-type controls   (MGI Ref ID J:100359)
    • following cigarette smoke exposure neutrophil influx into and beta-glucuronidase activity in the lungs are increased compared to similarly exposed wild-type controls   (MGI Ref ID J:118646)
    • following cigarette smoke exposure perivascular infiltrates are more pronounced   (MGI Ref ID J:118646)
    • inflammatory response in the lungs following aerosol exposure to LPS is increased compared to similarly treated controls   (MGI Ref ID J:118646)
  • pulmonary edema
    • severe edema is seen after exposure to hyperoxia   (MGI Ref ID J:100359)
    • pulmonary alveolar edema
      • severe alveolar flooding after exposure to hyperoxia   (MGI Ref ID J:100359)
  • hematopoietic system phenotype
  • abnormal macrophage physiology
    • macrophages from BAL fluid exposed to LPS in vitro produce more IL6 and TNF   (MGI Ref ID J:118646)
    • exposure to an NFKB inhibitor (helenalin or SN50) blocks LPS induced IL6 and TNF expression in both mutant and wild-type mice   (MGI Ref ID J:118646)

Ahrtm1Bra/Ahrtm1Bra

        B6.129-Ahrtm1Bra
  • homeostasis/metabolism phenotype
  • abnormal circulating hormone level
    • serum concentration of 5alpha-androstane-3alpha,17beta-diol are reduced at P21   (MGI Ref ID J:126176)
  • decreased physiological sensitivity to xenobiotic
    • exposure to 2,3,7,8-tetrachrlorodibenzo-p-dioxin (TCDD) has no effect on anterior, ventral or dorsolateral prostate weights unlike in similarly exposed littermate controls   (MGI Ref ID J:126176)
    • exposure to TCDD increased rather than decreased seminal vesicle weight on P35   (MGI Ref ID J:126176)
    • however, by P90 seminal vesicle weight is reduced   (MGI Ref ID J:126176)
  • cardiovascular system phenotype
  • abnormal blood vessel morphology
    • in the eye the limbal vasculature is exaggerated with loops that extend centrally and invade the corneal stroma   (MGI Ref ID J:64483)
    • abnormal kidney blood vessel morphology
      • vascular architecture is altered and appears less dense   (MGI Ref ID J:64483)
    • abnormal liver sinusoid morphology
      • the sinusoidal pattern retains the neonatal structure with failure of the resolution of sinusoidal junctions that normally occurs during liver development   (MGI Ref ID J:64483)
      • sinusoids are highly anastomotic throughout the liver   (MGI Ref ID J:64483)
    • patent ductus venosus
      • the ductus venosus remains open in adults resulting in portosystemic shunting and impaired liver perfusion   (MGI Ref ID J:64483)
  • liver/biliary system phenotype
  • abnormal hepatocyte morphology
    • total cellular area is reduced by about 36% compared to control littermates   (MGI Ref ID J:64483)
    • cytoplasmic area is reduced by nearly 50% compared to control littermates   (MGI Ref ID J:64483)
  • abnormal liver sinusoid morphology
    • the sinusoidal pattern retains the neonatal structure with failure of the resolution of sinusoidal junctions that normally occurs during liver development   (MGI Ref ID J:64483)
    • sinusoids are highly anastomotic throughout the liver   (MGI Ref ID J:64483)
  • decreased liver weight
    • about a 25% reduction in relative liver weight compared to controls   (MGI Ref ID J:64483)
  • vision/eye phenotype
  • persistent hyaloid artery
    • a persistent hyaloid artery is commonly seen   (MGI Ref ID J:64483)
    • in 25% of mice the hyaloid artery extends to the posterior lens capsule membrane   (MGI Ref ID J:64483)
  • reproductive system phenotype
  • decreased seminal vesicle weight
    • on P35 and P90   (MGI Ref ID J:126176)
  • small prostate gland anterior lobe
    • anterior prostate weight is reduced on P35 but not on P90   (MGI Ref ID J:126176)
  • small prostate gland dorsolateral lobe
    • dorsolateral prostate weight is reduced on P35 and P90   (MGI Ref ID J:126176)
  • growth/size/body phenotype
  • increased body weight
    • 7% heavier than littermate controls of P90   (MGI Ref ID J:126176)
  • endocrine/exocrine gland phenotype
  • decreased seminal vesicle weight
    • on P35 and P90   (MGI Ref ID J:126176)
  • small prostate gland anterior lobe
    • anterior prostate weight is reduced on P35 but not on P90   (MGI Ref ID J:126176)
  • small prostate gland dorsolateral lobe
    • dorsolateral prostate weight is reduced on P35 and P90   (MGI Ref ID J:126176)
  • renal/urinary system phenotype
  • abnormal kidney blood vessel morphology
    • vascular architecture is altered and appears less dense   (MGI Ref ID J:64483)
  • cellular phenotype
  • patent ductus venosus
    • the ductus venosus remains open in adults resulting in portosystemic shunting and impaired liver perfusion   (MGI Ref ID J:64483)
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Research Applications
This mouse can be used to support research in many areas including:

Ahrtm1Bra related

Cancer Research
Toxicology

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Growth Defects
Internal/Organ Defects
      liver

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Hematopoietic Defects

Internal/Organ Research
Kidney Defects
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Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Ahrtm1Bra
Allele Name targeted mutation 1, Christopher A Bradfield
Allele Type Targeted (Null/Knockout)
Common Name(s) Ahr-; AhrKO;
Mutation Made ByDr. Christopher Bradfield,   University of Wisconsin Medical School
Strain of Origin(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
ES Cell Line NameR1
ES Cell Line Strain(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Gene Symbol and Name Ahr, aryl-hydrocarbon receptor
Chromosome 12
Gene Common Name(s) Ah; Ahh; Ahre; In; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; bHLHe76; dioxin receptor; inflammatory reactivity;
Molecular Note A neomycin selection cassette replaced a genomic fragment containing exon 2, which encodes the basic-HLH domain essential for dimerization and DNA binding. Western blot analysis on liver cytosol demonstrated that the protein was not detectable in homozygous mice. [MGI Ref ID J:33827]

Genotyping

Genotyping Information

Genotyping Protocols

Ahrtm1Bra, Separated PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Schmidt JV; Su GH; Reddy JK; Simon MC; Bradfield CA. 1996. Characterization of a murine Ahr null allele: involvement of the Ah receptor in hepatic growth and development. Proc Natl Acad Sci U S A 93(13):6731-6. [PubMed: 8692887]  [MGI Ref ID J:33827]

Additional References

Lahvis GP; Bradfield CA. 1998. Ahr null alleles: distinctive or different? Biochem Pharmacol 56(7):781-7. [PubMed: 9774139]  [MGI Ref ID J:49883]

Ahrtm1Bra related

Abdelrahim M; Ariazi E; Kim K; Khan S; Barhoumi R; Burghardt R; Liu S; Hill D; Finnell R; Wlodarczyk B; Jordan VC; Safe S. 2006. 3-Methylcholanthrene and other aryl hydrocarbon receptor agonists directly activate estrogen receptor alpha. Cancer Res 66(4):2459-67. [PubMed: 16489053]  [MGI Ref ID J:106646]

Apetoh L; Quintana FJ; Pot C; Joller N; Xiao S; Kumar D; Burns EJ; Sherr DH; Weiner HL; Kuchroo VK. 2010. The aryl hydrocarbon receptor interacts with c-Maf to promote the differentiation of type 1 regulatory T cells induced by IL-27. Nat Immunol 11(9):854-61. [PubMed: 20676095]  [MGI Ref ID J:163922]

Baglole CJ; Maggirwar SB; Gasiewicz TA; Thatcher TH; Phipps RP; Sime PJ. 2008. The aryl hydrocarbon receptor attenuates tobacco smoke-induced cyclooxygenase-2 and prostaglandin production in lung fibroblasts through regulation of the NF-kappaB family member RelB. J Biol Chem 283(43):28944-57. [PubMed: 18697742]  [MGI Ref ID J:142470]

Barnett KR; Tomic D; Gupta RK; Babus JK; Roby KF; Terranova PF; Flaws JA. 2007. The aryl hydrocarbon receptor is required for normal gonadotropin responsiveness in the mouse ovary. Toxicol Appl Pharmacol 223(1):66-72. [PubMed: 17594909]  [MGI Ref ID J:124374]

Barnett KR; Tomic D; Gupta RK; Miller KP; Meachum S; Paulose T; Flaws JA. 2007. The aryl hydrocarbon receptor affects mouse ovarian follicle growth via mechanisms involving estradiol regulation and responsiveness. Biol Reprod 76(6):1062-70. [PubMed: 17329597]  [MGI Ref ID J:122009]

Basu R; O'Quinn DB; Silberger DJ; Schoeb TR; Fouser L; Ouyang W; Hatton RD; Weaver CT. 2012. Th22 Cells Are an Important Source of IL-22 for Host Protection against Enteropathogenic Bacteria. Immunity 37(6):1061-75. [PubMed: 23200827]  [MGI Ref ID J:191059]

Beamer CA; Seaver BP; Shepherd DM. 2012. Aryl hydrocarbon receptor (AhR) regulates silica-induced inflammation but not fibrosis. Toxicol Sci 126(2):554-68. [PubMed: 22273745]  [MGI Ref ID J:183699]

Benedict JC; Lin TM; Loeffler IK; Peterson RE; Flaws JA. 2000. Physiological role of the aryl hydrocarbon receptor in mouse ovary development. Toxicol Sci 56(2):382-8. [PubMed: 10910997]  [MGI Ref ID J:83527]

Benedict JC; Miller KP; Lin TM; Greenfeld C; Babus JK; Peterson RE; Flaws JA. 2003. Aryl hydrocarbon receptor regulates growth, but not atresia, of mouse preantral and antral follicles. Biol Reprod 68(5):1511-7. [PubMed: 12606443]  [MGI Ref ID J:82983]

Bessede A; Gargaro M; Pallotta MT; Matino D; Servillo G; Brunacci C; Bicciato S; Mazza EM; Macchiarulo A; Vacca C; Iannitti R; Tissi L; Volpi C; Belladonna ML; Orabona C; Bianchi R; Lanz TV; Platten M; Della Fazia MA; Piobbico D; Zelante T; Funakoshi H; Nakamura T; Gilot D; Denison MS; Guillemin GJ; DuHadaway JB; Prendergast GC; Metz R; Geffard M; Boon L; Pirro M; Iorio A; Veyret B; Romani L; Grohmann U; Fallarino F; Puccetti P. 2014. Aryl hydrocarbon receptor control of a disease tolerance defence pathway. Nature 511(7508):184-90. [PubMed: 24930766]  [MGI Ref ID J:213564]

Bui P; Solaimani P; Wu X; Hankinson O. 2012. 2,3,7,8-Tetrachlorodibenzo-p-dioxin treatment alters eicosanoid levels in several organs of the mouse in an aryl hydrocarbon receptor-dependent fashion. Toxicol Appl Pharmacol 259(2):143-51. [PubMed: 22230337]  [MGI Ref ID J:181214]

Bunger MK; Glover E; Moran SM; Walisser JA; Lahvis GP; Hsu EL; Bradfield CA. 2008. Abnormal liver development and resistance to 2,3,7,8-tetrachlorodibenzo-p-dioxin toxicity in mice carrying a mutation in the DNA-binding domain of the aryl hydrocarbon receptor. Toxicol Sci 106(1):83-92. [PubMed: 18660548]  [MGI Ref ID J:141978]

Bunger MK; Moran SM; Glover E; Thomae TL; Lahvis GP; Lin BC; Bradfield CA. 2003. Resistance to 2,3,7,8-tetrachlorodibenzo-p-dioxin toxicity and abnormal liver development in mice carrying a mutation in the nuclear localization sequence of the aryl hydrocarbon receptor. J Biol Chem 278(20):17767-74. [PubMed: 12621046]  [MGI Ref ID J:83597]

Camacho IA; Singh N; Hegde VL; Nagarkatti M; Nagarkatti PS. 2005. Treatment of mice with 2,3,7,8-tetrachlorodibenzo-p-dioxin leads to aryl hydrocarbon receptor-dependent nuclear translocation of NF-kappaB and expression of Fas ligand in thymic stromal cells and consequent apoptosis in T cells. J Immunol 175(1):90-103. [PubMed: 15972635]  [MGI Ref ID J:100624]

Chavan H; Krishnamurthy P. 2012. Polycyclic aromatic hydrocarbons (PAHs) mediate transcriptional activation of the ATP binding cassette transporter ABCB6 gene via the aryl hydrocarbon receptor (AhR). J Biol Chem 287(38):32054-68. [PubMed: 22761424]  [MGI Ref ID J:190243]

Fan Y; Boivin GP; Knudsen ES; Nebert DW; Xia Y; Puga A. 2010. The aryl hydrocarbon receptor functions as a tumor suppressor of liver carcinogenesis. Cancer Res 70(1):212-20. [PubMed: 19996281]  [MGI Ref ID J:155744]

Fritz WA; Lin TM; Cardiff RD; Peterson RE. 2007. The aryl hydrocarbon receptor inhibits prostate carcinogenesis in TRAMP mice. Carcinogenesis 28(2):497-505. [PubMed: 17052998]  [MGI Ref ID J:118152]

Fritz WA; Lin TM; Peterson RE. 2008. The aryl hydrocarbon receptor (AhR) inhibits vanadate-induced vascular endothelial growth factor (VEGF) production in TRAMP prostates. Carcinogenesis 29(5):1077-82. [PubMed: 18359762]  [MGI Ref ID J:138497]

Fuchs A; Vermi W; Lee JS; Lonardi S; Gilfillan S; Newberry RD; Cella M; Colonna M. 2013. Intraepithelial Type 1 Innate Lymphoid Cells Are a Unique Subset of IL-12- and IL-15-Responsive IFN-gamma-Producing Cells. Immunity 38(4):769-81. [PubMed: 23453631]  [MGI Ref ID J:196056]

Funatake CJ; Marshall NB; Steppan LB; Mourich DV; Kerkvliet NI. 2005. Cutting edge: activation of the aryl hydrocarbon receptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin generates a population of CD4+ CD25+ cells with characteristics of regulatory T cells. J Immunol 175(7):4184-8. [PubMed: 16177056]  [MGI Ref ID J:118998]

Harrill JA; Hukkanen RR; Lawson M; Martin G; Gilger B; Soldatow V; Lecluyse EL; Budinsky RA; Rowlands JC; Thomas RS. 2013. Knockout of the aryl hydrocarbon receptor results in distinct hepatic and renal phenotypes in rats and mice. Toxicol Appl Pharmacol 272(2):503-18. [PubMed: 23859880]  [MGI Ref ID J:203445]

Harstad EB; Guite CA; Thomae TL; Bradfield CA. 2006. Liver deformation in Ahr-null mice: evidence for aberrant hepatic perfusion in early development. Mol Pharmacol 69(5):1534-41. [PubMed: 16443691]  [MGI Ref ID J:135797]

Herlin M; Finnila MA; Zioupos P; Aula A; Risteli J; Miettinen HM; Jamsa T; Tuukkanen J; Korkalainen M; Hakansson H; Viluksela M. 2013. New insights to the role of aryl hydrocarbon receptor in bone phenotype and in dioxin-induced modulation of bone microarchitecture and material properties. Toxicol Appl Pharmacol 273(1):219-26. [PubMed: 24035824]  [MGI Ref ID J:205158]

Hernandez-Ochoa I; Barnett-Ringgold KR; Dehlinger SL; Gupta RK; Leslie TC; Roby KF; Flaws JA. 2010. The ability of the aryl hydrocarbon receptor to regulate ovarian follicle growth and estradiol biosynthesis in mice depends on stage of sexual maturity. Biol Reprod 83(5):698-706. [PubMed: 20631400]  [MGI Ref ID J:168372]

Hines IN; Hartwell HJ; Feng Y; Theve EJ; Hall GA; Hashway S; Connolly J; Fecteau M; Fox JG; Rogers AB. 2011. Insulin resistance and metabolic hepatocarcinogenesis with parent-of-origin effects in AxB mice. Am J Pathol 179(6):2855-65. [PubMed: 21967816]  [MGI Ref ID J:180106]

Hollingshead BD; Patel RD; Perdew GH. 2006. Endogenous hepatic expression of the hepatitis B virus X-associated protein 2 is adequate for maximal association with aryl hydrocarbon receptor-90-kDa heat shock protein complexes. Mol Pharmacol 70(6):2096-107. [PubMed: 16988012]  [MGI Ref ID J:135626]

Hoyler T; Klose CS; Souabni A; Turqueti-Neves A; Pfeifer D; Rawlins EL; Voehringer D; Busslinger M; Diefenbach A. 2012. The Transcription Factor GATA-3 Controls Cell Fate and Maintenance of Type 2 Innate Lymphoid Cells. Immunity 37(4):634-48. [PubMed: 23063333]  [MGI Ref ID J:188553]

Hu P; Herrmann R; Bednar A; Saloupis P; Dwyer MA; Yang P; Qi X; Thomas RS; Jaffe GJ; Boulton ME; McDonnell DP; Malek G. 2013. Aryl hydrocarbon receptor deficiency causes dysregulated cellular matrix metabolism and age-related macular degeneration-like pathology. Proc Natl Acad Sci U S A 110(43):E4069-78. [PubMed: 24106308]  [MGI Ref ID J:201965]

Hushka LJ; Williams JS; Greenlee WF. 1998. Characterization of 2,3,7,8-tetrachlorodibenzofuran-dependent suppression and AH receptor pathway gene expression in the developing mouse mammary gland. Toxicol Appl Pharmacol 152(1):200-10. [PubMed: 9772216]  [MGI Ref ID J:51158]

Jiang W; Welty SE; Couroucli XI; Barrios R; Kondraganti SR; Muthiah K; Yu L; Avery SE; Moorthy B. 2004. Disruption of the Ah receptor gene alters the susceptibility of mice to oxygen-mediated regulation of pulmonary and hepatic cytochromes P4501A expression and exacerbates hyperoxic lung injury. J Pharmacol Exp Ther 310(2):512-9. [PubMed: 15123765]  [MGI Ref ID J:100359]

Jurisicova A; Taniuchi A; Li H; Shang Y; Antenos M; Detmar J; Xu J; Matikainen T; Benito Hernandez A; Nunez G; Casper RF. 2007. Maternal exposure to polycyclic aromatic hydrocarbons diminishes murine ovarian reserve via induction of Harakiri. J Clin Invest 117(12):3971-8. [PubMed: 18037991]  [MGI Ref ID J:130754]

Jux B; Kadow S; Esser C. 2009. Langerhans cell maturation and contact hypersensitivity are impaired in aryl hydrocarbon receptor-null mice. J Immunol 182(11):6709-17. [PubMed: 19454665]  [MGI Ref ID J:148870]

Jux B; Kadow S; Luecke S; Rannug A; Krutmann J; Esser C. 2011. The aryl hydrocarbon receptor mediates UVB radiation-induced skin tanning. J Invest Dermatol 131(1):203-10. [PubMed: 20861855]  [MGI Ref ID J:179854]

Kadow S; Jux B; Zahner SP; Wingerath B; Chmill S; Clausen BE; Hengstler J; Esser C. 2011. Aryl hydrocarbon receptor is critical for homeostasis of invariant gammadelta T cells in the murine epidermis. J Immunol 187(6):3104-10. [PubMed: 21844385]  [MGI Ref ID J:179245]

Kerkvliet NI; Shepherd DM; Baecher-Steppan L. 2002. T lymphocytes are direct, aryl hydrocarbon receptor (AhR)-dependent targets of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD): AhR expression in both CD4+ and CD8+ T cells is necessary for full suppression of a cytotoxic T lymphocyte response by TCDD. Toxicol Appl Pharmacol 185(2):146-52. [PubMed: 12490139]  [MGI Ref ID J:153343]

Kiss EA; Vonarbourg C; Kopfmann S; Hobeika E; Finke D; Esser C; Diefenbach A. 2011. Natural aryl hydrocarbon receptor ligands control organogenesis of intestinal lymphoid follicles. Science 334(6062):1561-5. [PubMed: 22033518]  [MGI Ref ID J:179017]

Klose CS; Kiss EA; Schwierzeck V; Ebert K; Hoyler T; d'Hargues Y; Goppert N; Croxford AL; Waisman A; Tanriver Y; Diefenbach A. 2013. A T-bet gradient controls the fate and function of CCR6-RORgammat+ innate lymphoid cells. Nature 494(7436):261-5. [PubMed: 23334414]  [MGI Ref ID J:194555]

Lahvis GP; Bradfield CA. 1998. Ahr null alleles: distinctive or different? Biochem Pharmacol 56(7):781-7. [PubMed: 9774139]  [MGI Ref ID J:49883]

Lahvis GP; Lindell SL; Thomas RS; McCuskey RS; Murphy C; Glover E; Bentz M; Southard J; Bradfield CA. 2000. Portosystemic shunting and persistent fetal vascular structures in aryl hydrocarbon receptor-deficient mice Proc Natl Acad Sci U S A 97(19):10442-7. [PubMed: 10973493]  [MGI Ref ID J:64483]

Lahvis GP; Pyzalski RW; Glover E; Pitot HC; McElwee MK; Bradfield CA. 2005. The aryl hydrocarbon receptor is required for developmental closure of the ductus venosus in the neonatal mouse. Mol Pharmacol 67(3):714-20. [PubMed: 15590894]  [MGI Ref ID J:110128]

Lawrence BP; Roberts AD; Neumiller JJ; Cundiff JA; Woodland DL. 2006. Aryl hydrocarbon receptor activation impairs the priming but not the recall of influenza virus-specific CD8+ T cells in the lung. J Immunol 177(9):5819-28. [PubMed: 17056506]  [MGI Ref ID J:140537]

Lee JS; Cella M; McDonald KG; Garlanda C; Kennedy GD; Nukaya M; Mantovani A; Kopan R; Bradfield CA; Newberry RD; Colonna M. 2011. AHR drives the development of gut ILC22 cells and postnatal lymphoid tissues via pathways dependent on and independent of Notch. Nat Immunol 13(2):144-51. [PubMed: 22101730]  [MGI Ref ID J:180367]

Li Y; Innocentin S; Withers DR; Roberts NA; Gallagher AR; Grigorieva EF; Wilhelm C; Veldhoen M. 2011. Exogenous stimuli maintain intraepithelial lymphocytes via aryl hydrocarbon receptor activation. Cell 147(3):629-40. [PubMed: 21999944]  [MGI Ref ID J:178527]

Lin TM; Ko K; Moore RW; Buchanan DL; Cooke PS; Peterson RE. 2001. Role of the aryl hydrocarbon receptor in the development of control and 2,3,7,8-tetrachlorodibenzo-p-dioxin-exposed male mice. J Toxicol Environ Health A 64(4):327-42. [PubMed: 11693491]  [MGI Ref ID J:153346]

Lin TM; Ko K; Moore RW; Simanainen U; Oberley TD; Peterson RE. 2002. Effects of aryl hydrocarbon receptor null mutation and in utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure on prostate and seminal vesicle development in C57BL/6 mice. Toxicol Sci 68(2):479-87. [PubMed: 12151645]  [MGI Ref ID J:126176]

Mezrich JD; Fechner JH; Zhang X; Johnson BP; Burlingham WJ; Bradfield CA. 2010. An Interaction between Kynurenine and the Aryl Hydrocarbon Receptor Can Generate Regulatory T Cells. J Immunol 185(6):3190-8. [PubMed: 20720200]  [MGI Ref ID J:163544]

Moran TB; Brannick KE; Raetzman LT. 2012. Aryl-hydrocarbon receptor activity modulates prolactin expression in the pituitary. Toxicol Appl Pharmacol 265(1):139-45. [PubMed: 22975028]  [MGI Ref ID J:189015]

Navid F; Bruhs A; Schuller W; Fritsche E; Krutmann J; Schwarz T; Schwarz A. 2013. The Aryl Hydrocarbon Receptor Is Involved in UVR-Induced Immunosuppression. J Invest Dermatol 133(12):2763-70. [PubMed: 23652795]  [MGI Ref ID J:203019]

Nukaya M; Lin BC; Glover E; Moran SM; Kennedy GD; Bradfield CA. 2010. The aryl hydrocarbon receptor-interacting protein (AIP) is required for dioxin-induced hepatotoxicity but not for the induction of the Cyp1a1 and Cyp1a2 genes. J Biol Chem 285(46):35599-605. [PubMed: 20829355]  [MGI Ref ID J:166864]

Robles R; Morita Y; Mann KK; Perez GI; Yang S; Matikainen T; Sherr DH; Tilly JL. 2000. The aryl hydrocarbon receptor, a basic helix-loop-helix transcription factor of the PAS gene family, is required for normal ovarian germ cell dynamics in the mouse. Endocrinology 141(1):450-3. [PubMed: 10614669]  [MGI Ref ID J:59155]

Shi LZ; Faith NG; Nakayama Y; Suresh M; Steinberg H; Czuprynski CJ. 2007. The aryl hydrocarbon receptor is required for optimal resistance to Listeria monocytogenes infection in mice. J Immunol 179(10):6952-62. [PubMed: 17982086]  [MGI Ref ID J:153858]

Shin JH; Zhang L; Murillo-Sauca O; Kim J; Kohrt HE; Bui JD; Sunwoo JB. 2013. Modulation of natural killer cell antitumor activity by the aryl hydrocarbon receptor. Proc Natl Acad Sci U S A 110(30):12391-6. [PubMed: 23836658]  [MGI Ref ID J:198789]

Singh KP; Wyman A; Casado FL; Garrett RW; Gasiewicz TA. 2009. Treatment of mice with the Ah receptor agonist and human carcinogen dioxin results in altered numbers and function of hematopoietic stem cells. Carcinogenesis 30(1):11-9. [PubMed: 18820284]  [MGI Ref ID J:144887]

Teske S; Bohn AA; Hogaboam JP; Lawrence BP. 2008. Aryl hydrocarbon receptor targets pathways extrinsic to bone marrow cells to enhance neutrophil recruitment during influenza virus infection. Toxicol Sci 102(1):89-99. [PubMed: 18007012]  [MGI Ref ID J:133909]

Thatcher TH; Maggirwar SB; Baglole CJ; Lakatos HF; Gasiewicz TA; Phipps RP; Sime PJ. 2007. Aryl Hydrocarbon Receptor-Deficient Mice Develop Heightened Inflammatory Responses to Cigarette Smoke and Endotoxin Associated with Rapid Loss of the Nuclear Factor-{kappa}B Component RelB. Am J Pathol 170(3):855-64. [PubMed: 17322371]  [MGI Ref ID J:118646]

Thompson KE; Bourguet SM; Christian PJ; Benedict JC; Sipes IG; Flaws JA; Hoyer PB. 2005. Differences between rats and mice in the involvement of the aryl hydrocarbon receptor in 4-vinylcyclohexene diepoxide-induced ovarian follicle loss. Toxicol Appl Pharmacol 203(2):114-23. [PubMed: 15710172]  [MGI Ref ID J:95935]

Veldhoen M; Hirota K; Westendorf AM; Buer J; Dumoutier L; Renauld JC; Stockinger B. 2008. The aryl hydrocarbon receptor links TH17-cell-mediated autoimmunity to environmental toxins. Nature 453(7191):106-9. [PubMed: 18362914]  [MGI Ref ID J:136053]

Wagage S; John B; Krock BL; Hall AO; Randall LM; Karp CL; Simon MC; Hunter CA. 2014. The aryl hydrocarbon receptor promotes IL-10 production by NK cells. J Immunol 192(4):1661-70. [PubMed: 24403534]  [MGI Ref ID J:209400]

Walisser JA; Bunger MK; Glover E; Bradfield CA. 2004. Gestational exposure of Ahr and Arnt hypomorphs to dioxin rescues vascular development. Proc Natl Acad Sci U S A 101(47):16677-82. [PubMed: 15545609]  [MGI Ref ID J:94465]

Wu D; Li W; Lok P; Matsumura F; Adam Vogel CF. 2011. AhR deficiency impairs expression of LPS-induced inflammatory genes in mice. Biochem Biophys Res Commun 410(2):358-63. [PubMed: 21683686]  [MGI Ref ID J:174950]

Xu CX; Wang C; Krager SL; Bottum KM; Tischkau SA. 2013. Aryl hydrocarbon receptor activation attenuates Per1 gene induction and influences circadian clock resetting. Toxicol Sci 132(2):368-78. [PubMed: 23291558]  [MGI Ref ID J:206907]

Yeager RL; Reisman SA; Aleksunes LM; Klaassen CD. 2009. Introducing the 'TCDD-inducible AhR-Nrf2 gene battery'. Toxicol Sci 111(2):238-46. [PubMed: 19474220]  [MGI Ref ID J:154083]

Zago M; Sheridan JA; Nair P; Rico de Souza A; Gallouzi IE; Rousseau S; Di Marco S; Hamid Q; Eidelman DH; Baglole CJ. 2013. Aryl hydrocarbon receptor-dependent retention of nuclear HuR suppresses cigarette smoke-induced cyclooxygenase-2 expression independent of DNA-binding. PLoS One 8(9):e74953. [PubMed: 24086407]  [MGI Ref ID J:207747]

Zelante T; Iannitti RG; Cunha C; De Luca A; Giovannini G; Pieraccini G; Zecchi R; D'Angelo C; Massi-Benedetti C; Fallarino F; Carvalho A; Puccetti P; Romani L. 2013. Tryptophan catabolites from microbiota engage aryl hydrocarbon receptor and balance mucosal reactivity via interleukin-22. Immunity 39(2):372-85. [PubMed: 23973224]  [MGI Ref ID J:208224]

Zhou Y; Tung HY; Tsai YM; Hsu SC; Chang HW; Kawasaki H; Tseng HC; Plunkett B; Gao P; Hung CH; Vonakis BM; Huang SK. 2013. Aryl hydrocarbon receptor controls murine mast cell homeostasis. Blood 121(16):3195-204. [PubMed: 23462117]  [MGI Ref ID J:197552]

de Souza AR; Zago M; Eidelman DH; Hamid Q; Baglole CJ. 2014. Aryl hydrocarbon receptor (AhR) attenuation of subchronic cigarette smoke-induced pulmonary neutrophilia is associated with retention of nuclear RelB and suppression of intercellular adhesion molecule-1 (ICAM-1). Toxicol Sci 140(1):204-23. [PubMed: 24752502]  [MGI Ref ID J:212832]

van Voorhis M; Knopp S; Julliard W; Fechner JH; Zhang X; Schauer JJ; Mezrich JD. 2013. Exposure to atmospheric particulate matter enhances Th17 polarization through the aryl hydrocarbon receptor. PLoS One 8(12):e82545. [PubMed: 24349309]  [MGI Ref ID J:209865]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Breeding & HusbandryHomozygous females are poor mothers and have small litters. When maintaining a live colony, this strain can be maintained by heterozygous sibling matings. Expected coat color from breeding:Black

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2140.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2782.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

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

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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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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.

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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.

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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