Strain Name:

B6.129-Ahrtm1Bra/J

Stock Number:

002831

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 Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Specieslaboratory mouse
Background Strain C57BL/6
Donor Strain 129X1 x 129S1 via R1 (+Kitl-SlJ) ES cell line
 
Donating Investigator Chris Bradfield,   McArdle Laboratory for Cancer Research

Appearance
black
Related Genotype: a/a

Description
Mice homozygous for the targeted mutation are viable. 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 removed exon 2 of the targeted gene. The original mutation has been crossed 10 times to C57BL/6 mice. Strain also backcrossed to C57BL/6J 2 times after arriving at JAX, so current generation is N12.

Control Information

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

Related Strains

Strains carrying   Ahrtm1Bra allele
002727   B6;129-Ahrtm1Bra/J
View Strains carrying   Ahrtm1Bra     (1 strain)

Strains carrying other alleles of Ahr
000645   A/HeJ
000646   A/J
000648   AKR/J
002920   B6(D2N).Spretus-Ahrb-3/J
006203   B6.129(FVB)-Ahrtm3.1Bra/J
000130   B6.C-H17c/(HW14)ByJ
000136   B6.C-H34c/(HW22)ByJ
000370   B6.C-H38c/(HW119)ByJ
002921   B6.D2N-Ahrd/J
001026   BALB/cByJ
000659   C3H/HeJ
000664   C57BL/6J
000669   C58/J
000926   CAROLI/EiJ
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
000677   MA/MyJ
000550   MOLF/EiJ
001146   SPRET/EiJ
View Strains carrying other alleles of Ahr     (26 strains)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms
      assigned by genotype

Ahrtm1Bra/Ahrtm1Bra

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

Ahrtm1Bra/Ahrtm1Bra

        B6.129-Ahrtm1Bra
  • homeostasis/metabolism phenotype
  • abnormal circulating hormone level (MGI Ref ID J:126176)
    • serum concentration of 5alpha-androstane-3alpha,17beta-diol are reduced at P21
  • decreased physiological sensitivity to xenobiotics (MGI Ref ID J:126176)
    • 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
    • exposure to TCDD increased rather than decreased seminal vesicle weight on P35
    • however, by P90 seminal vesicle weight is reduced
  • cardiovascular system phenotype
  • abnormal blood vessel morphology (MGI Ref ID J:64483)
    • in the eye the limbal vasculature is exaggerated with loops that extend centrally and invade the corneal stroma
    • abnormal kidney vasculature (MGI Ref ID J:64483)
      • vascular architecture is altered and appears less dense
    • abnormal vascular regression (MGI Ref ID J:64483)
      • a persistent hyaloid artery is commonly seen
      • in 25% of mice the hyaloid artery extends to the posterior lens capsule membrane
      • patent ductus venosus (MGI Ref ID J:64483)
        • the ductus venosus remains open in adults resulting in portosystemic shunting and impaired liver perfusion
  • liver/biliary system phenotype
  • abnormal hepatocyte morphology (MGI Ref ID J:64483)
    • total cellular area is reduced by about 36% compared to control littermates
    • cytoplasmic area is reduced by nearly 50% compared to control littermates
  • abnormal liver sinusoid morphology (MGI Ref ID J:64483)
    • the sinusoidal pattern retains the neonatal structure with failure of the resolution of sinusoidal junctions that normally occurs during liver development
    • sinusoids are highly anastomotic throughout the liver
  • decreased liver weight (MGI Ref ID J:64483)
    • about a 25% reduction in relative liver weight compared to controls
  • vision/eye phenotype
  • abnormal eye development (MGI Ref ID J:64483)
    • a persistent hyaloid artery is commonly seen
    • in 25% of mice the hyaloid artery extends to the posterior lens capsule membrane
  • abnormal vitreous body (MGI Ref ID J:64483)
    • a persistent hyaloid artery is commonly seen
    • in 25% of mice the hyaloid artery extends to the posterior lens capsule membrane
  • reproductive system phenotype
  • decreased seminal vesicle weight (MGI Ref ID J:126176)
    • on P35 and P90
  • small prostate gland anterior lobe (MGI Ref ID J:126176)
    • anterior prostate weight is reduced on P35 but not on P90
  • small prostate gland dorsolateral lobe (MGI Ref ID J:126176)
    • dorsolateral prostate weight is reduced on P35 and P90
  • growth/size phenotype
  • increased body weight (MGI Ref ID J:126176)
    • 7% heavier than littermate controls of P90
  • endocrine/exocrine gland phenotype
  • decreased seminal vesicle weight (MGI Ref ID J:126176)
    • on P35 and P90
  • small prostate gland anterior lobe (MGI Ref ID J:126176)
    • anterior prostate weight is reduced on P35 but not on P90
  • small prostate gland dorsolateral lobe (MGI Ref ID J:126176)
    • dorsolateral prostate weight is reduced on P35 and P90
  • renal/urinary system phenotype
  • abnormal kidney vasculature (MGI Ref ID J:64483)
    • vascular architecture is altered and appears less dense

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Ahrtm1Bra/Ahrtm1Bra

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

Ahrtm1Bra/Ahrtm1Bra

        involves: 129S1/Sv * 129X1/SvJ
  • cardiovascular system phenotype
  • patent ductus venosus (MGI Ref ID J:94465)
    • a patent ductus venosus (shunting blood around the liver) was seen in all mutants
    • 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
  • reproductive system phenotype
  • abnormal branching of the mammary ductal tree (MGI Ref ID J:51158)
    • 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
  • abnormal ovarian folliculogenesis (MGI Ref ID J:82983)
    • reduced numbers preantral and antral follicles
    • no increase in atresia relative to wild-type
    • 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
    • reduced numbers preantral and antral follicles at 53 days of age
  • abnormal ovary physiology (MGI Ref ID J:124374)
    • following treatment with a low dose equine chorionic gonadotropin (eCG) fewer corpora lutea are present compared to similarly treated controls
  • abnormal ovulation (MGI Ref ID J:82983)
    • fewer corpora lutea by 45 days of age
    • abnormal superovulation (MGI Ref ID J:124374)
      • following treatment with low doses of exogenous gonadotropins fewer oocytes are collected compared to similarly treated controls
      • however, ovulation in response to higher doses of exogenous gonadotropins is similar to controls
  • decreased corpora lutea number (MGI Ref ID J:83527)
    • fewer corpora lutea by 45 days of age
  • decreased germ cell number (MGI Ref ID J:83527)
    • similar number of germ cells as wild-type at E18
    • 70% reduction in the number of ovarian germ cells at 2 days of age
  • small ovary (MGI Ref ID J:82983)
    • decreased ovary weight (MGI Ref ID J:124374)
      • following treatment with a low dose equine chorionic gonadotropin (eCG) ovarian weights are significantly less than similarly treated controls
      • however, in the absence of treatment or after treatment with a high dose of eCG ovarian weights are similar to controls
  • endocrine/exocrine gland phenotype
  • abnormal branching of the mammary ductal tree (MGI Ref ID J:51158)
    • 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
  • abnormal ovarian folliculogenesis (MGI Ref ID J:82983)
    • reduced numbers preantral and antral follicles
    • no increase in atresia relative to wild-type
    • 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
    • reduced numbers preantral and antral follicles at 53 days of age
  • abnormal ovary physiology (MGI Ref ID J:124374)
    • following treatment with a low dose equine chorionic gonadotropin (eCG) fewer corpora lutea are present compared to similarly treated controls
  • decreased corpora lutea number (MGI Ref ID J:83527)
    • fewer corpora lutea by 45 days of age
  • small ovary (MGI Ref ID J:82983)
    • decreased ovary weight (MGI Ref ID J:124374)
      • following treatment with a low dose equine chorionic gonadotropin (eCG) ovarian weights are significantly less than similarly treated controls
      • however, in the absence of treatment or after treatment with a high dose of eCG ovarian weights are similar to controls
View Research Applications

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

Ahrtm1Bra related

Cancer Research
Toxicology

Developmental Biology Research
Growth Defects
Internal/Organ Defects
      liver

Hematological Research
Hematopoietic Defects

Internal/Organ Research
Kidney Defects
Liver Defects

Metabolism Research

Research Tools
Toxicology Research

Genes & Alleles

Gene & Allele Information

 
Allele Symbol Ahrtm1Bra
Allele Name targeted mutation 1, Christopher A Bradfield
Allele Type Targeted (knock-out)
Common Name(s) Ahr-; AhrKO;
Mutation Made By Chris Bradfield,   McArdle Laboratory for Cancer Research
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, Standard PCR

Helpful Links

Genotyping resources and troubleshooting

References

References

Selected Reference(s)

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

Additional References

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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

Colony Maintenance

Breeding & HusbandryHomozygous females are poor mothers and have small litters. Expected coat color from breeding:Black

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Pricing for USA, Canada and Mexico shipping destinations View International pricing
Price (US dollars $)
Cryorecovery Fee $1900.00
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.

Additional Supply Details

Pricing for International shipping destinations View USA Canada and Mexico pricing
Price (US dollars $)
Cryorecovery Fee $2470.00
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.

Additional Supply Details

Supply Details

Standard SupplyCryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
Supply Notes
  • Cryorecovery - Standard.
    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. The total number of animals provided, their gender and genotype will vary. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 13 and 16 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).

  • This strain is included in the Induced Mutant Resource Colony collection.
  • Genomic DNA is available for this strain from the Mouse DNA Resource.

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains.
  International - Control Pricing Information for Genetically Engineered Mutant Strains.

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

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

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Contact Information
Orders & Technical Support
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


Contact information

General inquiries

Contracts Administration

phone:207-288-6470
fax:207-288-6655

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. 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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