JAX
Mouse Strain Datasheet - 002727
B6;129-Ahrtm1Bra/J
Also Known As: Ahr null
These Ahr knock-out mice exhibit hepatic defects.
Donating Investigator
Christopher A Bradfield, University of Wisconsin-Madison
Genetic overview
| Genetic Background | Generation |
|---|---|
|
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Ahrtm1Bra
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Targeted (Null/Knockout) | Ahr | aryl-hydrocarbon receptor |
Research Applications
- Cancer Research
- Developmental Biology Research
- Hematological Research
- Internal/Organ Research
- Metabolism Research
- Research Tools
Detailed 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 Suggestions
- Wild-type from the colony
Approximate Controls
Additional Information
Selected 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: 8692887MGI: J:33827
Ahrtm1Bra
Allele Symbol: Ahrtm1Bra
| Allele Name | targeted mutation 1, Christopher A Bradfield |
|---|---|
| Allele Type | Targeted (Null/Knockout) |
| Allele Synonym(s) | Ahr-; AhrKO |
| Gene Symbol and Name | Ahr, aryl-hydrocarbon receptor |
| Gene Synonym(s) | Ah; Ahh; Ahre; In; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; bHLHe76; dioxin receptor; inflammatory reactivity |
| Strain of Origin | (129X1/SvJ x 129S1/Sv)F1-Kitl<+> |
| Chromosome | 12 |
| 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. |
| Mutations Made By | Christopher Bradfield, University of Wisconsin-Madison |
Disease Terms
Research Areas By Genotype
This mouse can be used to support research in many areas including:
Genotype: 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
Mammalian Phenotype Terms by Genotype
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)
cellular phenotype
- patent ductus venosus
- (MGI Ref ID J:83597)
cardiovascular system phenotype
- patent ductus venosus
- (MGI Ref ID J:83597)
growth/size/body region phenotype
- decreased body weight
- (MGI Ref ID J:33827)
- postnatal growth retardation
- (MGI Ref ID J:33827)
immune system phenotype
- abnormal Langerhans cell morphology
- abnormal Langerhans cell physiology
- 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
liver/biliary system phenotype
- decreased liver weight
- reduced liver weight (28% less than wild-type) (MGI Ref ID J:83597)
- hepatic steatosis
- 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)
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
- decreased spleen germinal center size
- smaller germinal centers (MGI Ref ID J:33827)
- enlarged spleen
- extramedullary hematopoiesis
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)
The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain
Genotype: Ahrtm1Bra/Ahrtm1Bra
B6.129-Ahrtm1Bra/J
homeostasis/metabolism phenotype
- abnormal chemokine level
- abnormal cytokine level
- levels of proinflammatory cytokines are increased in bronchoalveolar lavage (BAL) fluid (MGI Ref ID J:118646)
- abnormal enzyme/coenzyme activity
- basal hepatic methoxyresorufin O-demethylase (MROD) activity is reduced (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 (MGI Ref ID J:100359)
- however, hyperoxia still induces an increase in MROD activity (MGI Ref ID J:100359)
- 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)
- 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 alveolar edema
- severe alveolar flooding after exposure to hyperoxia (MGI Ref ID J:100359)
- pulmonary edema
- severe edema is seen 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 chemokine level
- abnormal cytokine level
- levels of proinflammatory cytokines are increased in bronchoalveolar lavage (BAL) fluid (MGI Ref ID J:118646)
- abnormal interleukin level
- increased levels of IL6 in BAL fluid (MGI Ref ID J:118646)
- abnormal macrophage physiology
- 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)
- increased susceptibility to bacterial infection
- lung inflammation
- 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)
- lung inflammation after exposure to hyperoxia is increased compared to wild-type controls (MGI Ref ID J:100359)
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
- 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)
- lung inflammation after exposure to hyperoxia is increased compared to wild-type controls (MGI Ref ID J:100359)
- pulmonary alveolar edema
- severe alveolar flooding after exposure to hyperoxia (MGI Ref ID J:100359)
- pulmonary edema
- severe edema is seen after exposure to hyperoxia (MGI Ref ID J:100359)
hematopoietic system phenotype
Genotype: 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
- 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
- abnormal liver sinusoid morphology
- 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
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 region 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)
Genotype: 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
- 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)
- no increase in atresia relative to wild-type (MGI Ref ID J:82983)
- reduced numbers preantral and antral follicles (MGI Ref ID J:82983)
- 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
- decreased corpora lutea number
- fewer corpora lutea by 45 days of age (MGI Ref ID J:83527)
- decreased germ cell number
- 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)
- small ovary
- (MGI Ref ID J:82983)
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
- 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)
- no increase in atresia relative to wild-type (MGI Ref ID J:82983)
- reduced numbers preantral and antral follicles (MGI Ref ID J:82983)
- 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)
- 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)
- small ovary
- (MGI Ref ID J:82983)
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
- decreased germ cell number
- 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)
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: 8692887MGI: J:33827
Additional References
- Lahvis GP; Bradfield CA. 1998. Ahr null alleles: distinctive or different? Biochem Pharmacol 56(7):781-7. PubMed: 9774139MGI: J:49883
Additional - 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: 16489053MGI: 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: 20676095MGI: 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: 18697742MGI: 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: 17594909MGI: 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: 17329597MGI: 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: 23200827MGI: 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: 22273745MGI: 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: 10910997MGI: 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: 12606443MGI: J:82983
- Bennett JA; Singh KP; Unnisa Z; Welle SL; Gasiewicz TA. 2015. Deficiency in Aryl Hydrocarbon Receptor (AHR) Expression throughout Aging Alters Gene Expression Profiles in Murine Long-Term Hematopoietic Stem Cells. PLoS One 10(7):e0133791. PubMed: 26208102MGI: J:238614
- 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: 24930766MGI: J:213564
- Bruhs A; Haarmann-Stemmann T; Frauenstein K; Krutmann J; Schwarz T; Schwarz A. 2015. Activation of the arylhydrocarbon receptor causes immunosuppression primarily by modulating dendritic cells. J Invest Dermatol 135(2):435-44. PubMed: 25251932MGI: J:218044
- 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: 22230337MGI: 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: 18660548MGI: 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: 12621046MGI: 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: 15972635MGI: 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: 22761424MGI: J:190243
- Choudhary M; Kazmin D; Hu P; Thomas RS; McDonnell DP; Malek G. 2015. Aryl hydrocarbon receptor knock-out exacerbates choroidal neovascularization via multiple pathogenic pathways. J Pathol 235(1):101-12. PubMed: 25186463MGI: J:216381
- 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: 19996281MGI: J:155744
- Frauenstein K; Sydlik U; Tigges J; Majora M; Wiek C; Hanenberg H; Abel J; Esser C; Fritsche E; Krutmann J; Haarmann-Stemmann T. 2013. Evidence for a novel anti-apoptotic pathway in human keratinocytes involving the aryl hydrocarbon receptor, E2F1, and checkpoint kinase 1. Cell Death Differ 20(10):1425-34. PubMed: 23912710MGI: J:229001
- 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: 17052998MGI: 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: 18359762MGI: 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: 23453631MGI: 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: 16177056MGI: 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: 23859880MGI: 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: 16443691MGI: J:135797
- Hayes MD; Ovcinnikovs V; Smith AG; Kimber I; Dearman RJ. 2014. The aryl hydrocarbon receptor: differential contribution to T helper 17 and T cytotoxic 17 cell development. PLoS One 9(9):e106955. PubMed: 25203682MGI: J:221520
- 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: 24035824MGI: 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: 20631400MGI: 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: 21967816MGI: 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: 16988012MGI: 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: 23063333MGI: 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: 24106308MGI: 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: 9772216MGI: 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: 15123765MGI: 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: 18037991MGI: 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: 19454665MGI: J:148870
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