Originally inbred at the Rockefeller Institute, AKR mice are widely used in cancer research for their high leukemia incidence (60-90%) and in immunology as a source of the Thy1.1 (theta AKR) antigen. AKR/J mice are viremic from birth, and express the ecotropic retrovirus AKV in all tissues. The hair interior defect (hid) mutation, a strain characteristic of AKR mice, causes alterations in hair development that is only evident microscopically. Adrenocortical lipid depletion (ald) in AKR mice is caused by a mutation in sterol O-acyltransferase 1 (Soat1), and leads to a truncated SOAT1 protein. AKR/J mice are relatively resistant to aortic lesion formation on a semi-synthetic high fat diet and are hyporesponsive to diets containing high levels of fat and cholesterol.
|Allele Name||d variant|
|Allele Type||Not Applicable|
|Allele Synonym(s)||Ahd; Ahk; AhRd; Ahhn; ah; in|
|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||Not Applicable|
|General Note|| |
Strain of origin - this allele was found in DBA/2J, AKR/J, 129, SWR, RF, NZB strains
|Molecular Note||This allele encodes a 104 kDa receptor that is stabilized by molybdate and has an affinity for ligand 10-100 fold lower than that of the receptor produced by the C57BL/6J allele. PCR sequencing of cDNA revealed ten nucleotide differences between the coding sequences of the DBA/2J and C57BL/6J receptors. Five of the ten differences would cause amino acid changes. One of these, an apparent T to C transition replaces the opal termination codon in the C57BL/6J allele with an arginine codon in the DBA/2J allele. This change would extend translation of the DBA/2J mRNA by 43 amino acids, accounting for the larger size of the peptide produced by this allele (104 kDa vs 95 kDa for the C57BL/6J allele). A second T to C transition changes a leucine codon in the C57BL/6J allele to a proline codon in the DBA/2J allele, and would likely change secondary structure of the peptide and thus ligand affinity.|
|Allele Synonym(s)||C5-; C5-d; C5-def; C5-deficient; HcHfib2; hco|
|Gene Symbol and Name||Hc, hemolytic complement|
|Gene Synonym(s)||C5; C5; C5D; C5a; C5b; CPAMD4; ECLZB; He; He; Hfib2; Hfib2; hepatic fibrogenesis 2|
|Strain of Origin||multiple strains|
|General Note|| |
This is an allele characteristic of various inbred mouse strains including the following: A/HeJ, A/J, AKR/J, DBA/2J, NZB/B1NJ, SWR/J, B10.D2/oSnJ
Hc was identified as a candidate gene for Abhr2 in a microarray analysis of lung mRNA from A/J, C3H/HeJ, and (A/J x C3H/HeJ)F1 x A/J backcross animals. Hc genotype shows statistically significant correlation to allergen-induced bronchial hyperresponsive phenotype. The A/J allele contains a 2 bp deletion resulting in deficient Hc mRNA and protein production and is associated with susceptibility to allergen-induced bronchial hyperresponsiveness. (J:108211)
|Molecular Note||A 2 base "TA" deletion at positions 62 and 63 of an 83 base pair exon near the 5' end of the gene is found in the following mouse strains: A/HeJ, A/J, AKR/J, DBA/2J, NZB/B1NJ, SWR/J, B10.D2/oSnJ. The consequence of this deletion is the creation of a stop codon starting four bases after the deletion. A truncated product of 216 amino acids is predicted as a result although contradictory reports exist that a larger pro-C5 protein may be synthesized. Nevertheless, macrophages from mouse strains carrying this allele do not secrete complement 5.|
|Allele Name||mutation 1|
|Allele Synonym(s)||Il3raA/J; Il3ran|
|Gene Symbol and Name||Il3ra, interleukin 3 receptor, alpha chain|
|Gene Synonym(s)||CD123; Cyrl; IL-3 receptor alpha chain; IL3R; IL3RAY; IL3RX; IL3RY; SUT-1; hIL-3Ra|
|Strain of Origin||A/J|
|Molecular Note||Sequence analysis revealed A/J mice lack the sequence corresponding to exon 8, which encodes 10 amino acid residues in the extracellular domain. Aberrant splicing was due to a 5 base pair deletion at the branch point in intron 7.|
|Gene Symbol and Name||Obq3, obesity QTL 3|
|Strain of Origin||AKR/J|
|General Note||Obq3 exhibits an additive mode of inheritance.|
|Molecular Note||This allele confers increased adiposity in male animals compared to C57L/J.|
|Allele Name||mutation 1|
|Allele Type||Spontaneous (Not Applicable)|
|Gene Symbol and Name||Ogg1, 8-oxoguanine DNA-glycosylase 1|
|Gene Synonym(s)||HMMH; HOGG1; MUTM; Mmh; OGH1|
|Strain of Origin||various|
|Molecular Note||A guanine to adenine change at the fifty-ninth nucleotide in exon 7 resulted in a substitution of the 336th amino acid, arginine, by histidine (R336H) in a putative nuclear localization signal. The mutation led to disruption of the nuclear localization of the enzyme, although the activity remained normal.|
|Allele Name||MCF sensitive|
|Gene Symbol and Name||Rmcf, resistance to MCF virus|
|Strain of Origin||multiple strains|
|General Note|| |
This locus controls resistance and susceptibility of cells in tissue culture to infection by mink cell focus-forming murine leukemia viruses. The allele Rmcfr determines resistance and occurs in strains DBA/1, DBA/2, and CBA/Ca; the allele Rmcfs determines susceptibility and occurs in strains AKR/J, C57BL/6, BALB/c, CBA/J, NFS, NZB, 129/J, and many others. Heterozygotes are as resistant as the resistant parent or nearly so. Rmcf is different from and independent of Fv1, a locus that controls susceptibility to infection by ecotropic viruses. Rmcf is located on Chr 5 close to Hm near the centromeric end (J:7108). Rmcfr protects (AKR x CBA/Ca)F1 and (AKR x DBA/2)F1 hybrids from development of spontaneous thymic lymphomas and reduces the incidence of MCF-induced thymic lymphomas (J:7175). It also reduces susceptibility of cells of Sxvs/Sxvr mice to exogenous xenotropic viruses (J:7951). In addition, in strains susceptible to Friend virus-induced erythroleukemia, a condition thought to be due to the replication of MCF virus, Rmcfr increases resistance to the virus-induced erythroleukemia. It may cause resistance by coding for or regulating the production of an MCF-related envelope glycoprotein that blocks the receptor for MCF viruses (J:8074). This conclusion is reinforced by the findings of Buller et al. (J:8497), who showed that the Rmcfr allele contains an endogenous MCF gp70 env gene and that the Rmcfs allele, at least in some strains (C57BL/6, CBA/J, and A/WySn), contains a xenotropic gp70 env gene. Presumably the MCF gp70 inhibits exogenous MCF infection in vitro by a mechanism of viral interference.
|Molecular Note||This locus controls resistance of cells to infection by mink cell focus-forming murine leukemia viruses. The recessive s (susceptible) allele is found in AKR/J, C57BL/6, BALB/c, CBA/J, NFS, NZB and 129/J.|
|Allele Name||adrenocortical lipid depletion|
|Allele Synonym(s)||Acact-; Soat1hid; ald; hid|
|Gene Symbol and Name||Soat1, sterol O-acyltransferase 1|
|Gene Synonym(s)||8430426K15Rik; 8430426K15Rik; ACACT; ACAT; ACAT-1; ACAT1; AW550831; Acact; Acact; Acat-1; RIKEN cDNA 8430426K15 gene; SOAT; STAT; acetyl coenzyme A cholesterol acyltransferase; adrenocortical lipid depletion; ald; expressed sequence AW550831; hair interior defect; hid; hid|
|Strain of Origin||AKR/O|
|General Note||All AKR sublines are homozygous for Soat1 |
|Molecular Note||Deletion of 118 bp in the a Soat1 mRNA. This region corresondes to the 5'UTR and the initial coding sequences. In addition, two missense mutations were observed: A1248G resulting in Ile to Val at amino acid 147 and C1422T resulting in His to Tyr at amino acid 205. Other nucleotide differences were observed that did not result in amino acid changes. A truncated protein is expressed from this allele, presumably due to internal initiation.|
When using the AKR mouse strain in a publication, please include JAX stock #000648 in your Materials and Methods section.
We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We 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.
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