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|A/J mice are widely used in cancer and immunology research.
Type Inbred Strain; Additional information on Inbred Strains. Visit our online Nomenclature tutorial. Mating System Sibling x Sibling (Female x Male) 01-MAR-06 Breeding Considerations This strain is a challenging breeder. Species laboratory mouse H2 Haplotype a Generation F297 (05-AUG-14)
Generation Definitions
View larger image
Related Genotype: a/a Tyrp1b/Tyrp1b Tyrc/Tyrc
Important Note
This strain is homozygous for Cdh23ahl, the age related hearing loss 1 mutation, and ahl4, which on this background result in progressive hearing loss with onset between three and five months of age.
Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A/J inbred strain is widely used in cancer and immunology research. It is highly susceptible to cortisone-induced congenital cleft palate. It has a high incidence of spontaneous lung adenomas, and lung tumors readily develop in response to carcinogens. A high percentage of mammary adenocarcinomas (a large proportion of acinar-type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains.
A/J mice fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid, and 15% fat) fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, Stock No. 000667, and SM/J, Stock No. 000687). In addition to atherosclerosis resistance, A/J mice are resistant to diabetes, obesity, insulin resistance and glucose intolerance. On either chow or high fat diet, A/J mice maintain low glucose and insulin levels.
A/J mice develop cigarette smoke-induced emphysema in approximately half the time when compared with C57BL/6J mice. Structural lung damage caused by induced asthma mimics the phenotype found in asthma patients more closely than does the induced damage in BALB/c mice.
A strain characteristic of A/J is a late onset (four to five months) progressive muscular dystrophy as a result of a homozygous retrotransposon insertion in the dysferlin (Dysf) gene. Myofibers in Dysfprmd homozygotes undergo degeneration and regeneration, and their nuclei are placed nuclei. Proximal muscles are more severely affected than distal muscles (Ho M, et al. 2004).
Sequencing of the mitochondrial genome of A/J reveals 10 adenines in a polymorphic adenine repeat sequence in the mt-Tr sequence. This repeat contains nine adenines in NOD/ShiLtJ, A/HeJ, A/WySnJ, and SKH2/J and 10 adenines in A/J, and NZB/B1NJ, and likely enhances the hearing loss associated with the Cdh23ahl allele (Johnson et al. 2001).
View A Strains (2 strains)Strains carrying Ahrb-2 allele
000645 A/HeJ 000130 B6.C-H17c/(HW14)ByJ 000370 B6.C-H38c/(HW119)ByJ 001026 BALB/cByJ 000653 BUB/BnJ 000659 C3H/HeJ 000656 CBA/J 000657 CE/J 000352 CXB2/ByJ 000353 CXB3/ByJ 000354 CXB4/ByJ 000355 CXB5/ByJ 000357 CXB7/ByJ 000673 HRS/J 000679 P/J 000930 PERA/EiJ 000644 SEA/GnJ 000280 SF/CamEiJView Strains carrying Ahrb-2 (18 strains)Strains carrying Cdh23ahl allele
001137 129P1/ReJ 000690 129P3/J 000691 129X1/SvJ 000647 A/WySnJ 003070 ALR/LtJ 003072 ALS/LtJ 004502 B6;AKR-Lxl2/GrsrJ 001026 BALB/cByJ 000653 BUB/BnJ 005494 C3.129S1(B6)-Grm1rcw/J 000664 C57BL/6J 004764 C57BL/6J-Cdh23v-8J/J 003129 C57BL/6J-Epha4rb-2J/GrsrJ 004820 C57BL/6J-Kcne12J/J 004703 C57BL/6J-Kcnq2Nmf134/J 004811 C57BL/6J-nmf110/J 004812 C57BL/6J-nmf111/J 004747 C57BL/6J-nmf118/J 004656 C57BL/6J-nmf88/J 004391 C57BL/6J-Chr 13A/J/NaJ 004385 C57BL/6J-Chr 7A/J/NaJ 000662 C57BLKS/J 000667 C57BR/cdJ 000668 C57L/J 000669 C58/J 010614 CBACa.B6-Cdh23ahl/Kjn 000657 CE/J 000670 DBA/1J 001140 DBA/1LacJ 000671 DBA/2J 007048 DBA/2J-Gpnmb+/SjJ 002106 KK/HlJ 000675 LG/J 000676 LP/J 000677 MA/MyJ 001976 NOD/ShiLtJ 002050 NOR/LtJ 000679 P/J 002747 SENCARB/PtJ 002335 SKH2/J 003392 STOCK Crb1rd8/JView Strains carrying Cdh23ahl (41 strains)Strains carrying Csahl4-A/J allele
014192 B6.A-(rs3676616-D10Utsw1)/Kjn 004388 C57BL/6J-Chr 10A/J/NaJView Strains carrying Csahl4-A/J (2 strains)Strains carrying Dysfprmd allele
012767 B6.A-Dysfprmd/GeneJ 017917 B6.Cg-Dysfprmd Prkdcscid/JView Strains carrying Dysfprmd (2 strains)Strains carrying Hc0 allele
000645 A/HeJ 000647 A/WySnJ 000648 AKR/J 000460 B10.D2-Hc0 H2d H2-T18c/o2SnJ 000461 B10.D2-Hc0 H2d H2-T18c/oSnJ 000657 CE/J 000671 DBA/2J 007048 DBA/2J-Gpnmb+/SjJ 001800 FVB/NJ 001491 FVB/NMob 000674 I/LnJ 001303 NOD.CB17-Prkdcscid/J 001976 NOD/ShiLtJ 000684 NZB/BlNJ 000682 RF/J 000688 ST/bJ 000689 SWR/JView Strains carrying Hc0 (17 strains)Strains carrying Il3ram1 allele
000645 A/HeJ 000647 A/WySnJ 000648 AKR/J 000653 BUB/BnJ 000669 C58/J 000657 CE/J 000684 NZB/BlNJ 000682 RF/J 000687 SM/JView Strains carrying Il3ram1 (9 strains)Strains carrying Micrln allele
000651 BALB/cJ 000009 BXH14/TyJ 000038 BXH6/TyJ 000014 BXH7/TyJ 000665 C57BL/10J 000664 C57BL/6J 000669 C58/JView Strains carrying Micrln (7 strains)Strains carrying Nrg3ska allele
001673 AXB1/PgnJ 001681 AXB10/PgnJ 001826 AXB13/PgnJ 001684 AXB13a/PgnJ 001687 AXB19/PgnJ 001688 AXB19b/PgnJ 001674 AXB2/PgnJ 001690 AXB23/PgnJ 001676 AXB4/PgnJ 001678 AXB6/PgnJ 001701 BXA13/PgnJ 001702 BXA14/PgnJ 001703 BXA16/PgnJ 001710 BXA24/PgnJ 001711 BXA25/PgnJ 001999 BXA26/PgnJ 001694 BXA4/PgnJ 001696 BXA7/PgnJ 001697 BXA8/PgnJView Strains carrying Nrg3ska (19 strains)Strains carrying Rmcfs allele
000648 AKR/J 000779 AKXD14/TyJ 000780 AKXD23/TyJ 000764 AKXD27/TyJ 000777 AKXD6/TyJ 000667 C57BR/cdJ 000668 C57L/J 000669 C58/J 000682 RF/J 000644 SEA/GnJ 000686 SJL/J 000688 ST/bJView Strains carrying Rmcfs (12 strains)Strains carrying Wnt9bclf1 allele
000645 A/HeJ 000647 A/WySnJ 001690 AXB23/PgnJView Strains carrying Wnt9bclf1 (3 strains)Strains carrying mt-Trm1 allele
003072 ALS/LtJ 001976 NOD/ShiLtJ 000684 NZB/BlNJView Strains carrying mt-Trm1 (3 strains)Strains carrying other alleles of Ahr
000690 129P3/J 000648 AKR/J 002920 B6(D2N).Spretus-Ahrb-3/J 002831 B6.129-Ahrtm1Bra/J 000136 B6.C-H34c/(HW22)ByJ 008599 B6.Cg-Del(9Cyp1a2-Cyp1a1)1Dwn Ahrd Tg(CYP1A1,CYP1A2)1Dwn/DwnJ 002921 B6.D2N-Ahrd/J 002727 B6;129-Ahrtm1Bra/J 000652 BDP/J 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 000351 CXB1/ByJ 000356 CXB6/ByJ 002937 D2.B6-Ahrb-1/J 000671 DBA/2J 000674 I/LnJ 000675 LG/J 000676 LP/J 000677 MA/MyJ 000550 MOLF/EiJ 000684 NZB/BlNJ 000726 RBF/DnJ 000682 RF/J 000686 SJL/J 001146 SPRET/EiJ 000688 ST/bJ 006203 STOCK Ahrtm3.1Bra/J 000689 SWR/J 000693 WC/ReJ KitlSl/J 000933 YBR/EiJView Strains carrying other alleles of Ahr (37 strains)Strains carrying other alleles of Cdh23
002552 B6(V)-Cdh23v-2J/J 002756 B6.CAST-Cdh23Ahl+/Kjn 010615 B6.CBACa-Cdh23CBA/CaJ/Kjn 002432 B6J x B6.C-H2-Kbm1/ByJ-Cdh23v-J/J 004764 C57BL/6J-Cdh23v-8J/J 004819 C57BL/6J-Cdh23v-9J/J 005016 CByJ;B6-Cdh23v-10J/J 000275 V/LeJView Strains carrying other alleles of Cdh23 (8 strains)Strains carrying other alleles of Dysf
006830 129-Dysftm1Kcam/J 011128 B10.SJL-Dysfim/AwaJ 013149 B6.129-Dysftm1Kcam/J 017644 B6;129S6-Dysftm2.1Kcam/J 000686 SJL/JView Strains carrying other alleles of Dysf (5 strains)Strains carrying other alleles of Hc
000470 AK.M-H2m H2-T18a/nSnJ 005308 B10.Cg-H2d Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ 000463 B10.D2-Hc1 H2d H2-T18c/nSnJ 003147 B10.D2-Hc1 H2d H2-T18c/nSnJ-Tg(DO11.10)10Dlo/J 024977 B6N(Cg)-Hctm1b(EUCOMM)Wtsi/J 022980 C57BL/6N-Hctm1a(EUCOMM)Wtsi/J 004306 NOD.CBALs-Hc1/LtJView Strains carrying other alleles of Hc (7 strains)Strains carrying other alleles of Micrl
000032 BXH10/TyJ 000033 BXH19/TyJ 000011 BXH4/TyJ 000076 BXH8/TyJ 000008 BXH9/TyJ 000260 JGBF/LeJ 000072 JGBF/LeTyJView Strains carrying other alleles of Micrl (7 strains)Strains carrying other alleles of Naip5
013574 FVB/N-Tg(149m19)M141Kunst/JView Strains carrying other alleles of Naip5 (1 strain)Strains carrying other alleles of Rmcf
000690 129P3/J 000765 AKXD13/TyJ 000954 AKXD15/TyJ 001093 AKXD18/TyJ 000947 AKXD22/TyJ 000763 AKXD9/TyJ 000654 CBA/CaJ 000670 DBA/1JView Strains carrying other alleles of Rmcf (8 strains)Strains carrying other alleles of Wnt9b
008469 STOCK Wnt9btm1.2Amc/JView Strains carrying other alleles of Wnt9b (1 strain)View Strains carrying other alleles of mt-Tr (2 strains)
JAX® NOTES, April 1988; 433. H-2 Haplotypes of Mice from Jackson Laboratory Production Colonies.
JAX® NOTES, Spring 2004; 493. Chromosome Substitution Strain Panel: A New Tool for Quantitative Trait Loci Analysis.
JAX® NOTES, Summer 1992; 450. Myoepitheliomas in Inbred Laboratory Mice.
JAX® NOTES, Winter 2006; 504. JAX® Mice: the Gold Standard Just Got Better.
Mouse Phenome Database / SNP Facility
National Center for Biotechnology Information / SNP Data
Sequence data is available from the Mouse Genomes Project at the Wellcome Trust Sanger Institute
View Phenotypic DataPhenotypic DataMouse Phenome Database
Festing Inbred Strain Characteristics: A
View Related Disease (OMIM) TermsRelated Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).Miyoshi Muscular Dystrophy 1; MMD1
Muscular Dystrophy, Limb-Girdle, Type 2B; LGMD2B
Myopathy, Distal, with Anterior Tibial Onset; DMAT
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.Complement Component 5 Deficiency; C5D (C5)
Deafness, Autosomal Recessive 12; DFNB12 (CDH23)
Eculizumab, Poor Response to (C5)
Usher Syndrome, Type ID; USH1D (CDH23)
View Mammalian Phenotype TermsMammalian Phenotype Terms provided by MGIassigned by genotype
- hearing/vestibular/ear phenotype
- cochlear hair cell degeneration
- at 30 days of age a hair cell lesion is found in the basal turn of the cochlea in A/J although the spiral ganglion appear normal in all turns including the basal turn (MGI Ref ID J:139222)
- at 9 weeks of age there is a massive loss of inner and outer hair cells from the mid-basal turn of the cochlea and a moderate loss of inner and outer hair cells from the mid-apical turn (MGI Ref ID J:139222)
- at 20 weeks of age there is a massive loss of inner and outer hair cells throughout the cochlea, except for the apical 10% (MGI Ref ID J:139222)
- loss of cochlear hair cells begins around 16 days of age, spreads from base to apex, and outer hair cells are more vulnerable to loss than are inner hair cells (MGI Ref ID J:139222)
- nervous system phenotype
- cochlear hair cell degeneration
- at 30 days of age a hair cell lesion is found in the basal turn of the cochlea in A/J although the spiral ganglion appear normal in all turns including the basal turn (MGI Ref ID J:139222)
- at 9 weeks of age there is a massive loss of inner and outer hair cells from the mid-basal turn of the cochlea and a moderate loss of inner and outer hair cells from the mid-apical turn (MGI Ref ID J:139222)
- at 20 weeks of age there is a massive loss of inner and outer hair cells throughout the cochlea, except for the apical 10% (MGI Ref ID J:139222)
- loss of cochlear hair cells begins around 16 days of age, spreads from base to apex, and outer hair cells are more vulnerable to loss than are inner hair cells (MGI Ref ID J:139222)
- immune system phenotype
- abnormal neutrophil physiology
- subsequent to ip injection of 15mg/kg LPS, A/J mice show highly diminished neutrophil infiltration into hepatic sinusoids compared with C57BL/6J controls (MGI Ref ID J:51631)
- decreased acute inflammation
- subsequent to ip injection of 15mg/kg LPS, A/J mice have decreased hepatic, pulmonary and intestinal neutrophil infiltrate compared with C57BL/6J mice (MGI Ref ID J:51631)
- hematopoietic system phenotype
- abnormal neutrophil physiology
- subsequent to ip injection of 15mg/kg LPS, A/J mice show highly diminished neutrophil infiltration into hepatic sinusoids compared with C57BL/6J controls (MGI Ref ID J:51631)
Cdh23ahl/Cdh23ahl mt-Trm1/?either: A/J X (A/J x CAST/Ei)F1 or A/J X (CAST/Ei x A/J)F1
- hearing/vestibular/ear phenotype
- increased or absent threshold for auditory brainstem response
- average ABR threshold is significantly increased by 3 months of age (MGI Ref ID J:67312)
- increased susceptibility to age-related hearing loss
- the presence of this mitochondrial sequence polymorphism in mice homozygous for the ahl allele results in age related hearing loss by 3 months of age, which is absent when the CAST/Ei mitochondrial sequence is instead present (MGI Ref ID J:67312)
- hearing/vestibular/ear phenotype
- impaired hearing (MGI Ref ID J:139222)
- increased or absent threshold for auditory brainstem response
- in A/J mice ABR thresholds at 16 and 32 kHz are elevated by 25 days of age and by 3 months of age the ABR thresholds are more than 50 dB above normal (MGI Ref ID J:139222)
- increased susceptibility to age-related hearing loss
- in A/J mice onset of hearing loss is found as early as 25 days of age and is much more severe at 6 months of age than that found in C57BL/6J (MGI Ref ID J:139222)
- behavior/neurological phenotype
- abnormal physical strength (MGI Ref ID J:92838)
- limb grasping
- muscle phenotype
- abnormal skeletal muscle morphology
- abnormal skeletal muscle fiber morphology
- centrally nucleated skeletal muscle fibers (MGI Ref ID J:92838)
- skeletal muscle fiber degeneration
- fibers with scattered degenerating and regenerating fibers by 4-5 months of age (MGI Ref ID J:92838)
- skeletal muscle fiber necrosis
- increased numbers of necrotic and regenerating fibers with time (MGI Ref ID J:92838)
- skeletal muscle endomysial fibrosis
- endomysial fibrosis at later stages (MGI Ref ID J:92838)
- hematopoietic system phenotype
- abnormal common myeloid progenitor cell morphology
- CFU-GM assays using bone marrow derived cells yield very few colonies in repsonse to interleukin 3, but normal colony growth occurs in response to GM-CSF (MGI Ref ID J:24918)
- abnormal leukopoiesis
- Il3 alone does not support granulocyte/macrophage colony formation in bone marrow cells from A/J mice but does in bone marrow from C57BL/6 controls; costimulation with both Il3 and SCF increases the number of colonies formed compared to SCF alone (MGI Ref ID J:23971)
- immune system phenotype
- abnormal leukopoiesis
- Il3 alone does not support granulocyte/macrophage colony formation in bone marrow cells from A/J mice but does in bone marrow from C57BL/6 controls; costimulation with both Il3 and SCF increases the number of colonies formed compared to SCF alone (MGI Ref ID J:23971)
- immune system phenotype
- increased susceptibility to bacterial infection
- peritoneal macrophages derived from A/J mice are susceptible to Legionella pneumophilia infection; infected macrophages show a 10-fold increase in bacterial burden after 1 day of infection compared to resistant controls (C57BL/6J) (MGI Ref ID J:20633)
- endocrine/exocrine gland phenotype
- abnormal mammary gland development
- 95% of female A/J mice display an altered pattern of mammary gland development compared with C57BL/6 which showed no abnormalities in this study (MGI Ref ID J:60708)
- abnormal mammary gland pattern
- 95% of females have abnormal mammary gland development (MGI Ref ID J:60708)
- abnormal nipple development (MGI Ref ID J:60708)
- ectopic nipples (MGI Ref ID J:60708)
- absent mammary gland
- increased mammary gland number
- increased nipple number
- most commonly observed laterally to a #4 gland and displaced away from the mid-line (MGI Ref ID J:60708)
- connected to distinct underlying ductal systems; not connected to the major ductal system of the normal gland (MGI Ref ID J:60708)
- easily observed at 21 days of age (MGI Ref ID J:60708)
- this phenotype or supernumerary mammary glands comprise 31% of mice observed (MGI Ref ID J:60708)
- integument phenotype
- abnormal mammary gland development
- 95% of female A/J mice display an altered pattern of mammary gland development compared with C57BL/6 which showed no abnormalities in this study (MGI Ref ID J:60708)
- abnormal mammary gland pattern
- 95% of females have abnormal mammary gland development (MGI Ref ID J:60708)
- abnormal nipple development (MGI Ref ID J:60708)
- ectopic nipples (MGI Ref ID J:60708)
- absent mammary gland
- increased mammary gland number
- increased nipple number
- most commonly observed laterally to a #4 gland and displaced away from the mid-line (MGI Ref ID J:60708)
- connected to distinct underlying ductal systems; not connected to the major ductal system of the normal gland (MGI Ref ID J:60708)
- easily observed at 21 days of age (MGI Ref ID J:60708)
- this phenotype or supernumerary mammary glands comprise 31% of mice observed (MGI Ref ID J:60708)View Research ApplicationsResearch ApplicationsThis mouse can be used to support research in many areas including:
Cdh23ahl related
Cancer Research
Increased Tumor Incidence
Adenomas: lung
Mammary Gland Tumors
Mammary Gland Tumors: late onset
Cardiovascular Research
Diet-Induced Atherosclerosis
Relatively Resistant
Developmental Biology Research
Craniofacial and Palate Defects
congenital cleft palate
Internal/Organ Defects
Internal/Organ Research
Lung Defects
Neurobiology Research
Hearing Defects
Age related hearing loss
Muscular Dystrophy
Limb-Girdle type
Research Tools
General Purpose
Immunology, Inflammation and Autoimmunity Research
hybridoma production
Infectious Disease
Sensorineural Research
Hearing Defects
Age related hearing loss
Hc0 related
Neurobiology Research
Hearing Defects
Age related hearing loss
Sensorineural Research
Hearing Defects
Age related hearing loss
Il3ram1 related
Immunology, Inflammation and Autoimmunity Research
specific complement deficiency
Research Tools
Immunology, Inflammation and Autoimmunity Research
specific complement deficiency, C5 complement
Naip5Lgn1-s related
Immunology, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
genes regulating susceptibility to infectious disease and endotoxin
Macrophage defects
|Allele Symbol
|Allele Name
|b-2 variant
|Allele Type
|Not Applicable
|Common Name(s)
|Ahb-2; Ahh;
|Strain of Origin
|Gene Symbol and Name
|Ahr, aryl-hydrocarbon receptor
|Gene Common Name(s)
|Ah; Ahh; Ahre; In; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; bHLHe76; dioxin receptor; inflammatory reactivity;
|General Note
C57BL/6 carries the responsive Ahrb allele; DBA/2 carries nonresponsive Ahrd. Heterozygotes (Ahrb/Ahrd) are responsive (J:5282). Later work identified a second (J:8895) and later a third (J:22144) allele conferring response. Thus the allele in C57, C58, and MA/My strains is now Ahrb-1; Ahrb-2 is carried by BALB/cBy, A, and C3H; and Ahrb-3 by Mus spretus, M. caroli, and MOLF/Ei. The nonresponsive strains AKR, DBA/2, and 129 carry Ahrd (J:22144). Nucleotide and amino acid sequence differences between Ahrb-1 and Ahrd have been determined (J:17460).
Strain of origin - this allele was found in BALB/cByJ, A/J, C3H/HeJ, CBA strains
|Molecular Note
|This allele encodes a high affinity, heat labile, 104 kDa receptor containing 848 amino acids. Sequencing studies of cDNA from C57BL/6J congenic mice homozygous for this allele identified nucleotide substitutions in the ORF that would cause 5 amino acid differences between the C57BL/6J and BALB/cBy peptides, and 2 amino acid differences between the BALB/cBy and DBA/2J peptides. A T to C transition in exon 11 replaces the opal termination codon in the C57BL/6J allele with an arginine codon in the BALB/cByallele. This change would extend translation of the BALB/cBy 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). [MGI Ref ID J:15153] [MGI Ref ID J:22144]
|Allele Symbol
|Allele Name
|Allele Type
|Strain of Origin
|Gene Symbol and Name
|Bhr1, bronchial hyperresponsiveness 1
|General Note
|Heterozygosity for A/J-derived alleles at both Bhr1 and Bhr5 is sufficient to confer the airway hyperresponsive phenotype.
|Molecular Note
|This allele confers increased airway hyperresponsiveness compared to C57BL/6J.
|Allele Symbol
|Allele Name
|Allele Type
|Strain of Origin
|Gene Symbol and Name
|Bhr5, bronchial hyperresponsiveness 5
|General Note
|Heterozygosity for A/J-derived alleles at both Bhr1 and Bhr5 is sufficient to confer the airway hyperresponsive phenotype.
|Molecular Note
|This allele confers susceptibility to airway hyperresponsiveness compared to C3H/HeJ. [MGI Ref ID J:33778]
|Allele Symbol
|Allele Name
|age related hearing loss 1
|Allele Type
|Common Name(s)
|Cdh23753A; mdfw;
|Strain of Origin
|multiple strains
|Gene Symbol and Name
|Cdh23, cadherin 23 (otocadherin)
|Gene Common Name(s)
|4930542A03Rik; CDHR23; RIKEN cDNA 4930542A03 gene; USH1D; W; age related hearing loss 1; ahl; bob; bobby; bus; bustling; mdfw; modifier of deaf waddler; neuroscience mutagenesis facility, 112; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; nmf112; nmf181; nmf252; sals; salsa; v; waltzer;
|Molecular Note
|Genetic complementation tests have shown allelism between the mdfw (modifier of deaf waddler) locus and the ahl locus. Further analysis has identified an association between ahl and a G to A transition at nucleotide position 753 of Cdh23. This hypomorphic allele causes in frame skipping of exon 7 and reduced message stability. Twenty-seven strains classified with ahl and carrying the 753A allele include: CD1, RBF/DnJ, PL/J, AKR/J, RF/J, BALB/cBy, A/WySnJ, P/J, SENCARA/PtJ, DBA/1J, ALS/LtJ, C58/J, C57BLKS/J, 129P1/ReJ, C57BR/cd, SKH2/J, BUB/Bn, MA/MyJ, LP/J, 129X1/SvJ, NOR/LtJ, A/J, C57BL/6, NOD/LtJ, DBA/2J, ALR/LtJ, C57L/J. Strains classified with ahl that DO NOT carry this mutation include: C3H/HeSnJ, I/LnJ,YBR/Ei, MRL/MpJ. [MGI Ref ID J:86905]
|Allele Symbol
|Allele Name
|Allele Type
|Strain of Origin
|Gene Symbol and Name
|Cs, citrate synthase
|Gene Common Name(s)
|2610511A05Rik; 9030605P22Rik; Ahl4; BB234005; Cis; RIKEN cDNA 2610511A05 gene; RIKEN cDNA 9030605P22 gene; age related hearing loss 4; ahl4; expressed sequence BB234005;
|Molecular Note
|The C to A nucleotide change in exon 3 of Cs in A/J (SNP rs29358506) mice causes a nonconservative amino acid change, from histidine (H) to asparagine (N) at position 55 of the CS protein (H55N). This histidine is highly conserved in the orthologous proteins of all mammals and in many other species indicating that it is likely to be functionally important.
|Allele Symbol
|Allele Name
|progressive muscular dystrophy
|Allele Type
|Mutation Made By
|Douglas Albrecht, Jain Foundation Inc
|Strain of Origin
|Gene Symbol and Name
|Dysf, dysferlin
|Gene Common Name(s)
|2310004N10Rik; AI604795; D6Pas3; DNA segment, Chr 6, Pasteur Institute 3; FER1L1; LGMD2B; MMD1; RIKEN cDNA 2310004N10 gene; expressed sequence AI604795;
|Molecular Note
|A retrotransposon insertion occurred within intron 4, causing aberrant splicing of the gene. Protein was abolished as shown by Northern blot and immunoblot analysis. The insertion was 6000bp in size. This allele was found only in A/J mice, not in A/WySnJ, A/HeJ, C57BL/6J, SJL/J, SWR/J or 129/SvJ mice. [MGI Ref ID J:149430] [MGI Ref ID J:149432] [MGI Ref ID J:92838]
|Allele Symbol
|Allele Name
|Allele Type
|Common Name(s)
|C5-; C5-d; C5-def; C5-deficient; hco;
|Strain of Origin
|multiple strains
|Gene Symbol and Name
|Hc, hemolytic complement
|Gene Common Name(s)
|C5; C5D; C5a; C5b; CPAMD4; ECLZB; He;
|General Note
This is an allele characteristic of various inbred mouse strains including the following: A/HeJ, 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, 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. [MGI Ref ID J:23983] [MGI Ref ID J:5016]
|Allele Symbol
|Allele Name
|mutation 1
|Allele Type
|Common Name(s)
|Il3raA/J; Il3ran;
|Strain of Origin
|Gene Symbol and Name
|Il3ra, interleukin 3 receptor, alpha chain
|Gene Common Name(s)
|CD123; Cyrl; IL-3 receptor alpha chain; IL3R; IL3RAY; IL3RX; IL3RY; SUT-1; hIL-3Ra;
|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. [MGI Ref ID J:23971]
|Allele Symbol
|Allele Name
|Allele Type
|Strain of Origin
|multiple strains
|Gene Symbol and Name
|Micrl, microwave induced increase in complement receptor B cells
|General Note
The following inbred strains are homozygous for the recessive QTL, Micrl
|Allele Symbol
|Allele Name
|Legionella, susceptiblility 1
|Allele Type
|Common Name(s)
|Strain of Origin
|Gene Symbol and Name
|Naip5, NLR family, apoptosis inhibitory protein 5
|Gene Common Name(s)
|Birc1; Birc1a; Birc1b; Birc1e; Legionella, susceptiblility 1; Lgn1; Naip; Naip-rs3; Naip2; RGD1559914; baculoviral IAP repeat-containing 1e; neuronal apoptosis inhibitory protein 5; neuronal apoptosis inhibitory protein, related sequence 3;
|Molecular Note
|A/J mice are susceptible to infection by Legionella pneumophilia. This susceptibility is heritable and is caused by a polymorphism in the Naip5 gene. Expression of BAC clones containing the Naip5 gene from resistant strains (C57BL/6J and 129X1/SvJ) in A/J mice rendered transgenic mice resistant to infection (J:81887, J:129300). In addition, Western blot experiments demonstrated that the NAIP5 protein is not expressed in A/J macrophages, while robust expression is seen in macrophages from resistant strains such as C57BL/6J. Sequence polymorphisms in this gene between susceptible and resistant strains were identified that may account for the difference in phenotype. In addition, morpholino antisense inhibition of NAIP5 activity in mouse macrophages fromresistant mice resulted in an increase in permissiveness of Legionella replication (J:129300). [MGI Ref ID J:129300] [MGI Ref ID J:81887]
|Allele Symbol
|Allele Name
|Allele Type
|Common Name(s)
|Strain of Origin
|Gene Symbol and Name
|Nrg3, neuregulin 3
|Gene Common Name(s)
|HRG3; RGD1559678; pro-NRG3; scaramanga; ska;
|Molecular Note
|This allele maps to an interval between the microsatellite markers D14Mit14 and D14Mit80 located at 10.0 cM and 13.5 cM. The mutation identified is a microsatellite repeat within intron 7 of the gene. This simple sequence repeat (SSR) was found to completely cosegregate with the ska phenotype. [MGI Ref ID J:100495]
|Allele Symbol
|Allele Name
|MCF sensitive
|Allele Type
|Strain of Origin
|multiple strains
|Gene Symbol and Name
|Rmcf, resistance to MCF virus
|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 theRmcfs 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 Symbol
|Allele Name
|cleft lip 1
|Allele Type
|Strain of Origin
|Gene Symbol and Name
|Wnt9b, wingless-type MMTV integration site family, member 9B
|Gene Common Name(s)
|WNT14B; WNT15; Wnt15; cleft lip; cleft lip 1; clf; clf1; wingless-type MMTV integration site 15;
|General Note
|Unequal duplicate epistasis - the normal allele at clf1 is a dominant suppressor of the recessive phenotype at clf2, and the normal allele at clf2 is a semidominant suppressor of the recessive phenotype at the clf1 locus.
|Molecular Note
|This mutation is a novel insertion of an IAP transposon 3' from the gene. In addition, a standard genetic test of allelism between clf1 and a Wnt9b targeted mutation demonstrated noncomplementation, showing clf1 is an allele of Wnt9b. [MGI Ref ID J:117594] [MGI Ref ID J:96061]
|Allele Symbol
|Allele Name
|mutation 1
|Allele Type
|Common Name(s)
|Strain of Origin
|Gene Symbol and Name
|mt-Tr, mitochondrially encoded tRNA arginine
|Gene Common Name(s)
|TrnR tRNA; tRNA; tRNA-Arg;
|General Note
|This polymorphism is present in A/J, NZB/B1NJ, ALS/Lt and NOD/ShiLtJ. A variant with 9 adenines is found in NOD/ShiLtDvs, ALR/Lt and SKH2/J.
|Molecular Note
|The adenine repeat in the D stem is polymorphic with 10 adenines in this allele. [MGI Ref ID J:67312] [MGI Ref ID J:97969]
Inbred mouse strains are maintained through sibling (sister x brother) matings; no genotyping required.
Genotyping resources and troubleshooting
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Schmitt J; Roderfeld M; Sabrane K; Zhang P; Tian Y; Mertens JC; Frei P; Stieger B; Weber A; Mullhaupt B; Roeb E; Geier A. 2012. Complement factor C5 deficiency significantly delays the progression of biliary fibrosis in bile duct-ligated mice. Biochem Biophys Res Commun 418(3):445-50. [PubMed: 22277671] [MGI Ref ID J:181268]
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Trendelenburg M; Fossati-Jimack L; Cortes-Hernandez J; Turnberg D; Lewis M; Izui S; Cook HT; Botto M. 2005. The role of complement in cryoglobulin-induced immune complex glomerulonephritis. J Immunol 175(10):6909-14. [PubMed: 16272350] [MGI Ref ID J:119691]
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Wright RJ; Bikoff EK; Stockinger B. 1998. The Ii41 isoform of invariant chain mediates both positive and negative selection events in T-cell receptor transgenic mice. Immunology 95(3):309-13. [PubMed: 9824491] [MGI Ref ID J:50737]
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Younger JG; Shankar-Sinha S; Mickiewicz M; Brinkman AS; Valencia GA; Sarma JV; Younkin EM; Standiford TJ; Zetoune FS; Ward PA. 2003. Murine complement interactions with Pseudomonas aeruginosa and their consequences during pneumonia. Am J Respir Cell Mol Biol 29(4):432-8. [PubMed: 14500254] [MGI Ref ID J:94613]
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Gainsford T; Roberts AW; Kimura S; Metcalf D; Dranoff G; Mulligan RC; Begley CG; Robb L; Alexander WS. 1998. Cytokine production and function in c-mpl-deficient mice: no physiologic role for interleukin-3 in residual megakaryocyte and platelet production. Blood 91(8):2745-52. [PubMed: 9531584] [MGI Ref ID J:47462]
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Animal Health ReportsRoom Number AX29
Room Number AX9
Room Number MP14
Room Number MP16
Room Number RB04
Colony Maintenance
Mating System Sibling x Sibling (Female x Male) 01-MAR-06 Breeding Considerations This strain is a challenging breeder. Diet Information LabDiet® 5K52/5K67
|Pricing for USA, Canada and Mexico shipping destinations
Weeks of Age Price per mouse (US dollars $) Gender 3 weeks $34.96 Female or Male 4 weeks $34.96 Female or Male 5 weeks $34.96 Female or Male 6 weeks $38.18 Female or Male 7 weeks $41.57 Female or Male 8 weeks $44.79 Female or Male 9 weeks $48.24 Female or Male 10 weeks $51.58 Female or Male 11 weeks $54.86 Female or Male 12 weeks $58.19 Female or Male 13 weeks $61.47 Female or Male 14 weeks $64.80 Female or Male 15 weeks $68.08 Female or Male 16 weeks $71.42 Female or Male 17 weeks $74.87 Female or Male 18 weeks $78.09 Female or Male 19 weeks $81.48 Female or Male 20 weeks $84.70 Female or Male
Standard Supply
Level 2. Up to 100 mice. Larger quantities or custom orders arranged upon request.
Supply Notes
Volume pricing is available for this strain. View our Volume Pricing Program for information.
- This strain is available from both the Bar Harbor, Maine and Sacramento, Calif. facilities.
- Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.
|Pricing for International shipping destinations
Weeks of Age Price per mouse (US dollars $) Gender 3 weeks $45.50 Female or Male 4 weeks $45.50 Female or Male 5 weeks $45.50 Female or Male 6 weeks $49.70 Female or Male 7 weeks $54.10 Female or Male 8 weeks $58.30 Female or Male 9 weeks $62.80 Female or Male 10 weeks $67.10 Female or Male 11 weeks $71.40 Female or Male 12 weeks $75.70 Female or Male 13 weeks $80.00 Female or Male 14 weeks $84.30 Female or Male 15 weeks $88.60 Female or Male 16 weeks $92.90 Female or Male 17 weeks $97.40 Female or Male 18 weeks $101.60 Female or Male 19 weeks $106.00 Female or Male 20 weeks $110.20 Female or Male
Standard Supply
Level 2. Up to 100 mice. Larger quantities or custom orders arranged upon request.
Supply Notes
- Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.
- This strain is available from some international Charles River (CR) breeding facilities in Japan and/or Europe. For more information, see the Worldwide Distributor List for JAX® Mice.
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.
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.

subset: commoncrawl


text:
For most taxpayers, tax-filing season is over. Tax scams, however, never seem to end.
It's true that tax-oriented scams are at their peak during the January-to-April filing season. But criminals use tax issues -- and taxpayers' concerns about their taxes -- to dupe unsuspecting filers year round.
Every year, the IRS tracks the multitude of schemes and compiles a list of the 12 most egregious tax-related scams.
Some scam artists come up with patently false schemes to wheedle personal information and money from unsuspecting taxpayers. Others take real tax breaks, or portions of legal write-offs, and illegally apply them.
Eleven of the scams are making a repeat appearance on this year's warning list, including the criminals' perennial favorite, phishing. Other cons still making the rounds include frivolous tax arguments, retirement scams, misuse of trusts and improper charity deductions. And some folks can't even trust their tax pros, with unscrupulous preparers once again making the annual list.
Each of these tax-oriented cons has serious consequences, not just for the perpetrators, but also for their victims.
If convicted of tax fraud or evasion, scam promoters face tax penalties, interest and criminal prosecution. And taxpayers who bought into a scam, even if they are unwitting victims, also could pay a steep tax price. They can end up owing not only the tax they thought they were avoiding, but also penalties and interest.
To help you avoid such unwanted tax consequences, be aware of these "dirty dozen" common, and potentially costly, tax scams.
1. Phishing
More identity thieves than ever are using tax-themed fake e-mails to try to get personal financial information. Once they do, you can say goodbye to your good financial reputation and hello to a prolonged hassle to clean up the mess. These criminals use the information to empty victims' bank accounts, run up credit card charges and apply for loans or credit in the victims' names.
Some phishing e-mails falsely claim to come from the IRS, usually asking the recipient to send the personal data in a reply e-mail or to click on a link that takes the reader to a fake IRS Web page. Don't fall for this fake bait. The IRS never uses e-mail to contact taxpayers about tax issues. Never respond to such a request and never follow any links in suspect e-mails. The only official IRS Web site is at www.irs.gov, and your safest move is to go there yourself directly if you have tax questions.
If you get such
a solicitation, forward the
e-mail to the IRS at email@example.com.
And if you ever have any doubt
as to whether any IRS contact
is authentic, call (800) 829-1040
to confirm it.


text:
The University Post Office provides the university with convenient access to mailing services. In addition to processing and distributing interoffice as well as all incoming and outgoing mail for the university, we provide express mail, priority mail, registered mail and delivery confirmation services. United States Postal Service money orders and postage stamps are also available for sale.
Hours of Operation:
Monday-Friday 8:00AM-5:00PM (Office)
Monday-Friday 9:00AM-5:00PM (Window)


text:
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