This widely used general purpose strain is the only CBA substrain that carries the Pde6brd1 mutation, which causes blindness by wean age. Renal tubulointerstitial lesions have been observed in this strain at a high frequency. Some CBA/J mice spontaneously develop exocrine pancreatic insufficiency syndrome. Research includes immunology and inflammation, metabolism, hearing and cochlear function, infectious disease, and fetal development.Read More +
This strain is homozygous for the retinal degeneration allele Pde6brd1. See article "Genetic Background Effects: Can Your Mice See?", JAX® NOTES Spring 2002, No. 485.
CBA/J inbred mice are widely used as a general purpose strain. CBA/J strain is the only CBA substrain that carries the Pde6brd1 mutation, which causes blindness by wean age. CBA/J mice are not histocompatible with the CBA/CaJ (Stock No. 000654) substrain (Green and Kaufer, 1965).
The CBA/J inbred mouse strain is used to study granulomatous experimental autoimmune thyroiditis (G-EAT), are relatively resistant to diet-induced atherosclerosis (Paigen et al. 1990), and develop a mild hearing loss late in life, with most of the hearing loss occurring in the higher frequencies (Sweet et al. 1988). Renal tubulointerstitial lesions have been observed in this strain at a high frequency (Rudofsky 1978). Some CBA/J mice spontaneously develop exocrine pancreatic insufficiency syndrome (Eppig and Leiter 1977, Leiter et al. 1977).
Beginning in 1920, Strong developed the CBA inbred strain from a cross of an unpedigreed Bagg albino female and an early DBA progenitor male. C3H mice are descended from the same cross. CBA was selected for a low incidence of mammary tumors. Strong sent the CBA mice to Andervont in 1947. Andervont sent the CBA mice to The Jackson Laboratory in 1948.
|Allele Name||retinal degeneration 1|
|Allele Synonym(s)||Pdebrd1; rd; rd-1; rd1; rodless retina|
|Gene Symbol and Name||Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide|
|Gene Synonym(s)||rd; rd1; Pdeb; r; rd; rd10; nmf137; r; retinal degeneration; retinal degeneration 1; retinal degeneration 10; CSNB3; CSNBAD2; rd1; rd-1; rd10; PDEB; RP40; phosphodiesterase, cGMP, rod receptor, beta polypeptide; Pdeb; GMP-PDEbeta|
|Strain of Origin||various|
|General Note||The following inbred strains are known to be homozygous for Pde6b |
|Molecular Note||Two mutations have been identified in rd1 mice. A murine leukimia virus (Xmv-28) insertion in reverse orientation in intron 1 is found in all mouse strains with the rd1 phenotype. Further, a nonsense mutation (C to A transversion) in codon 347 that results in a truncation eliminating more than half of the predicted encoded protein, including the catalytic domain has also been identified in all rd1 strains of mice. A specific degradation of mutant transcript during or after pre-mRNA splicing is suggested.|
|Allele Name||b-2 variant|
|Allele Type||Not Applicable|
|Allele Synonym(s)||Ahb-2; Ahh|
|Gene Symbol and Name||Ahr, aryl-hydrocarbon receptor|
|Gene Synonym(s)||bHLHe76; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; Ahh; dioxin receptor; In; Ah; Ahre; inflammatory reactivity|
|Strain of Origin||BALB/cBy|
|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/cBy allele. 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).|
|Allele Name||a variant|
|Allele Synonym(s)||CD5.1; Ly-1.1|
|Gene Symbol and Name||Cd5, CD5 antigen|
|Gene Synonym(s)||Ly-12; lymphocyte antigen 1; T1; T-lymphocyte antigen 1; LEU1; Ly-1; Lyt-1; lymphocyte antigen 12; Ly-12; Lyt-1; Ly-A; Ly-1|
|Strain of Origin||multiple strains|
|Molecular Note||Sequence analysis of C3H/HeJ showed that this polymorphic variant has point mutations relative to the b variant that result in valine instead of isoleucine at amino acid 9, leucine instead of glutamine at amino acid 52, and isoleucine instead of phenylalanine at amino acid 71, all within the amino terminal scavenger receptor cysteine-rich D1 domain, in addition to 7 silent point mutations. This allele is found in many inbred strains including CBA/J, C3H and DBA substrains.|
Older mice are prone to seizures.
Volume Pricing Program
Quantities: Volume pricing is automatically applied when a minimum quantity per strain for a shipment is reached
Sexes: Sexes of the same strain may be combined to reach minimum quantity levels to receive the volume pricing
Shipment: All shipping destinations qualify
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.
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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