LG/J mice develop antinuclear antibodies and rheumatoid factor as well as renal disease characterized by glomerulonephritis, interstitial nephritis, and perivasculitis. LG/J mice are often compared to SM/J (Stock No. 000687) for quantitative trait locus analysis in the areas of atherosclerosis, obesity, and mandible size . These mice are susceptible to diet-induced obesity and diet-induced atherosclerosis. This strain is among the least responsive to phytohemagglutinin.Read More +
This strain is homozygous for Cdh23ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss with onset after 10 months of age.
LG/J mice develop antinuclear antibodies and rheumatoid factor as well as renal disease characterized by glomerulonephritis, interstitial nephritis, and perivasculitis (Peng et al., 1996). LG/J was the predominant strain used to develop the MRL/LpJ (Stock No. 000486) inbred strain, a model for autoimmunity. LG/J mice are often compared to SM/J (Stock No. 000687) for quantitative trait locus analysis in the areas of atherosclerosis, obesity, and mandible size . These mice are susceptible to diet-induced obesity and diet-induced atherosclerosis. This strain is among the least responsive to phytohemagglutinin (Heiniger et al., 1975).
Developed by Goodale with selection for large body size begining in 1931. Inbred by M.N. Runner. Two substrains, J and Ckc, were separated at F27.
|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 Name||age related hearing loss 1|
|Allele Synonym(s)||Cdh23753A; mdfw|
|Gene Symbol and Name||Cdh23, cadherin 23 (otocadherin)|
|Gene Synonym(s)||4930542A03Rik; 4930542A03Rik; CDHR23; PITA5; RIKEN cDNA 4930542A03 gene; USH1D; W; age related hearing loss 1; ahl; ahl; bob; bob; bobby; bus; bustling; mdfw; mdfw; modifier of deaf waddler; neuroscience mutagenesis facility, 112; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; nmf112; nmf112; nmf181; nmf181; nmf252; nmf252; sals; sals; salsa; v; waltzer|
|Strain of Origin||multiple strains|
|Molecular Note||Genetic complementation tests have shown allelism between the mdfw (modifier of deaf waddler) locus and the ahl locus. Further analysis has shown this is caused by a G to A transition at nucleotide position 753 of Cdh23. This hypomorphic allele causes in frame skipping of exon 7, which is predicted to delete part of the 2nd and 3rd ectodomains, and cause reduced message stability. Twenty-seven strains classified with ahl and carrying the 753A allele include: CD-1, 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.|
|Allele Type||Spontaneous (Not Specified)|
|Gene Symbol and Name||Gpr84, G protein-coupled receptor 84|
|Gene Synonym(s)||EX33; GPCR4|
|Strain of Origin||multiple strains|
|Molecular Note||This spontaneously arising frameshift deletion is located in exon 2 at position 103308576 bp (NCBI Build 37) and results in a premature stop codon. The mutation is predicted to result in a truncated protein lacking the transmembrane domains 4-7. The inbred strains BDP/J, DBA/1J, DBA/2J, I/LnJ, FVB/NJ, LG/J, MRL/MpJ, NODShi/LtJ, NOR/LtJ, P/J, PL/J, SKHIN/Sprd, SJL/J, SM/J are homozygous for the deletion. The allele is segregating in the outbred stocks ICR and CD-1.|
When using the Large mouse strain in a publication, please include JAX stock #000675 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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