Homozygous C3ar1tm1Cge knock-out mice have elevated IgG1 and decreased IgG2a, IgG3, and IgA in serum. This mutant may be suitable for use in studies related to asthma, allergic skin disease, and innate-immunity studies.
Craig Gerard, Childrens' Hospital Boston, Harvard MS
Mice homozygous for the targeted mutation are viable, fertile, normal in size, and do not display any behavioral abnormalities when maintained under barrier conditions. No transcripts from the targeted gene are detected in bone marrow. Homozygous mice have normal T and B cell development but elevated IgG1 and decreased IgG2a, IgG3, and IgA in serum. In standard models of airway hyperresponsiveness (intraperitoneal (i.p.) sensitization followed by aerosol challenge), mutant mice are protected from allergic airway disease. Following epicutaneous, but not i.p., sensitization, homozygotes have significantly greater serum IgG1, dermal eosinophilia, and splenocyte Th2 cytokine secretion. Antigen presenting cells from null mice induce stronger Th2 responses. This mutant may be suitable for use in studies related to asthma, allergic skin disease, T helper cell polarization/B cell isotype switching, and other Th2- and innate-immunity studies.
A targeting vector was designed to replace 736 base pairs of the N-terminal region of the targeted gene (including the start codon) with a mouse phosphoglycerate kinase promoter driven neomycin resistance gene. The construct was electroporated into the 129S4/SvJae-derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric males were backcrossed to BALB/cAnNCrl females. Heterozygotes were mated to BALB/cAnNCrl mice for 15 generations before arriving at The Jackson Laboratory. Upon arrival, mutants were bred to BALB/cJ mice for one generation. The resulting heterozygotes were bred together to create a homozygous colony.
|Allele Name||targeted mutation 1, Craig Gerard|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||C3aR -|
|Gene Symbol and Name||C3ar1, complement component 3a receptor 1|
|Gene Synonym(s)||AZ3B; C3AR; C3aR; HNFAG09; anaphylatoxin C3a receptor|
|Strain of Origin||129S4/SvJae|
|Molecular Note||A 736 bp DNA fragment containing the translation start site and coding sequences for the N-terminal part of the protein was replaced with a neomycin selection cassette. RT-PCR analysis on RNA derived from bone marrow cells of homozygous mice confirmed that no detectable transcript is produced from this allele.|
|Mutations Made By|| |
Craig Gerard, Childrens' Hospital Boston, Harvard MS
Upon arrival, mutant mice were bred together to create homozygotes. To maintain the live colony, homozygous mice are bred together.
|Please inquire about possible genotypes.|
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided,
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