Homozygous Il4ra knockout mice show no overt phenotypic abnormalities, but exhibit a loss of IL4-mediated signal transduction.
Dr. Leonard D. Shultz, The Jackson Laboratory
Homozygous Il4ra (interleukin 4 receptor, alpha) knockout mice show no overt phenotypic abnormalities, but exhibit a loss of IL4 signal transduction. This results in a diminished TH2 helper T cell response to helminthic parasite infections. These mutant mice provide a tool for analyzing the role of IL4/IL4RA in immunological pathways, including those that prime TH2 responses in infectious disease and other pathologies.
Exons 7, 8, and 9 were replaced with a PGKneomycin resistance cassette inserted in reverse transcriptional orientation. The mutation was created through homologous recombination in BALB/cJ-derived BALB/c-I embryonic stem (ES) cells. Resultant chimeric males were bred to BALB/cJ females once before sibling matings were set up by the donating laboratory.
|Allele Name||targeted mutation 1, Leonard Shultz|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||IL-4R-; IL-4R KO; Il4ratm1; IL-4Ralpha-; Il-4ralphatm1Sz|
|Gene Symbol and Name||Il4ra, interleukin 4 receptor, alpha|
|Strain of Origin||BALB/cJ|
|Molecular Note||A neomycin resistance cassette replaced exons 7 - 9 of the gene.|
|Mutations Made By|| |
Dr. Leonard Shultz, The Jackson Laboratory
When using the Il4rα KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #003514 in your Materials and Methods section.