These Il10rb knock-out mice may be useful in studies of the role of interleukin-10 in inflammatory diseases such as chronic colitis.
Sherman Fong, Genentech, Inc.
Genetic Background | Generation |
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?+N2F3
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Allele Type | Gene Symbol | Gene Name |
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Targeted (Null/Knockout) | Il10rb | interleukin 10 receptor, beta |
Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis of ES cells. After 12 weeks of age, approximately 60% of mutant mice develop chronic colitis and increased numbers of splenocytes resulting in splenomegaly. Bone marrow-derived macrophages, splenocytes and peritoneal cells derived from homozygotes do not respond to IL-10. Mutant mice housed in non-SPF conditions do not breed well. This mutant mouse strain may be useful in studies of the role of interleukin-10 in inflammatory diseases such as chronic colitis.
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt exons 1 and 2, which encode the signal peptide and the first 39 amino acids. The construct was electroporated into 129S2/SvPas-derived D3 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The donating investigator reported that the resulting male chimeric animals were crossed to C57BL/6 female mice, and then backcrossed to C57BL/6J mice for 6 generations using a speed congenic protocol (see SNP note below).
A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, all 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a C57BL/6N genetic background.
Allele Name | Targeted mutation 1, Michael Aguet |
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Allele Type | Targeted (Null/Knockout) |
Allele Synonym(s) | CRFB4-; IL-10-; IL-10R2- |
Gene Symbol and Name | Il10rb, interleukin 10 receptor, beta |
Gene Synonym(s) | |
Strain of Origin | 129S2/SvPas |
Chromosome | 16 |
Molecular Note | The first two exons, encoding 39 amino acids including the signal peptide, were replaced with a neomycin cassette. Northern blot analysis of homozygous mutant ES cells showed an absence of transcript. |
Mutations Made By | Sherman Fong, Genentech, Inc. |
When using the CRFB4- mouse strain in a publication, please cite the originating article(s) and include JAX stock #005027 in your Materials and Methods section.
Service/Product | Description | Price |
---|---|---|
Heterozygous for Il10rb<tm1Agt> |
Frozen Mouse Embryo | B6.129S2-Il10rb<tm1Agt>/J Frozen Embryos | $2595.00 |
Frozen Mouse Embryo | B6.129S2-Il10rb<tm1Agt>/J Frozen Embryos | $2595.00 |
Frozen Mouse Embryo | B6.129S2-Il10rb<tm1Agt>/J Frozen Embryos | $3373.50 |
Frozen Mouse Embryo | B6.129S2-Il10rb<tm1Agt>/J Frozen Embryos | $3373.50 |
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.
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