This knockout allele causes severely impaired T helper cell (Th2) immune responses, retinal detachment, as well as abnormal insulin signaling and glucose transport. These mice are suitable for use in applications related to T cell development, Th2-mediated disease, asthma, diabetes, and exudative retinal detachment.Read More +
|Allele Type||Gene Symbol||Gene Name|
|Spontaneous||Crb1||crumbs family member 1, photoreceptor morphogenesis associated|
|Allele Type||Gene Symbol||Gene Name|
|Targeted (Null/Knockout)||Prkcq||protein kinase C, theta|
Mice homozygous for the Prkcqtm1Litt targeted allele are viable, fertile, normal in size, and do not display any behavioral abnormalities. No endogenous or truncated protein product was detected in thymocytes or T cells. Mature T lymphocytes from null mice have blunted proliferative responses with decreased levels of both IL-2 and IL-2 receptor, and defective T cell receptor-initiated IkappaB-degradation/NF-kappaB activation. Homozygous mice exhibit severely impaired Th2, but normal Th1, immune responses as well as abnormal insulin signaling and glucose transport. Mutant mice also have defective regulatory T cell development (very low CD25 expression). Additionally, homozygotes develop retinal detachments and late-onset retinal pigment epithelium atrophy. This strain is also homozygous for the Crb1rd8 mutation, which itself causes retinal spotting and retinal degeneration. Crb1rd8 is also absent from Stock No. 028488. This mutant may be suitable for use in studies related to T cell proliferation/signal transduction/immunodeficiency, Th2-mediated disease, asthma, diabetes, and exudative retinal detachment. No significant difference in ocular phenotype has been detected between mice homozygous for Prkcqtm1Litt and wild-type at Crb1 with those doubly homozygous for both Prkcqtm1Litt and Crb1rd8.
A targeting vector replaced the endogenous exon coding for the ATP-binding site of the kinase domain (amino acids 396-451) with the neomycin resistance gene. The construct was electroporated into the 129P2/OlaHsd-derived E14 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric mice were bred to C57BL/6. Heterozygotes were backcrossed to an undefined C57BL/6 subline for 15 generations before being made homozygous. These mice were imported into The Jackson Laboratory from Dr. Dan Littman and embryos were cryopreserved from homozygous males bred to C57BL/6J females, see stock #005711. An ocular screen of cryo-recovered mice by Dr. Bo Chang identified the retinal detachments and late-onset retinal pigment epithelium atrophy, attributable to Prkcq mutations. It was also discovered that the Crb1rd8 mutation, which is homozygous in C57BL/6N and C57BL/6By sublines but absent from C57BL/6J, was segregating in the cryo-recovered mice. These mice were again backcrossed to C57BL/6J, intercrossed and selected for the presence or absence of Crb1rd8 along with the presence of Prkdctm1Litt, yielding this strain, homozygous for both Crb1rd8 and Prkdctm1Litt and stock #028488, B6.Cg-Crb1+ Prkcqtm1Litt/Boc.
|Allele Name||retinal degeneration 8|
|Allele Synonym(s)||Crb1rd8; retinal degeneration 8|
|Gene Symbol and Name||Crb1, crumbs family member 1, photoreceptor morphogenesis associated|
|Gene Synonym(s)||7530426H14Rik; A930008G09Rik; RIKEN cDNA 7530426H14 gene; RIKEN cDNA A930008G09 gene; LCA8; 7530426H14Rik; RP12; A930008G09Rik|
|Strain of Origin||C57BL/6By or C57BL/6N|
|Molecular Note||The mutation in the rd8 mouse has been identified as a single base deletion at nt3481 in the gene. This deletion causes a frame shift and a premature stop codon that truncates the transmembrane and cytoplasmic domain of the protein after amino acid 1207. This mutation has been found to be present in all sublines of C57BL/6N and in C57BL/6ByJ, but not in any C57BL/6J subline. It occurred sometime between transfer of mice from JAX to NIH, in 1951, and from NIH to Donald Bailey, in 1961.|
|Allele Name||targeted mutation 1, Dan Littman|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||Prkcqtm1Litt; targeted mutation 1, Dan Littman|
|Gene Symbol and Name||Prkcq, protein kinase C, theta|
|Gene Synonym(s)||nPKC-theta; Pkcq; A130035A12Rik; A130035A12Rik; PRKCT; PKC theta; Pkcq; PKCtheta; PKC-0; PKC-theta; RIKEN cDNA A130035A12 gene; AW494342; expressed sequence AW494342|
|Strain of Origin||129P2/OlaHsd|
|Molecular Note||The exon encoding the ATP-binding site of the kinase domain (aa 396 - 451) was replaced with a neo cassette inserted by homologous recombination. Protein was undetected in thymocytes or T cells obtained from mutant mice.|
|Mutations Made By|| |
Dr. Dan Littman, New York University Medical Center
This strain is maintained by sibling intercrossing mice homozygous for both Crb1rd8 and Prkcqtm1Litt.
When using the B6.Cg-Crb1rd8 Prkcqtm1Litt/JBoc mouse strain in a publication, please cite the originating article(s) and include JAX stock #031293 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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