DR3-/- KO Mouse

The DR3-/- mouse exhibits complete knockout of DR3, a death domain-containing tumour necrosis factor receptor. which mediates one of the key regulators of the cell division cycle.

Contributors

Inventor Institute
Eddie Wang ; Mike Owen Cancer Research UK, London Research Institute: Lincoln's Inn Fields
Cat. #: 151474
Research Fields: Apoptosis and autophagy;Cancer;Cell biology;Cell signaling and signal transduction;Genetics;Immunology
Target: DR3 (Death Domain Receptor 3)
disease: Progressive neurological disease
Model: Knock-Out
Zygosity: Homozygous
Phenotype: Immune abnormalities (T cell development);
Primary citation: Wang et al. 2001. Mol Cell Biol. 21(10):3451-61. PMID: 11313471
Product description: The DR3-/- mouse exhibits complete knockout of DR3, a death domain-containing tumour necrosis factor receptor, which mediates one of the key regulators of the cell division cycle. Negative selection and anti-CD3-induced apoptosis are significantly impaired in DR3-null mice. In contrast, both superantigen-induced negative selection and positive selection are normal. The pre-T-cell receptor-mediated checkpoint, which is dependent on TNFR signaling, is also unaffected in DR3-deficient mice. These data reveal a nonredundant in vivo role for this TNF receptor family member in the removal of self-reactive T cells in the thymus. Other behavioral studies on DR3 KO mice indicated that DR3 plays a key nonredundant role in the retention of normal motor control function during aging in mice and implicate DR3 in progressive neurological disease
Conditional: No
Genetic background: A DR3 targeting vector, replacing the entire DR3 coding region with a loxP flanked resistance cassette, was transfected into GK129 ES cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. Chimeric offspring were bred with C57BL/6 mice to yield mice heterozygous for the mutant allele.
Production details: A DR3 targeting vector, replacing the entire DR3 coding region with a loxP flanked resistance cassette, was transfected into GK129 ES cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. Chimeric offspring were bred with C57BL/6 mice to yield mice heterozygous for the mutant allele.
Shipping conditions: Dry Ice
References:

Twohig et al. 2010. J Neurosci. 30(10):3782-92. PMID: 20220013

Wang et al. 2001. Mol Cell Biol. 21(10):3451-61. PMID: 11313471

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