MGI phenotypes (allele matching)
B6.129P2-Casp3tm1Mak/Cnbc
| Status | Available to order |
| EMMA ID | EM:06370 |
| International strain name | B6.129P2-Casp3tm1Mak/Cnbc |
| Alternative name | Caspase 3 |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Casp3tm1Mak, |
| Gene/Transgene symbol | Casp3 |
Information from provider
| Provider | Tak W Mak |
| Provider affiliation | Mak Lab, Campbell Family Breast Cancer reseach Institute |
| Genetic information | The CPP32 (Casp3) gene was disrupted in ES cells by use of a targeting vector that deleted exon 3 of CPP32 gene, leading to the introduction of termination codons in all three reading frames. |
| Phenotypic information | CPP32ex3 mutant mice were born at lower than the expected Mendelian frequency (9%). Most survived until only 4-5 weeks of age. Consistent with the previously reported CPP32 mutant mice, our CPP32ex3-/- mice were smaller than their littermates, showed neurological abnormalities, and had visible masses in their heads that represent ectopic masses of supernumerary cells in place of pyknotic clusters that represent normal apoptosis that occur during brain development. |
| Breeding history | CPP32ex3 mutant mice were born at lower than the expected Mendelian frequency (9%). Most survived until only 4-5 weeks of age. Currently pure C57BL/6. |
| References |
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| Homozygous fertile | no |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | CNB-CSIC, Centro Nacional de Biotecnologia, Madrid, Spain |
| Animals used for archiving | heterozygous C57BL/6J |
Disease and phenotype information
Literature references
- Essential contribution of caspase 3/CPP32 to apoptosis and its associated nuclear changes.;Woo M, Hakem R, Soengas M S, Duncan G S, Shahinian A, Kägi D, Hakem A, McCurrach M, Khoo W, Kaufman S A, Senaldi G, Howard T, Lowe S W, Mak T W, ;1998;Genes & development;12;806-19; 9512515
- Caspase 3 is not essential for the induction of anergy or multiple pathways of CD8+ T-cell death.;Murakami Kiichi, Liadis Nicole, Sarmiento Janice, Elford Alisha R, Woo Minna, Nguyen Linh T, Mak Tak W, Ohashi Pamela S, ;2010;European journal of immunology;40;3372-7; 21110320