IMPC phenotypes (gene matching)
129(C)-Eif2ak2tm1Jcbe/Cnbc
| Status | Available to order |
| EMMA ID | EM:09405 |
| International strain name | 129(C)-Eif2ak2tm1Jcbe/Cnbc |
| Alternative name | Eif2ak2_PKR-deficient |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Eif2ak2tm1Jcbe |
| Gene/Transgene symbol | Eif2ak2 |
Information from provider
| Provider | Juanjo Berlanga |
| Provider affiliation | Genome Dynamics and Function, Centro de Biología Molecular Severo Ochoa (CSIC-UAM) |
| Additional owner | Dr. John S. Bell, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada |
| Genetic information | Pkr (Eif2ak2, alpha subunit of eukaryotic initiation factor 2 kinase-eIF2 alpha kinase) mutant allele, with target disruption of the catalytic domain (exon 12, encoding subdomains V and VI) of the double-stranded RNA-dependent protein kinase, PKR. |
| Phenotypic information | Homozygous:Mice homozygous for Pkr disruption (Pkr 0/0) develop normally and are fertile with average-sized litters. Interferon-alpha and -beta induction of transcription is intact, and the mice show normal hematopoiesis. Pkr 0/0 mice show responses to vaccinia and influenza infection comparable to control animals or cells. Catalytic disruption of Pkr is not sufficient to ablate eIF-2alpha phosphorylation.Heterozygous:Mice heterozygous for Pkr disruption (Pkr P/0) develop normally and are fertile with average sized litters. Interferon-alpha and -beta induction of transcription is intact, and the mice show normal hematopoiesis. Pkr 0/0 mice show responses to vaccinia and influenza infection comparable to control animals or cells. Catalytic disruption of Pkr is not sufficient to ablate eIF-2alpha phosphorylation. |
| References |
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| Homozygous fertile | yes |
| 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 | homozygous 129/Sv (synonym: 129Sv), homozygous 129/Sv (synonym: 129Sv) |
| Stage of embryos | 2-cell |
Disease and phenotype information
Orphanet associated rare diseases, based on orthologous gene matching
- Early-onset generalized limb-onset dystonia / Orphanet_256
MGI phenotypes (allele matching)
- neoplasm / MGI
- cellular phenotype / MGI
- immune system phenotype / MGI
- decreased erythroid progenitor cell number / MGI
- increased susceptibility to viral infection / MGI
- increased sensitivity to induced cell death / MGI
- decreased sensitivity to induced cell death / MGI
- increased sensitivity to induced morbidity/mortality / MGI
MGI phenotypes (gene matching)
- neoplasm / MGI
- increased susceptibility to viral infection / MGI
- increased T cell proliferation / MGI
- cellular phenotype / MGI
- immune system phenotype / MGI
- increased susceptibility to type IV hypersensitivity reaction / MGI
- abnormal cell physiology / MGI
- increased interleukin-4 secretion / MGI
- increased sensitivity to induced cell death / MGI
- decreased sensitivity to induced cell death / MGI
- decreased erythroid progenitor cell number / MGI
- increased sensitivity to induced morbidity/mortality / MGI
Literature references
- Characterization of transgenic mice with targeted disruption of the catalytic domain of the double-stranded RNA-dependent protein kinase, PKR.;Abraham N, Stojdl D F, Duncan P I, Méthot N, Ishii T, Dubé M, Vanderhyden B C, Atkins H L, Gray D A, McBurney M W, Koromilas A E, Brown E G, Sonenberg N, Bell J C, ;1999;The Journal of biological chemistry;274;5953-62; 10026221