IMPC phenotypes (gene matching)
129(C)-Eif2ak2tm1Jcbe/Cnbc
| Status | Available to order |
| EMMA ID | EM:09405 |
| Citation information | RRID:IMSR_EM:09405 Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information. |
| 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) males, homozygous 129/Sv (synonym: 129Sv) females |
| 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