| 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 |
| 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 |
| 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 |
Orphanet associated rare diseases, based on orthologous gene matching
