IMPC phenotypes (gene matching)
B6NCrl.129P2(Cg)-Tyk2tm3.1Biat/Biat
| Status | Available to order |
| EMMA ID | EM:09905 |
| Citation information | RRID:IMSR_EM:09905 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 | B6NCrl.129P2(Cg)-Tyk2tm3.1Biat/Biat |
| Alternative name | B6NCrl.129P2(C)-Tyk2 |
| Strain type | Targeted Mutant Strains : Point mutation |
| Allele/Transgene symbol | Tyk2tm3.1Biat |
| Gene/Transgene symbol | Tyk2 |
Information from provider
| Provider | Mathias Müller |
| Provider affiliation | Department for Biomedical Sciences, University of Veterinary Medicine Vienna (Vetmeduni Vienna) |
| Additional owner | Prof. Thomas Rülicke, University of Veterinary Medicine, Institute of Laboratory Animal Science, Vienna, Austria |
| Genetic information | Exon 20 was replaced with a modified one in which nucleotide substitutions (AAG GCC CTG to GAG GCC CTT) results in the amino acid substitution of glutamic acid for lysine at position 923 (K923E) and introduced a BspTI restriction enzyme site. A floxed neo cassette inserted downstream of exon 21 was removed by cre-mediated recombination. In vitro kinase activity confirmed the absence of activity. (PubMed ID:22723949) |
| Phenotypic information | Homozygous:immune defectsHeterozygous:none |
| References |
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| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | yes |
Information from EMMA
| Archiving centre | University of Veterinary Medicine, Vienna, Austria |
Disease and phenotype information
MGI phenotypes (allele matching)
- increased susceptibility to viral infection induced morbidity/mortality / MGI
MGI phenotypes (gene matching)
- increased body weight / MGI
- obese / MGI
- increased circulating free fatty acid level / MGI
- abnormal body temperature homeostasis / MGI
- decreased IgG level / MGI
- increased circulating insulin level / MGI
- abnormal T cell differentiation / MGI
- increased susceptibility to viral infection / MGI
- abnormal T cell physiology / MGI
- abnormal brown adipose tissue morphology / MGI
- abnormal cell cycle / MGI
- decreased susceptibility to induced arthritis / MGI
- abnormal nitric oxide homeostasis / MGI
- increased cholesterol level / MGI
- decreased energy expenditure / MGI
- abnormal response to infection / MGI
- increased susceptibility to parasitic infection / MGI
- impaired glucose tolerance / MGI
- abnormal T-helper 1 physiology / MGI
- abnormal mitochondrial physiology / MGI
- abnormal common myeloid progenitor cell morphology / MGI
- decreased IgG1 level / MGI
- decreased IgG2a level / MGI
- decreased interferon-gamma secretion / MGI
- increased circulating interleukin-12 level / MGI
- abnormal splenocyte physiology / MGI
- increased susceptibility to viral infection induced morbidity/mortality / MGI
- impaired adaptive thermogenesis / MGI
- decreased macrophage nitric oxide production / MGI
- abnormal fat cell differentiation / MGI
- disorganized mitochondrial cristae / MGI
Literature references
- TYK2 kinase activity is required for functional type I interferon responses in vivo.;Prchal-Murphy Michaela, Semper Christian, Lassnig Caroline, Wallner Barbara, Gausterer Christian, Teppner-Klymiuk Ingeborg, Kobolak Julianna, Müller Simone, Kolbe Thomas, Karaghiosoff Marina, Dinnyés Andras, Rülicke Thomas, Leitner Nicole R, Strobl Birgit, Müller Mathias, ;2012;PloS one;7;e39141; 22723949