IMPC phenotypes (gene matching)
B6J;129-Tniktm1.1grnt/WtsiH
| Status | Available to order |
| EMMA ID | EM:15866 |
| Citation information | RRID:IMSR_EM:15866 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 | B6J;129-Tniktm1.1grnt/WtsiH |
| Alternative name | B6J;129-Tnik |
| Strain type | Targeted Mutant Strains : Knock-in |
| Allele/Transgene symbol | TnikTM1.1Grnt |
| Gene/Transgene symbol | Tnik |
Information from provider
| Provider | Seth Grant |
| Provider affiliation | Wellcome Trust Sanger Institute |
| Genetic information | Information sourced from PMID: 23035106: Traf2 and NcK interacting kinase (TNiK) contains serine-threonine kinase and scaffold domains and has been implicated in cell proliferation and glutamate receptor regulation in vitro. This strain carries a TNiK knockout. |
| Phenotypic information | Mice showed a marked impairment in neurogenesis of dentate gyrus granule cells and exhibit deficits in pattern separation and were significantly impaired in learning the association of an object and its location. Mice displayed enhanced phosphorylation of NeuroD1 S274, which would be expected to contribute to the observed reduction in neurogenesis and number of dentate gyrus neurons. . NeuroD1-positive cells were decreased in the dentate gyrus of homozygous mice and this decrease in precursor/progenitor cells was paralleled with a decrease in the number of newly born neurons and total number of dentate gyrus granule cells. |
| Breeding history | Crossed TnikTAP-TNiK (GIA) and CAG-Cre (GFZ). Maintained as Het x JAXJ (C57BL/6J). Hom viability and fertilty unknown. Maintained on a mixed background: C57BL/6J 129P2/OlaHsdWtsi 129S5/SvEvBrdWtsi |
| References |
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| Homozygous fertile | not known |
| Homozygous viable | yes |
| Homozygous matings required | not known |
| Immunocompromised | not known |
Information from EMMA
| Archiving centre | Mary Lyon Centre at MRC Harwell, Oxford, United Kingdom |
Disease and phenotype information
Orphanet associated rare diseases, based on orthologous gene matching
- Autosomal recessive non-syndromic intellectual disability / Orphanet_88616
MGI phenotypes (gene matching)
- decreased circulating HDL cholesterol level / MGI
- decreased body weight / MGI
- hyperactivity / MGI
- abnormal object recognition memory / MGI
- no abnormal phenotype detected / MGI
- abnormal discrimination learning / MGI
- abnormal excitatory postsynaptic potential / MGI
- enhanced paired-pulse facilitation / MGI
- nervous system phenotype / MGI
- decreased incidence of tumors by chemical induction / MGI
- abnormal miniature excitatory postsynaptic currents / MGI
- decreased circulating cholesterol level / MGI
- immune system phenotype / MGI
- decreased circulating glucose level / MGI
- decreased cerebellar granule cell number / MGI
- abnormal neuron differentiation / MGI
Literature references
- TNiK is required for postsynaptic and nuclear signaling pathways and cognitive function.;Coba Marcelo P, Komiyama Noboru H, Nithianantharajah Jess, Kopanitsa Maksym V, Indersmitten Tim, Skene Nathan G, Tuck Ellie J, Fricker David G, Elsegood Kathryn A, Stanford Lianne E, Afinowi Nurudeen O, Saksida Lisa M, Bussey Timothy J, O'Dell Thomas J, Grant Seth G N, ;2012;The Journal of neuroscience : the official journal of the Society for Neuroscience;32;13987-99; 23035106