IMPC phenotypes (gene matching)
C57BL/6-Cldn12tm1(KOMP)Vlcg/Ph
| Status | Available to order |
| EMMA ID | EM:11196 |
| Citation information | RRID:IMSR_EM:11196 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 | C57BL/6-Cldn12tm1(KOMP)Vlcg/Ph |
| Alternative name | Cldn12 |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Cldn12tm1(KOMP)Vlcg |
| Gene/Transgene symbol | Cldn12 |
Information from provider
| Provider | Rosel Blasig |
| Provider affiliation | Molecular Cellphysiology, Leibniz Institute of Molecular Pharmacology |
| Genetic information | Cldn12 region (1 exon) in Chromosome 5, ES cell clones from KOMP Repository (http://www.velocigene.com/komp/detail/13208). Cassette with lacZ reporter gene and floxed neomycin gene replaced the Cldn12 exon. ES cell clones were injected into albinotic donor embryos with C57BL/6 background resulting in chimeric mice. Male chimeras with germline transmission after breeding with C57BL/6 females were used to create cohorts for observing the impact of Cldn12 deletion. |
| Phenotypic information | Homozygous:Cldn12 deficient mice reach normal age and size, and are fertile. The mice were further analyzed in accordance to guidelines of the International Mouse Phenotyping Consortium and the International Mouse Phenotyping Resource of Standardized Screens covering the main physiological functions. The mutated mice show good general health and normal activity. No macroscopic or microscopic lesions were found. Most of all phenotypic parameters are the same compared to wild-type littermates. In behavioral studies, small differences were indicated with the Cldn12 mutants in a few tests. Single alterations in the leukocyte fraction may occur in Cldn12 deficient mice not detectable in control mice. Cardiovascular analyses suggest myocardial disturbances and electrophysiological impairment due to the Cldn12 knock-out. In conclusion, the phenotype of Cldn12-deficient mice is characterised by extenuated neurotransmission and a slight inflammatory syndrome.Heterozygous:Heterozygous mice were not analysed in detail, but reach also normal age and size, and are fertile. |
| Breeding history | Always backcrossing with C57BL/6 females. |
| References | None available |
| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Institute of Molecular Genetics, Prague, Czech Republic |
| Animals used for archiving | heterozygous C57BL/6 males |