IMPC phenotypes (gene matching)
BALB/c-Cd1d1em1Kblg/Orl
| Status | Available to order |
| EMMA ID | EM:15248 |
| Citation information | RRID:IMSR_EM:15248 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 | BALB/c-Cd1d1em1Kblg/Orl |
| Alternative name | BALB/C CD1d1 KO |
| Strain type | Endonuclease-mediated |
| Allele/Transgene symbol | Cd1d1em1Kblg |
| Gene/Transgene symbol | Cd1d1 |
Information from provider
| Provider | Kamel Benlagha |
| Provider affiliation | Immunology, IRSL-Inserm U1160 |
| Genetic information | Mutation in exon 1 of the Cd1d1 gene: additional T in position 17, starting ATG, which induced a downstream STOP codon producing a truncated 19-aa protein. CRISPR technology details: Cas9 mRNA and sgRNAs targeting exon1 were mixed and electroporated (NEPA21) into the pronuclei of the one-cell embryos. SgRNA1 5′- CCCACAGCAACAGCCATGGT-3′ and SgRNA3 5′-CCTACCATGGCTG TTGCTGT-3′ |
| Phenotypic information | Homozygous:Mice deficient in innate natural killer T (NKT) cell subsets.Heterozygous:Altered distribution of NKT cell subsets. |
| Breeding history | Mutation generated by CRISPR/Cas9 on BALB/c background. Maintained by breeding of homozygous mice. |
| References |
|
| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | CNRS-TAAM – Typing and Archiving of Animal Models, Orléans, France |
| Animals used for archiving | heterozygous BALB/c males |
Disease and phenotype information
MGI phenotypes (gene matching)
- abnormal liver morphology / MGI
- decreased IgG level / MGI
- arrested T cell differentiation / MGI
- abnormal T cell activation / MGI
- abnormal antigen presentation / MGI
- autoimmune response / MGI
- kidney inflammation / MGI
- lung inflammation / MGI
- increased susceptibility to bacterial infection / MGI
- abnormal dendritic cell antigen presentation / MGI
- glomerulonephritis / MGI
- increased urine protein level / MGI
- increased susceptibility to ischemic brain injury / MGI
- renal interstitial fibrosis / MGI
- decreased susceptibility to induced arthritis / MGI
- increased anti-double stranded DNA antibody level / MGI
- increased anti-nuclear antigen antibody level / MGI
- decreased regulatory T cell number / MGI
- decreased acute inflammation / MGI
- glomerulosclerosis / MGI
- increased blood urea nitrogen level / MGI
- abnormal NK T cell morphology / MGI
- decreased NK T cell number / MGI
- abnormal NK T cell physiology / MGI
- abnormal CD4-positive T cell differentiation / MGI
- increased IgG3 level / MGI
- decreased tumor necrosis factor secretion / MGI
- decreased interferon-gamma secretion / MGI
- decreased interleukin-2 secretion / MGI
- abnormal interleukin-4 secretion / MGI
- decreased interleukin-4 secretion / MGI
- decreased physiological sensitivity to xenobiotic / MGI
- increased susceptibility to bacterial infection induced morbidity/mortality / MGI
- renal tubule atrophy / MGI
- glomerular crescent / MGI
Literature references
- Intrinsic factors and CD1d1 but not CD1d2 expression levels control invariant natural killer T cell subset differentiation.;Amable Ludivine, Ferreira Martins Luis Antonio, Pierre Remi, Do Cruseiro Marcio, Chabab Ghita, Sergé Arnauld, Kergaravat Camille, Delord Marc, Viret Christophe, Jaubert Jean, Liu Chaohong, Karray Saoussen, Marie Julien C, Irla Magali, Georgiev Hristo, Clave Emmanuel, Toubert Antoine, Lucas Bruno, Klibi Jihene, Benlagha Kamel, ;2023;Nature communications;14;7922; 38040679