- abnormal immune system physiology / MGI
- decreased inflammatory response / MGI
- abnormal dendritic cell physiology / MGI
- increased susceptibility to viral infection / MGI
- abnormal macrophage physiology / MGI
- abnormal B cell physiology / MGI
- abnormal cytokine secretion / MGI
- abnormal leukocyte migration / MGI
- decreased susceptibility to experimental autoimmune encephalomyelitis / MGI
- abnormal response to infection / MGI
- decreased susceptibility to parasitic infection / MGI
- impaired natural killer cell mediated cytotoxicity / MGI
- decreased B cell proliferation / MGI
- immune system phenotype / MGI
- abnormal T-helper 1 physiology / MGI
- abnormal NK T cell physiology / MGI
- increased susceptibility to induced colitis / MGI
- decreased tumor necrosis factor secretion / MGI
- decreased interferon-alpha secretion / MGI
- decreased interferon-beta secretion / MGI
- decreased interferon-gamma secretion / MGI
- decreased interleukin-12b secretion / MGI
- abnormal plasmacytoid dendritic cell physiology / MGI
- abnormal NK cell physiology / MGI
C57BL/6N-Tlr9tm1.2Arte/Ieg
Status | Available to order |
EMMA ID | EM:05496 |
Citation information | RRID:IMSR_EM:05496 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/6N-Tlr9tm1.2Arte/Ieg |
Alternative name | Tlr9 KO conv |
Strain type | Targeted Mutant Strains : Knock-out |
Allele/Transgene symbol | Tlr9tm1.2 |
Gene/Transgene symbol | Tlr9 |
Information from provider
Provider | Helmholtz Zentrum Muenchen |
Provider affiliation | Institute of Experimental Genetics, Helmholtz Zentrum Muenchen German Research Center for Environmental Health (GmbH) |
Genetic information | Exon 2 has been flanked by loxP sites, as its genetic ablation should result in loss of function by deletion of most of the open reading frame (see EMMA strain EM:05497). The constitutive knock-out mutation has been obtained by in vivo cre recombinase-mediated deletion. |
Phenotypic information | TO BE PROVIDED |
Breeding history | Targeting performed in C57BL/6N ES cells and confirmed by Southern blotting. Tlr9 floxed mice were crossed to C57BL/6N cre-deleter mice to obtain the Tlr9 null allele. Maintained on C57BL/6N background. |
References | None available |
Homozygous fertile | not known |
Homozygous viable | not known |
Homozygous matings required | not known |
Immunocompromised | not known |
Information from EMMA
Archiving centre | Helmholtz Zentrum Muenchen - German Research Center for Environmental Health (GmbH), Oberschleißheim, Germany |
Animals used for archiving | heterozygous C57BL/6NTac males, wild-type C57BL/6N females |
Stage of embryos | 2-cell |
Disease and phenotype information
MGI phenotypes (gene matching)
Information on how we integrate external resources can be found here
INFRAFRONTIER® and European Mouse Mutant Archive - EMMA® are registered trademarks at the European Union Intellectual Property Office (EUIPO).