- improved glucose tolerance / IMPC
- decreased circulating fructosamine level / IMPC
- decreased monocyte cell number / IMPC
- decreased KLRG1-positive NK cell number / IMPC
- increased circulating creatinine level / IMPC
- abnormal vibrissa morphology / IMPC
- increased bone mineral content / IMPC
- increased circulating amylase level / IMPC
STOCK Tg(H2-K1-Ifnb1)10Seif Ifnar1tm1Agt/Orl
Status | Available to order |
EMMA ID | EM:07149 |
International strain name | STOCK Tg(H2-K1-Ifnb1)10Seif Ifnar1tm1Agt/Orl |
Alternative name | Ifnar1tm1Agt/Ifnar1tm1Agt Tg(H2-K1-Ifnb1)10Seif/Tg(H2- K1-Ifnb1)10Seif |
Strain type | Targeted Mutant Strains : Knock-out |
Allele/Transgene symbol | Ifnar1tm1Agt, Tg(H2-K1-Ifnb1)10Seif |
Gene/Transgene symbol | Ifnar1, Tg(H2-K1-Ifnb1)10Seif |
Information from provider
Provider | Isabelle Seif |
Provider affiliation | Neuropharmacologie, Faculte de pharmacie (Universite Paris-Sud) |
Genetic information | Random integration of a transgene for IFN beta expressed under the control of a H2-K1 promoter resulted in insertion of the transgene into exon 2 of Prps1l3 and a partial duplication of Prps1l3 and Slc25a21. |
Phenotypic information | Excess type I interferon signaling in the seminiferous tubules of Tg10 mice leads to germ cell loss and sterility. Testicular integrity and normal fertility is maintained in Tg10 mice invalidated for the type I IFN receptor (Tg10-Ifnar1-/-). |
Breeding history | Inbred for 5 generations. |
References |
|
Homozygous fertile | yes |
Homozygous viable | yes |
Homozygous matings required | yes |
Immunocompromised | yes |
Information from EMMA
Archiving centre | Institut de Transgenose, INTRAGENE, Orléans, France |
Animals used for archiving | homozygous C3H/He, homozygous C3H/He |
Breeding at archiving centre | Males: transgenic for Tg(H2-K1-Ifnb1)10Seif and homozygous knock-out for Ifnar1-tm1Agt. Females: transgenic and homozygous knock-out. |
Disease and phenotype information
IMPC phenotypes (gene matching)
MGI phenotypes (allele matching)
- decreased bone mineral density / MGI
- increased tumor growth/size / MGI
- abnormal osteoclast morphology / MGI
- abnormal response to infection / MGI
- impaired natural killer cell mediated cytotoxicity / MGI
- decreased tumor necrosis factor secretion / MGI
- decreased interferon-alpha secretion / MGI
- decreased interferon-beta secretion / MGI
- decreased interleukin-6 secretion / MGI
- increased susceptibility to bacterial infection induced morbidity/mortality / MGI
- abnormal inflammatory response / MGI
- abnormal dendritic cell physiology / MGI
- increased susceptibility to viral infection / MGI
- abnormal immunoglobulin level / MGI
- abnormal cytokine secretion / MGI
- corneal vascularization / MGI
- increased susceptibility to viral infection induced morbidity/mortality / MGI
- abnormal NK cell physiology / MGI
- altered susceptibility to infection / MGI
- immune system phenotype / MGI
- abnormal CD8-positive, alpha-beta T cell physiology / MGI
- abnormal interferon-gamma secretion / MGI
- increased circulating interleukin-12 level / MGI
- abnormal testis morphology / MGI
- seminiferous tubule degeneration / MGI
- reduced male fertility / MGI
- male infertility / MGI
- abnormal spermiogenesis / MGI
- decreased litter size / MGI
- abnormal seminiferous tubule morphology / MGI
- oligozoospermia / MGI
- abnormal male reproductive system physiology / MGI
- decreased testis weight / MGI
- reproductive system phenotype / MGI
- abnormal male germ cell apoptosis / MGI
- early reproductive senescence / MGI
MGI phenotypes (gene matching)
- decreased bone mineral density / MGI
- increased leukocyte cell number / MGI
- altered susceptibility to infection / MGI
- abnormal inflammatory response / MGI
- increased incidence of induced tumors / MGI
- abnormal dendritic cell physiology / MGI
- increased susceptibility to viral infection / MGI
- abnormal macrophage physiology / MGI
- abnormal immunoglobulin level / MGI
- abnormal cytokine secretion / MGI
- no phenotypic analysis / MGI
- increased tumor growth/size / MGI
- abnormal CD8-positive, alpha-beta T cell physiology / MGI
- increased incidence of tumors by chemical induction / MGI
- abnormal osteoclast morphology / MGI
- abnormal response to infection / MGI
- impaired natural killer cell mediated cytotoxicity / MGI
- immune system phenotype / MGI
- corneal vascularization / MGI
- abnormal enzyme/coenzyme activity / MGI
- decreased NK cell number / MGI
- abnormal interferon-gamma secretion / MGI
- decreased tumor necrosis factor secretion / MGI
- decreased interferon-alpha secretion / MGI
- decreased interferon-beta secretion / MGI
- increased circulating interleukin-12 level / MGI
- decreased interleukin-6 secretion / MGI
- increased susceptibility to bacterial infection induced morbidity/mortality / MGI
- increased susceptibility to viral infection induced morbidity/mortality / MGI
- abnormal NK cell physiology / MGI
- abnormal testis morphology / MGI
- seminiferous tubule degeneration / MGI
- reduced male fertility / MGI
- male infertility / MGI
- abnormal spermiogenesis / MGI
- decreased litter size / MGI
- abnormal seminiferous tubule morphology / MGI
- oligozoospermia / MGI
- abnormal male reproductive system physiology / MGI
- decreased testis weight / MGI
- reproductive system phenotype / MGI
- abnormal male germ cell apoptosis / MGI
- early reproductive senescence / MGI
Literature references
- Excess type I interferon signaling in the mouse seminiferous tubules leads to germ cell loss and sterility.;Satie Anne-Pascale, Mazaud-Guittot Severine, Seif Isabelle, Mahé Dominique, He Zhiguo, Jouve Guilhem, Jégou Bernard, Dejucq-Rainsford Nathalie, ;2011;The Journal of biological chemistry;286;23280-95; 21515676
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