Overview

Also Known As:IFN-αβR-

Mice homozygous for this Ifnar1 knock-out mutation are more susceptible to viral infection, have an abnormal NK antitumor response, and reduced bone mass. This mutant mouse strain may be useful in studies of immunological responses to infection, and bone homeostasis. Mouse mutants involving this gene have been used in studies of Zika virus pathogenesis. Note: these mice carry the same allele as 'A129' mice, although on a congenic C57BL/6, not 129, genetic background.

Donating Investigator

Dr. Michel Aguet, EPFL, Ecole polytechnique fédérale de Lausanne

Genetic overview

Genetic Background	Generation
	N6+N2 (2021-07-22 00:00:00)

Ifnar1^tm1Agt

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Ifnar1	interferon (alpha and beta) receptor 1

View Genetics

Research Applications

Immunology, Inflammation and Autoimmunity Research
Research Tools
Cancer Research
Cell Biology Research
Endocrine Deficiency Research

View All Research Applications

Details

Detailed Description

Mice that are homozygous for the targeted mutation are viable, fertile, and normal in size. No gene product (mRNA) is detected by Northern blot analysis of homozygous primary embryonic fibroblasts. Mice that are homozygous for this targeted allele lack type I IFN receptor function, exhibit enhanced osteoclastogenesis with decreased bone density, and impaired response to protozoan parasite (Leishmania) infection. NK cell mediated tumor regression does not occur in homozygotes in response to B16 melanoma tumor implant model. Mouse mutants involving this gene have been used in studies of Zika virus pathogenesis.

Development

A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt exon 3. The construct was electroporated into 129S2/SvPas derived D3 embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient blastocysts. The mice were backcrossed to C57Bl/6 for at least 5 generations, as reported by the donating investigator.

Control Suggestions

000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Muller U; Steinhoff U; Reis LF; Hemmi S; Pavlovic J; Zinkernagel RM; Aguet M. 1994. Functional role of type I and type II interferons in antiviral defense. Science 264(5167):1918-21PubMed: 8009221 MGI: J:36115

View All References

Genetics

Ifnar1^tm1Agt

Allele Symbol: Ifnar1^tm1Agt

Allele Name	targeted mutation 1, Michel Aguet
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	A 129; A^-; A129; IFN Alpha Ro/o; IFN type I receptor; IFN-alpha/betaR-; IFN-alpha/betaR/A129; IFN-alpha/betaR⁰; IFN-alphabetaR-; IFN-alphabeta-R KO; IFNAR(0); IFNAR^-; Ifnar1-; IFN-IR KO; IFN-IR^-; IFNR^-; IFNRA1,-.; IFNRI -; IFNRI KO
Gene Symbol and Name	Ifnar1, interferon (alpha and beta) receptor 1
Gene Synonym(s)
Strain of Origin	129S2/SvPas
Chromosome	16
Molecular Note	A neomycin cassette was inserted into exon 3 at a position corresponding to amino acid 88.
Mutations Made By	Dr. Michel Aguet, EPFL, Ecole polytechnique fédérale de Lausanne

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Immunology, Inflammation and Autoimmunity Research
- Intracellular Signaling Molecules
- Immunodeficiency
  - NK Cell Deficiency
- CD Antigens, Antigen Receptors, and Histocompatibility Markers
  - genes regulating susceptibility to infectious disease and endotoxin
- Growth Factors/Receptors/Cytokines
Research Tools
- Infectious Disease
- Immunology, Inflammation and Autoimmunity Research
  - genes regulating susceptibility to infectious disease and endotoxin
  - NK Cell Deficiency
- Cancer Research
  - tumor immunology
Cancer Research
- Growth Factors/Receptors/Cytokines
Cell Biology Research
- Signal Transduction
Endocrine Deficiency Research
- Bone/Bone Marrow Defects

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Ifnar1^tm1Agt/Ifnar1^tm1Agt
involves: 129S2/SvPas

behavior/neurological phenotype

abnormal gait
- mice inoculated intracerebrally with MV-Edm show initial hyperactivity followed by awkward gait and lack of mobility

induced hyperactivity
- mice inoculated intracerebrally with MV-Edm show initial hyperactivity following infection

lethargy
- mice inoculated intracerebrally with MV-Edm show initial hyperactivity that is followed by awkward gait and lethargy

homeostasis/metabolism phenotype

increased circulating alanine transaminase level
- MHV-infected mice show rapidly rising liver enzyme values in serum

immune system phenotype

increased susceptibility to viral infection
- plasmacytoid dendritic cells (pDCs) are more susceptible to MHV infection than wild-type pDCs
- mice infected with HSV-2 strain 186 exhibit more severe clinical scores of disease (genital lesions, redness and swelling) compared with wild-type mice
- increased susceptibility of encephalomyocarditis virus induced lethality
- elevated virus titers in all organs tested after primary infection but much improved after secondary infections
- increased susceptibility to Ectromelia virus
- 100% mortality by day 6-12 after primary infection infection
- survive secondary infections
- mice show increased susceptibility to infection with murine hepatitis virus (MHV) A59 (a coronavirus), showing increased viral titers and developing a rapidly lethal acute hemorrhagic liver disease
- mice are 100-fold more susceptible to MCMV viral infection than controls

increased susceptibility to Paramyxoviridae infection induced morbidity/mortality
- 50% of mice inoculated with the rodent brain-adapted neurotrophic measles virus strain CAM/RBH succumb 5-11 days post infection
- 8 of 18 mice inoculated intracerebrally with the attenuated Edmonston measles virus (MV-Edm) die between days 4 and 7 post infection

increased susceptibility to Paramyxoviridae infection
- susceptibility to MV-Edm infection is more pronounced if less virus is inoculated
- mice inoculated intranasally with the attenuated Edmonston measles virus (MV-Edm) show macroscopic purple lesion areas in the lungs
- 8 of 18 mice inoculated intracerebrally with MV-Edm die between days 4 and 7 post infection and show signs of neurological disease including initial hyperactivity followed by awkward gait, lethargy, lack of mobility, and death

increased susceptibility to Coronaviridae infection
- plasmacytoid dendritic cells (pDCs) are more susceptible to MHV infection than wild-type pDCs
- mice show increased susceptibility to infection with murine hepatitis virus (MHV) A59 (a coronavirus) , showing increased viral titers and developing a rapidly lethal acute hemorrhagic liver disease

impaired natural killer cell mediated cytotoxicity
- NK cells from MCMV-infected mice have 10-fold less cytotoxicity than wild-type NK cells

abnormal cytokine secretion
- upon viral infection, interferon alpha induction is normal initially, but in later phases does not reach wild-type levels

increased susceptibility to Poxviridae infection
- elevated virus titers in all organs tested after primary infection but much improved after secondary infections
- increased susceptibility to Ectromelia virus
- survive secondary infections
- 100% mortality by day 6-12 after primary infection infection

increased susceptibility to Herpesvirales infection
- mice are 100-fold more susceptible to murine cytomegalovirus, Smith strain (MCMV) viral infection than controls
- mice infected with herpes simplex type 2 (HSV-2) strain 186 exhibit more severe clinical scores of disease (genital lesions, redness and swelling) compared with wild-type mice

abnormal NK cell physiology
- there is 50% less actively proliferating NK cells in the spleen after MCMV infection compared to controls
- NK cells in vivo make much about a fifth less IFN-gamma in response to injections of the TLR9 agonist CpG

abnormal dendritic cell physiology
- in mutant dendritic cells, induction of MHC and costimulatory molecules does not occur in response poly(I:C), in contrast to wild-type cells; LPS or CpG-dependent induction of MHC I and costimulatory molecules is also suppressed
- ulated cells
- induction of MHC and costimulatory molecules is abolished in dendritic cells upon infection with Newcastle disease virus (NDC)
- Ifn beta stimulation of dendritic cells elicits a significantly lower response in mutant cells than in wild-type
- stimulatory activity of CD4+ and CD8+ T cells by poly(I:C) is impaired in poly(I:C)-stimulated mutant dendritic cells; stimulatory activity of CD8+ T cells is impaired in the LPS- or CpG-stimulated dendritic cells to a lesser extent than in poly(I:C)-stimulated cells
- maturation of dendritic cells is impaired when stimulated by poly(I:C), LPS or NDV, but migration in T cell zone of spleen is not affected
- amplification of dendritic signaling is suppressed in mutant dendritic cells stimulated with poly(I:C); RelA activation is suppressed

increased susceptibility to viral infection induced morbidity/mortality
- MCMV-treated mice exhibit a 800-fold lower LD50 compared with similarly treated wild-type mice
- mice infected with 5 pfu MHV die within 48 hours while wild-type mice survive

abnormal inflammatory response
- MHC I induction is severely impaired in response to all three stimuli
- in mutant dendritic cells, induction of MHC and costimulatory molecules does not occur in response poly(I:C), in contrast to wild-type cells; LPS or CpG-dependent induction of MHC I and costimulatory molecules is also suppressed

increased susceptibility to Picornaviridae infection
- increased susceptibility of encephalomyocarditis virus induced lethality

increased susceptibility to Herpesvirales infection induced morbidity/mortality
- MCMV-treated mice exhibit a 800-fold lower LD50 compared with similarly treated wild-type mice

increased susceptibility to Coronaviridae infection induced morbidity/mortality
- mice infected with 5 pfu MHV die within 48 hours while wild-type mice survive

abnormal immunoglobulin level
- levels of IgG1a, IgG2a and IgG2b neutralizing antibodies are reduced relative to controls after secondary infection with Ectromelia virus

cardiovascular system phenotype

liver hemorrhage
- MHV-infected mice develop an acute hemorrhagic liver disease with massive hepatocyte necrosis

corneal vascularization
- corneal injection of a plasmid encoding short hairpin RNA targeting the C terminus of the secreted form of Flt1 (pshRNA-sflt1) induces corneal vascularization within 3 days of injection in wild-type and mutant mice

liver/biliary system phenotype

liver hemorrhage
- MHV-infected mice develop an acute hemorrhagic liver disease with massive hepatocyte necrosis

mammalian phenotype

immune system phenotype
- Normal - mice infected with the Urbani strain of severe acute respiratory syndrome coronavirus (SARS-CoV) or a recombinant isogenic mouse-adapted SARS-CoV (rMA15) that contains six virulence modifying mutations show no increase in susceptibility, pathogenesis, or histological outcomes to infection compared to wild-type controls

mortality/aging

increased susceptibility to Paramyxoviridae infection induced morbidity/mortality
- 50% of mice inoculated with the rodent brain-adapted neurotrophic measles virus strain CAM/RBH succumb 5-11 days post infection
- 8 of 18 mice inoculated intracerebrally with the attenuated Edmonston measles virus (MV-Edm) die between days 4 and 7 post infection

increased susceptibility to Coronaviridae infection induced morbidity/mortality
- mice infected with 5 pfu MHV die within 48 hours while wild-type mice survive

increased susceptibility to viral infection induced morbidity/mortality
- MCMV-treated mice exhibit a 800-fold lower LD50 compared with similarly treated wild-type mice
- mice infected with 5 pfu MHV die within 48 hours while wild-type mice survive

increased susceptibility to Herpesvirales infection induced morbidity/mortality
- MCMV-treated mice exhibit a 800-fold lower LD50 compared with similarly treated wild-type mice

vision/eye phenotype

corneal vascularization
- corneal injection of a plasmid encoding short hairpin RNA targeting the C terminus of the secreted form of Flt1 (pshRNA-sflt1) induces corneal vascularization within 3 days of injection in wild-type and mutant mice

hematopoietic system phenotype

abnormal NK cell physiology
- there is 50% less actively proliferating NK cells in the spleen after MCMV infection compared to controls
- NK cells in vivo make much about a fifth less IFN-gamma in response to injections of the TLR9 agonist CpG

abnormal immunoglobulin level
- levels of IgG1a, IgG2a and IgG2b neutralizing antibodies are reduced relative to controls after secondary infection with Ectromelia virus

impaired natural killer cell mediated cytotoxicity
- NK cells from MCMV-infected mice have 10-fold less cytotoxicity than wild-type NK cells

Genotype: Ifnar1^tm1Agt/Ifnar1^tm1Agt
involves: 129S2/SvPas * 129S6/SvEvTac

hematopoietic system phenotype

abnormal CD8-positive, alpha-beta T cell physiology
- the antigen specificity of CD8 T cells to common LCMV-derived peptides differs from controls with a higher percentage being specific for the GP33-41 peptide

immune system phenotype

increased susceptibility to viral infection
- mice took much longer to clear virus, around 28 days, compared to 7 days for wild-type mice
- mice have a 2-log higher viral titer in the spleen, and a 4-log higher viral titer in the liver, 4.5 days after infection with LCMV virus

abnormal interferon-gamma secretion
- splenic leukocyte production of IFN-gamma is increased 3-fold 8 days after infection with LCMV compared to controls
- these T cells produce less IFN-gamma on a per cell basis
- two-thirds of this IFN-gamma production is dependent on CD8 T cells

abnormal CD8-positive, alpha-beta T cell physiology
- the antigen specificity of CD8 T cells to common LCMV-derived peptides differs from controls with a higher percentage being specific for the GP33-41 peptide

increased circulating interleukin-12 level
- 3-4 pg/ml of IL-12 heterodimer are present in the serum 1.5- and 3- days after infection with LCMV while no IL-12 is detected at this timepoint in wild-type mice

increased susceptibility to Riboviria infection
- mice took much longer to clear virus, around 28 days, compared to 7 days for wild-type mice
- mice have a 2-log higher viral titer in the spleen, and a 4-log higher viral titer in the liver, 4.5 days after infection with LCMV virus

homeostasis/metabolism phenotype

increased circulating interleukin-12 level
- 3-4 pg/ml of IL-12 heterodimer are present in the serum 1.5- and 3- days after infection with LCMV while no IL-12 is detected at this timepoint in wild-type mice

Genotype: Ifnar1^tm1Agt/Ifnar1^tm1Agt
involves: 129S2/SvPas * C57BL/6

immune system phenotype

abnormal susceptibility to infection
- infection with lvPR8 produces low titers of 5x10⁴
- infection with hvPR8 produces high titers of 5x10⁷

mammalian phenotype

immune system phenotype
- Normal - mice do not develop chronic polyarthritis

Genotype: Ifnar1^tm1Agt/Ifnar1^tm1Agt
involves: 129S2/SvPas * BALB/c

cellular phenotype

decreased T cell apoptosis
- SARS-CoV-MA15-infected mice show lower levels of CD8 and CD4 T cell apoptos

immune system phenotype

increased CD8-positive, alpha-beta T cell number
- SARS-CoV-MA15-infected mice show increased numbers of virus-specific CD8 T cells in lungs

increased CD4-positive, alpha beta T cell number
- SARS-CoV-MA15-infected mice show increased numbers of virus-specific CD4 T cells in lungs

decreased susceptibility to Coronaviridae infection
- SARS-CoV-MA15 virus is completely cleared from the lungs by 10 dpi
- middle-aged (8-9 month old) mice show increased survival after SARS-CoV-MA15 infection compared to middle-aged BALB/c control mice
- mice infected with a lethal dose of the mouse adapted severe acute respiratory syndrome coronavirus (SARS-CoV-MA15) survive the infection, exhibiting only a moderate 15% weight loss and mild to moderate clinical disease
- SARS-CoV-MA15-infected mice show nearly normal lungs at 3 and 5 dpi compared to hyperemia and congestion in controls, with minimal alveolar edema and increased peribronchial-perivascular immune cell infiltration, and reduced lung microvascular leakage
- total lung virus loads after SARS-CoV-MA15 infection are the same as in control mice, except for a modest increase at 3 days post infection (dpi) in mutants

abnormal cytokine level
- SARS-CoV-MA15- infected mice have reduced levels of cytokines and chemokines in the broncho-alveolar lavage fluid

abnormal mononuclear phagocyte morphology
- SARS-CoV-MA15-infected mice show a decrease in the percentage and numbers of inflammatory monocyte-macrophages that produce the pro-inflammatory cytokines TNF, IL-6, IL1-beta, and iNOS
- SARS-CoV-MA15-infected mice do show an increase in highly activated inflammatory monocyte-macrophages as is seen in infected BALB/c controls

increased susceptibility to Coronaviridae infection induced morbidity/mortality
- all mice infected with murine hepatitis virus strain 1 (MHV-1) succumb to a sub-lethal dose compared to only about 10% of control BALB/c mice

decreased Ly6C high monocyte number
- SARS-CoV-MA15-infected mice do not show an increase in Ly6C^hiCD11b⁺ cells in the lungs as is seen in controls

increased susceptibility to Orthomyxoviridae infection induced morbidity/mortality
- mice infected with the mouse-adapted H1N1 influenza A virus, PR8 strain, succumb to a sub-lethal dose compared to only about 20% of control BALB/c mice

decreased T cell apoptosis
- SARS-CoV-MA15-infected mice show lower levels of CD8 and CD4 T cell apoptos

mortality/aging

increased susceptibility to Coronaviridae infection induced morbidity/mortality
- all mice infected with murine hepatitis virus strain 1 (MHV-1) succumb to a sub-lethal dose compared to only about 10% of control BALB/c mice

increased susceptibility to Orthomyxoviridae infection induced morbidity/mortality
- mice infected with the mouse-adapted H1N1 influenza A virus, PR8 strain, succumb to a sub-lethal dose compared to only about 20% of control BALB/c mice

hematopoietic system phenotype

increased CD8-positive, alpha-beta T cell number
- SARS-CoV-MA15-infected mice show increased numbers of virus-specific CD8 T cells in lungs

decreased T cell apoptosis
- SARS-CoV-MA15-infected mice show lower levels of CD8 and CD4 T cell apoptos

increased CD4-positive, alpha beta T cell number
- SARS-CoV-MA15-infected mice show increased numbers of virus-specific CD4 T cells in lungs

decreased Ly6C high monocyte number
- SARS-CoV-MA15-infected mice do not show an increase in Ly6C^hiCD11b⁺ cells in the lungs as is seen in controls

abnormal mononuclear phagocyte morphology
- SARS-CoV-MA15-infected mice show a decrease in the percentage and numbers of inflammatory monocyte-macrophages that produce the pro-inflammatory cytokines TNF, IL-6, IL1-beta, and iNOS
- SARS-CoV-MA15-infected mice do show an increase in highly activated inflammatory monocyte-macrophages as is seen in infected BALB/c controls

homeostasis/metabolism phenotype

abnormal cytokine level
- SARS-CoV-MA15- infected mice have reduced levels of cytokines and chemokines in the broncho-alveolar lavage fluid

Genotype: Ifnar1^tm1Agt/Ifnar1^tm1Agt
involves: 129S2/SvPas * BALB/c * C57BL/6 * SJL

immune system phenotype

increased susceptibility to viral infection
- mice infected with Thogoto virus all succumb within 3 days compared to 5 days for littermate controls

increased susceptibility to Orthomyxoviridae infection
- mice infected with Thogoto virus all succumb within 3 days compared to 5 days for littermate controls

The following phenotype relates to a compound genotype created using this strain

Genotype: Ifnar1^tm1Agt/Ifnar1^tm1Agt
B6.129S2-Ifnar1

hematopoietic system phenotype

abnormal osteoclast morphology
- osteoclastogenesis is enhanced

impaired natural killer cell mediated cytotoxicity
- natural killer cells from polyI:C-treated mice do not display cytotoxicity towards B16 melanoma cells

mortality/aging

increased susceptibility to bacterial infection induced morbidity/mortality
- all mice treated with LPS die unlike control mice

neoplasm

increased tumor growth/size
- in mice treated with polyI:C the reduction in tumor growth of injected B16 melanoma cells is less than in polyI:C treated control mice

skeleton phenotype

decreased bone mineral density

abnormal osteoclast morphology
- osteoclastogenesis is enhanced

immune system phenotype

decreased tumor necrosis factor secretion
- from bone marrow-derived macrophage stimulated with LPS or E. coli K1 E-R8

decreased interferon-alpha secretion
- following infection with Leishmania

abnormal osteoclast morphology
- osteoclastogenesis is enhanced

decreased interleukin-6 secretion
- from bone marrow-derived macrophage stimulated with LPS or E. coli K1 E-R8

increased susceptibility to bacterial infection induced morbidity/mortality
- all mice treated with LPS die unlike control mice

decreased interferon-beta secretion
- following infection with Leishmania

impaired natural killer cell mediated cytotoxicity
- natural killer cells from polyI:C-treated mice do not display cytotoxicity towards B16 melanoma cells

abnormal response to infection
- murine cytomegalovirus replication in macrophages is increased greater than 10,000-fold compared to that in wild-type macrophages

References

Muller U; Steinhoff U; Reis LF; Hemmi S; Pavlovic J; Zinkernagel RM; Aguet M. 1994. Functional role of type I and type II interferons in antiviral defense. Science 264(5167):1918-21PubMed: 8009221 MGI: J:36115

Additional References

Rossi SL; Tesh RB; Azar SR; Muruato AE; Hanley KA; Auguste AJ; Langsjoen RM; Paessler S; Vasilakis N; Weaver SC. 2016. Characterization of a Novel Murine Model to Study Zika Virus. Am J Trop Med Hyg 94(6):1362-9PubMed: 27022155 MGI: J:230104

Additional - Ifnar1^tm1Agt related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Ifnar1
- Standard PCR:Ifnar1
- Probe:Ifnar1 Probe
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

When maintaining a live colony, these mice can be bred as homozygotes. SPF conditions are recommended.
- Additional Breeding and Husbandry Support
Mating System
- Homozygote x Homozygote
Citation
When using the IFN-αβR- mouse strain in a publication, please cite the originating article(s) and include MMRRC stock #32045 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX10 (Standard)

Terms Of Use

General Terms and Conditions

See MMRRC for Additional Conditions of Distribution

Questions about Terms of Use

Additional Use Restrictions Apply

Notice regarding distribution of this strain.

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:IFN-αβR-

Donating Investigator

Genetic overview

Research Applications

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Ifnar1tm1Agt

Allele Symbol: Ifnar1tm1Agt

Disease Terms

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Mammalian Phenotype Terms by Genotype

Genotype: Ifnar1tm1Agt/Ifnar1tm1Agtinvolves: 129S2/SvPas

behavior/neurological phenotype

homeostasis/metabolism phenotype

immune system phenotype

cardiovascular system phenotype

liver/biliary system phenotype

mammalian phenotype

mortality/aging

vision/eye phenotype

hematopoietic system phenotype

Genotype: Ifnar1tm1Agt/Ifnar1tm1Agtinvolves: 129S2/SvPas * 129S6/SvEvTac

hematopoietic system phenotype

immune system phenotype

homeostasis/metabolism phenotype

Genotype: Ifnar1tm1Agt/Ifnar1tm1Agtinvolves: 129S2/SvPas * C57BL/6

immune system phenotype

mammalian phenotype

Genotype: Ifnar1tm1Agt/Ifnar1tm1Agtinvolves: 129S2/SvPas * BALB/c

cellular phenotype

immune system phenotype

mortality/aging

hematopoietic system phenotype

homeostasis/metabolism phenotype

Genotype: Ifnar1tm1Agt/Ifnar1tm1Agtinvolves: 129S2/SvPas * BALB/c * C57BL/6 * SJL

immune system phenotype

Genotype: Ifnar1tm1Agt/Ifnar1tm1AgtB6.129S2-Ifnar1

hematopoietic system phenotype

mortality/aging

neoplasm

skeleton phenotype

immune system phenotype

References

Additional References

Additional - Ifnar1tm1Agt related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Citation

Animal Health Reports

The Jackson Laboratory's Genotype Promise

Terms Of Use

Additional Use Restrictions Apply

Licensing Information

Ifnar1^tm1Agt

Allele Symbol: Ifnar1^tm1Agt

Genotype: Ifnar1^tm1Agt/Ifnar1^tm1Agt
involves: 129S2/SvPas

Genotype: Ifnar1^tm1Agt/Ifnar1^tm1Agt
involves: 129S2/SvPas * 129S6/SvEvTac

Genotype: Ifnar1^tm1Agt/Ifnar1^tm1Agt
involves: 129S2/SvPas * C57BL/6

Genotype: Ifnar1^tm1Agt/Ifnar1^tm1Agt
involves: 129S2/SvPas * BALB/c

Genotype: Ifnar1^tm1Agt/Ifnar1^tm1Agt
involves: 129S2/SvPas * BALB/c * C57BL/6 * SJL

Genotype: Ifnar1^tm1Agt/Ifnar1^tm1Agt
B6.129S2-Ifnar1

Additional - Ifnar1^tm1Agt related