- 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 Ifnar1tm1Agt/Cnrm
Status | Under development - register interest |
EMMA ID | EM:13140 |
Citation information | RRID:IMSR_EM:13140 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 | STOCK Ifnar1tm1Agt/Cnrm |
Alternative name | IFNAR |
Strain type | Targeted Mutant Strains : Knock-out |
Allele/Transgene symbol | Ifnar1tm1Agt |
Gene/Transgene symbol | Ifnar1 |
Information from provider
Provider | Eleonora Aricò |
Provider affiliation | Core Facilities, Istituto Superiore di Sanità |
Genetic information | Mice are homozygous for the knocked out gene encoding interferon alpha/beta receptor 1. |
Phenotypic information | Homozygous:Homozygotes Ifnar1 (IFNAR) knock-out mice lack type I interferon receptor function and are viable, fertile and phenotypically normal but show increased susceptibility to viral infections and diminished cancer immune surveillance. Heterozygous:Heterozygous Ifnar1 (IFNAR) knock-out mice are viable, fertile and phenotypically normal. No data are available on their susceptibility to viral infections. |
Breeding history | 129/Sv Ifnar1-/- female mice (A129; Muller et al., Science, 1994) were originally purchased from B&K Universal LTD, UK (now Marshall BioResoures, US). |
References |
|
Homozygous fertile | yes |
Homozygous viable | yes |
Homozygous matings required | no |
Immunocompromised | yes |
Information from EMMA
Archiving centre | CNR, Consiglio Nazionale delle Ricerche, Monterotondo, Italy |
Breeding at archiving centre | 1 backcross to C57BL/6N |
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
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
Literature references
- Disruption of IFN-I Signaling Promotes HER2/Neu Tumor Progression and Breast Cancer Stem Cells.;Castiello Luciano, Sestili Paola, Schiavoni Giovanna, Dattilo Rosanna, Monque Domenica M, Ciaffoni Fiorella, Iezzi Manuela, Lamolinara Alessia, Sistigu Antonella, Moschella Federica, Pacca Anna Maria, Macchia Daniele, Ferrantini Maria, Zeuner Ann, Biffoni Mauro, Proietti Enrico, Belardelli Filippo, Aricò Eleonora, ;2018;Cancer immunology research;6;658-670; 29622580
- Anticancer Effects of Sublingual Type I IFN in Combination with Chemotherapy in Implantable and Spontaneous Tumor Models.;Ciccolella Maria, Andreone Sara, Mancini Jacopo, Sestili Paola, Negri Donatella, Pacca Anna Maria, D'Urso Maria Teresa, Macchia Daniele, Canese Rossella, Pang Ken, SaiYing Ko Thomas, Decadt Yves, Schiavoni Giovanna, Mattei Fabrizio, Belardelli Filippo, Aricò Eleonora, Bracci Laura, ;2021;Cells;10;; 33917958
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).