- abnormal cochlea morphology / MGI
- abnormal lateral semicircular canal morphology / MGI
- delayed bone ossification / MGI
- abnormal hair follicle morphology / MGI
- decreased hair follicle number / MGI
- small hair follicles / MGI
- abnormal liver morphology / MGI
- muscle hypoplasia / MGI
- decreased oligodendrocyte progenitor number / MGI
- abnormal spinal cord morphology / MGI
- atelectasis / MGI
- translucent skin / MGI
- thin epidermis / MGI
- thin epidermis stratum spinosum / MGI
- decreased body weight / MGI
- cyanosis / MGI
- postnatal growth retardation / MGI
- respiratory failure / MGI
- abnormal postnatal growth/weight/body size / MGI
- abnormal muscle morphology / MGI
- hydrops fetalis / MGI
- abnormal semicircular canal morphology / MGI
- abnormal posterior semicircular canal morphology / MGI
- abnormal cochlear sensory epithelium morphology / MGI
- abnormal bony labyrinth / MGI
- abnormal cochlear inner hair cell morphology / MGI
- decreased cochlear inner hair cell number / MGI
- abnormal cochlear outer hair cell morphology / MGI
- decreased cochlear outer hair cell number / MGI
- decreased cochlear hair cell number / MGI
- abnormal cochlear hair cell stereociliary bundle morphology / MGI
- abnormal cochlear hair cell development / MGI
- abnormal brainstem morphology / MGI
- homeostasis/metabolism phenotype / MGI
- growth/size/body region phenotype / MGI
- decreased birth weight / MGI
- prenatal growth retardation / MGI
- abnormal inner hair cell kinocilium morphology / MGI
- neonatal lethality, complete penetrance / MGI
129(Cg)-Igf1rtm1.1Mhz/Orl
| Status | Available to order |
| EMMA ID | EM:15696 |
| Citation information | RRID:IMSR_EM:15696 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 | 129(Cg)-Igf1rtm1.1Mhz/Orl |
| Alternative name | 129-Igf1rflox |
| Strain type | Targeted Mutant Strains : Conditional mutation |
| Allele/Transgene symbol | Igf1rtm1.1Mhz |
| Gene/Transgene symbol | Igf1r |
Information from provider
| Provider | Martin HOLZENBERGER |
| Provider affiliation | Sorbonne Université INSERM, U938, Centre de recherche Saint Antoine |
| Genetic information | Mutants were generated by targeting the endogenous Igf1r (IGF type 1 receptor) gene with a replacement construct to flox the essential exon 3. The mutant Igf1r allele harbors 2 loxP sites flanking exon 3. This Igf1rflox strain is useful for generating conditional Igf1r gene knockout, for instance by crossing with mice that express cre recombinase. |
| Phenotypic information | Homozygous:Homozygous 129-Igf1r-flox mice show no phenotypic difference to wild-type 129S2/SvPas, including growth, fertility and adult body weight. They are phenotypically strictly normal.Heterozygous:Heterozygous 129-Igf1r-flox mice show no phenotypic difference to wild-type 129S2/SvPas. |
| Breeding history | This mutation was generated by homologous recombination, targeting the endogenous Igf1r gene with a replacement construct containing a floxed exon 3 and a floxed neomycin resistance cassette (tri-lox-construct). The selection cassette was subsequently eliminated in vivo by the cre recombinase deleter transgene EIIa-Cre. The resulting Igf1r-flox mutant devoid of the neo cassette was extensively backcrossed to the 129S2/SvPas genetic background. Homozygous 129-Igf1r-flox mice were obtained by mating siblings. This strain is maintained since on 129S2/SvPas genetic background. |
| 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 | homozygous 129S2/SvPas males |
Disease and phenotype information
Orphanet associated rare diseases, based on orthologous gene matching
- Growth delay due to insulin-like growth factor I resistance / Orphanet_73273
MGI phenotypes (gene matching)
Literature references
- A targeted partial invalidation of the insulin-like growth factor I receptor gene in mice causes a postnatal growth deficit.;Holzenberger M, Leneuve P, Hamard G, Ducos B, Perin L, Binoux M, Le Bouc Y, ;2000;Endocrinology;141;2557-66; 10875258
- Cre-mediated germline mosaicism: a method allowing rapid generation of several alleles of a target gene.;Holzenberger M, Lenzner C, Leneuve P, Zaoui R, Hamard G, Vaulont S, Bouc Y L, ;2000;Nucleic acids research;28;E92; 11058142
- Experimental IGF-I receptor deficiency generates a sexually dimorphic pattern of organ-specific growth deficits in mice, affecting fat tissue in particular.;Holzenberger M, Hamard G, Zaoui R, Leneuve P, Ducos B, Beccavin C, Périn L, Le Bouc Y, ;2001;Endocrinology;142;4469-78; 11564712
- Hepatocyte proliferation during liver regeneration is impaired in mice with liver-specific IGF-1R knockout.;Desbois-Mouthon Christèle, Wendum Dominique, Cadoret Axelle, Rey Colette, Leneuve Patricia, Blaise Annick, Housset Chantal, Tronche François, Le Bouc Yves, Holzenberger Martin, ;2006;FASEB journal : official publication of the Federation of American Societies for Experimental Biology;20;773-5; 16484330
- Brain IGF-1 receptors control mammalian growth and lifespan through a neuroendocrine mechanism.;Kappeler Laurent, De Magalhaes Filho Carlos, Dupont Joëlle, Leneuve Patricia, Cervera Pascale, Périn Laurence, Loudes Catherine, Blaise Annick, Klein Rüdiger, Epelbaum Jacques, Le Bouc Yves, Holzenberger Martin, ;2008;PLoS biology;6;e254; 18959478
- Disrupting IGF Signaling in Adult Mice Conditions Leanness, Resilient Energy Metabolism, and High Growth Hormone Pulses.;François Jean-Christophe, Aïd Saba, Chaker Zayna, Lacube Philippe, Xu Jie, Fayad Racha, Côté Francine, Even Patrick, Holzenberger Martin, ;2017;Endocrinology;158;2269-2283; 28881863
- IGF-1R contributes to stress-induced hepatocellular damage in experimental cholestasis.;Cadoret Axelle, Rey Colette, Wendum Dominique, Elriz Khaldoun, Tronche François, Holzenberger Martin, Housset Chantal, ;2009;The American journal of pathology;175;627-35; 19628767
- The Alzheimer's disease transcriptome mimics the neuroprotective signature of IGF-1 receptor-deficient neurons.;George Caroline, Gontier Géraldine, Lacube Philippe, François Jean-Christophe, Holzenberger Martin, Aïd Saba, ;2017;Brain : a journal of neurology;140;2012-2027; 28595357
- Blocking IGF Signaling in Adult Neurons Alleviates Alzheimer's Disease Pathology through Amyloid-β Clearance.;Gontier Géraldine, George Caroline, Chaker Zayna, Holzenberger Martin, Aïd Saba, ;2015;The Journal of neuroscience : the official journal of the Society for Neuroscience;35;11500-13; 26290229
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