Search Criteria: Research Area is "Metabolism Research: Iron Metabolism"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 013039 | 129S-Spictm1Kmm/J | Repository- Live |
| In these mutant mice a loxP-flanked neomycin resistance (neo) cassette replaces exons 2-5 of the Spi-C transcription factor (Spi-1/PU.1 related) gene (Spic), abolishing gene function. Heterozygous mice are viable and fertile, while homozygotes are born at a frequency lower than the expected Mendelian ratio and they have small litters. Spi-C is highly expressed in red pulp macrophages which are a distinct splenic subset required for red blood cell recycling and iron homeostasis. These Spi-C-/- mice exhibit a defect in the development of red pulp macrophages, which fail to efficiently phagocytose red blood cells trapped in the spleen. They also develop an iron overload localized selectively to splenic red pulp. These mice may be useful for studying the development and function of red pulp macrophages. | ||
| 016235 | B6(Cg)-Narfltm1.1Fsl/J | Repository- Live |
| These Iop1flox mutant mice possess loxP sites flanking exon 1 of the nuclear prelamin A recognition factor-like (Narfl or Iop1) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. IOP1 is required for cytosolic iron-sulfur protein assembly pathways. Iron-sulfur proteins are involved in the Krebs Cycle, oxidative phosphorylation, translation, iron regulatory pathways, and purine metabolism. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exon 1 deleted in the cre-expressing tissues. This strain may be useful for conditional deletion of IOP1 to study the cytoplasmic iron-sulfur complex assembly pathway. | ||
| 012932 | B6.129S4-Ftmttm1Mdf/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis of testes from homozygotes. Homozygotes do not exhibit any overt phenotype. | ||
| 003333 | C57BL/6-Tg(TF-CAT)48Gsa/J | Cryopreserved - Ready for recovery |
| Transferrin is regulated by iron at the level of translation. This transgenic strain carries a chimeric gene composed of the human TF 5'-flanking sequences fused to the CAT reporter gene. Iron administration to transgenic mice results in a significant decrease of transferrin-directed CAT enzyme activity and CAT protein in the liver. This strain is useful for understanding the expression of the human TF gene and its age-related regulation. During aging, expression of the transgene decreases in the liver, but not in the brain, and liver expression is suppressed by iron and lipopolysaccharide. | ||
| 008660 | FVB.129S2(B6)-Hmox2tm1Poss/J | Cryopreserved - Ready for recovery |
| Homozygotes have reduced total heme oxygenase activity in brain and testes, diminished inflammatory pain response and are more susceptible to hyperoxia with attenuated hypoxic ventilatory response. Cultured neurons from homozygotes exhibit increased neurotoxicity and cell death. Neuronal and endothelial cell damage due to transient focal ischemia and glutamate induced cytotoxicity is increased. Olfactory epithelial neurons have decreased proliferation of neuronal precursors and increased apoptosis. Mutant pulmonary venous myocardium is hypertrophic. After hyperoxic exposure, total lung iron content increased 3.5 fold in homozygotes compared to wild-type. Homozygotes have a slower overall gastrointestinal transit time than wild-type. Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Although homozygous male animals exhibit ejaculatory abnormalities, both male and female homozygotes are fertile ..... For more information please see the full phenotype on the strain data sheet | ||
| 003582 | STOCK Cptm1Hrs/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Cp gene demonstrate a progressive accumulation of iron in hepatocytes and reticuloendothelial cells. By one year of age, iron content of the liver and spleen reaches three to six-fold that observed in wild-type litter mates. The Cp gene product appears to be necessary for proper iron efflux from these cell types. This strain represents a viable murine model for aceruloplasminemia. At one year of age there is no evidence of anemia, diabetes, or neurological symptoms despite iron accumulation at the corresponding tissue sites. | ||
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