Search Criteria: Research Area is "Developmental Biology Research: Skeletal Defects (osteopetrosis)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000231 | B6C3Fe a/a-Csf1op/J | Repository- Live |
| Mice homozygous for the osteopetrosis spontaneous mutation (Csf1op) are viable and exhibit osteopetrosis. The osteoclasts are the primary cell type affected in homozygous mutant mice. This results in a generalized macrophage deficiency, monocytopenia, and defective bone remodeling. Homozygous mutant mice also have abnormal calcium regulation, impaired dental growth and female mice fail to lactate. Total leukocyte counts are reduced and marrow cells are decreased to one-tenth of normal control mice. Homozygous mutant mice have a deficient microglia and macrophage response, and therefore may be useful tools to study the role of glia in neurological disease if mated to transgenic models of neurodegenerative disease. | ||
| 001573 | B6C3Fe a/a-MitfMi/J | Repository- Live |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice heterozygous for the MitfMi mutation have less iris pigment than wildtype and often have white spotting on the belly, head, and tail. Homozygous mutant mice have small eyes and are devoid of pigment in the eyes, inner ear, and skin. Homozygotes are deaf at an early age. There is a decrease of mast cells in the spleen and gut. Most homozygotes die around weaning but some may live for several months. There is a deficiency of secondary bone resorption (osteopetrosis) and the incisors fail to erupt. Immunological defects include decreased macrophage chemotactic responses, impaired proliferative responses to B cell and T cell mitogens, diminished responses in vitro to T-dependent and T-independent antigens and reduced NK cell activity. | ||
| 002277 | B6.129S7-Srctm1Sor/J | Repository-Cryopreserved |
| Mice homozygous for the Srctm1Sor targeted mutation display osteopetrosis. Homozygous mutant mice are approximately one-third the size of normal wildtype siblings. Incisors fail to erupt. In general, long bones are shorter in length and show a partial absence of bone marrow. Src has been implicated in development, but its role may be masked by other tyrosine kinases. No overt phenotype is found in brain or platelets, where it is most highly expressed. Mice heterozygous for the Srctm1Sor mutation have no apparent abnormalities. | ||
| 000158 | B6.Cg-MitfMi-wh/MitfMi/J | Repository-Cryopreserved |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes white mutant mice show slight microphthalmia but normal skeleton. Mice heterozygous for the microphthalmia (MitfMi) mutation have less iris pigment than wildtype and often have white spotting on the belly, head, and tail. Homozygous mutant mice have small eyes and are devoid of pigment in the eyes, inner ear, and skin. Homozygotes are deaf at an early age. There is a decrease of mast cells in the spleen and gut. Most homozygotes die around weaning but some may live for several months. There is a deficiency of secondary bone resorption (osteopetrosis) and the incisors fail to erupt. Immunological defects include decreased macrophage chemotac
..... For more information please see the full descriiption on the strain data sheet | ||
| 002381 | B6;129S7-Srctm1Sor/J | Repository-Cryopreserved |
| Mice homozygous for the Srctm1Sor targeted mutation display osteopetrosis. Homozygous mutant mice are approximately one-third the size of normal wildtype siblings. Incisors fail to erupt. In general, long bones are shorter in length and show a partial absence of bone marrow. Src has been implicated in development, but its role may be masked by other tyrosine kinases. No overt phenotype is found in brain or platelets, where it is most highly expressed. Mice heterozygous for the Srctm1Sor mutation have no apparent abnormalities. | ||
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