Search Criteria: Research Area is "Hematological Research: Hemoglobin Defects"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 007858 | B6.129S6(Cg)-Eraftm1.1Mjwe/J | Repository- Live |
| Mice homozygous for this targeted allele (AHSP-/- or ERAF-/-) are fertile with normal lifespans up to at least 18 months of age. No RNA or protein from the targeted gene is detected in hematopoietic tissues from homozygotes. AHSP-/- mice exhibit abnormal erythrocyte morphology with intracellular inclusion bodies that stain positively for denatured hemoglobin (Heinz bodies). Homozygous mice also have reduced lifespan of circulating red blood cells, increased apoptosis of erythroid precursors, and increased production of reactive oxygen species (ROS) with consequent damage to hemoglobin A and other cellular components. As the a-hemoglobin stabilizing protein specifically binds the cytotoxic free a-Hb subunit of hemoglobin A, these AHSP-mutant mice may be useful in studying erythroid development/erythropoiesis, thalassemia, Heinz body hemolytic anemia, and other hemoglobinopathies.
In an attem
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| 008369 | B6.129S6-Rpsatm1Ells/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, and do not display any gross behavioral abnormalities. Homozygous null mice have an embryonic lethal phenotype, failing to develop past embryonic days 3.5. Heterozygotes exhibit delayed embryonic growth that normalizes postnatally. On a mixed B6;129 background some cranifacial defects are observed. These abnormalities were no longer observed after the fourth generation backcross (N4) onto the C57BL/6 background. Mean corpuscular hemoglobin concentration (MCHC) is significantly lower in heterozygotes treated with myelosuppressor, Flourauracil, when compared to wild-type controls. Heterozygotes display slightly decreased insulin content in pancreatic islet cells, but have normal glucose tolerance, insulin senstivity and insulin secretion. A significant reduction of gene product (mRNA) is detected by Northern blot analysis of embryonic liver and MEFs isolated from heterozygotes. The MEFs exhibit a delayed productio
..... For more information please see the full descriiption on the strain data sheet | ||
| 000899 | C.B6-Tyr+ Hbbs/J | Repository- Live |
| 003516 | FVB.Cg-Tg(CAG-EGFP)B5Nagy/J | Repository- Live |
| This transgenic strain expresses an Enhanced Green Fluorescent Protein (Clontech) driven by chicken beta-actin promoter and CMV intermediate early enhancer. Mice, and cells derived from them, are distinguished from wildtype on the basis of fluorescence. The transgene is expressed in all nucleated embryonic tissues. Cells and tissues with increased hemoglobin content exhibit reduced fluorescence as development progresses. In newborn and adult mice, the entire organ system expresses EGFP. Though widespread, expression levels vary between different organs. This strain can be used as a source of fluorescently marked cells or tissues. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results b
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| 003342 | STOCK Hbatm1Paz Hbbtm1Tow Tg(HBA-HBBs)41Paz/J | Repository- Live |
| This strain was engineered so that it no longer expresses mouse Hba and Hbb, but does express human HBA and HBB. It mimics the genetic, hematologic and histopathologic features that are found in humans afflicted with sickle cell anemia, including irreversibly sickled red blood cells, anemia and multiorgan pathology. A significant percentage of sickle cell mice do not survive to adulthood. | ||
| 003115 | STOCK Tg(CAG-EGFP)B5Nagy/J | Repository- Live |
| This transgenic strain expresses an Enhanced Green Fluorescent Protein (Clontech) driven by chicken beta-actin promoter and CMV intermediate early enhancer. Mice, and cells derived from them, are distinguished from wildtype on the basis of fluorescence. The transgene is expressed in all nucleated embryonic tissues. Cells and tissues with increased hemoglobin content exhibit reduced fluorescence as development progresses. In newborn and adult mice, the entire organ system expresses EGFP. Though widespread, expression levels vary between different organs. This strain can be used as a source of fluorescently marked cells or tissues. | ||
| 000409 | B10.129P-H1b Hbbd Tyrc Ea7a/(5M)oSnJ | Repository-Cryopreserved |
| 000418 | B10.129P-H1b Tyrc Hbbd/(5M)nSnJ | Repository-Cryopreserved |
| 000432 | B10.C-H1b Hbbd Tyrc/(41N)SnJ | Repository-Cryopreserved |
| 000562 | B6(Cg)-Tubtub/J | Repository-Cryopreserved |
| Mice homozygous for the tubby spontaneous mutation experience maturity-onset obesity. Homozygous mutant mice are recognizable by increased body weight at 3 to 4 months in males and at 4 to 6 months in females. Both sexes are fertile. The increased weight is composed of excess adipose tissue. Blood glucose is normal, but plasma insulin is increased prior to obvious signs of obesity and may rise to 20 times normal by 6 months. Despite elevated plasma total cholesterol, triglycerides, and high-density lipoprotein cholesterol, homozygous mutant mice do not exhibit atherosclerotic fatty streak blood vessel lesions. Tubby mutant mice also exhibit retinal degeneration, initially believed due to the presence of another mutation which was called rd5, but since demonstrated to be a pleiotropic effect of the Tubtub mutation (Ohlemiller et al., 1997); the retinal phenotype is moderated by a QTL on Chromosome 11 (Ikeda et al., 2002). Tubby homozygotes additionally exhibit p
..... For more information please see the full descriiption on the strain data sheet | ||
| 002683 | B6.129P2-Hbb-b1tm1Unc Hbb-b2tm1Unc/J | Repository-Cryopreserved |
| Homozygous mice die perinatally. Heterozygous mice show "characteristics typical of severe thalassemia" and are fertile. | ||
| 002204 | B6.129P2-Hbbtm1Unc/J | Repository-Cryopreserved |
| Mice homozygous for this mutation die perinatally due to severe anemia. | ||
| 002949 | B6.129S4-Klf1tm1Sho/J | Repository-Cryopreserved |
| Homozygotes die at embryonic day 15 due to severe anemia during erythropoiesis of the fetal liver. There is a defect in beta-globin expression in these mice. This strain may serve as a model for the human disease beta-thalassemia. | ||
| 002616 | B6.129S7-Hbatm1Paz/J | Repository-Cryopreserved |
| Mice homozygous for this mutation die in utero. The apparent cause of death is severe anemia as no alpha-globin polypeptide is found in these animals. | ||
| 000383 | B6.C-Tyrc H1b Hbbd/ByJ | Repository-Cryopreserved |
| 001622 | B6.CAST-Gpi1a.Cg-Hbath-J | Repository-Cryopreserved |
| 001044 | B6.Cg-Exoc6hbd/J | Repository-Cryopreserved |
| Mice homozygous for the spontaneous mutation hbd exhibit microcytic anemia, red cell hypochromia and microcytosis, reticulocytosis (Bannerman et al., 1986), and low levels of hemoglobin. Microcytic anemia can be cured by bone marrow transplantation from normal donors (Bloom et al., 1997). Homozygotes can live to 23 months of age, however, B-cell homeostasis is compromised in older mice (Lipovsky et al., 2003). Heterozygotes do not display a clinical phenotype. | ||
| 002074 | B6.Cg-Gpi1a Hbbd H1b/DehJ | Repository-Cryopreserved |
| 001175 | B6.Cg-Hbap/J | Repository-Cryopreserved |
| 000745 | B6.SEC-Hbab/J | Repository-Cryopreserved |
| 006086 | B6.SJL-Tg(HBB-GH1)420King/J | Repository-Cryopreserved |
| Mice hemizygous for this transgene are viable. While males are fertile, transgenic females are unreliable breeders and mothers. Homozygotes are sterile. In both fetal and adult tissues, erythroid-specific expression of the transgene is observed. Transgenic mice have 120-150% greater mature body mass and increased bone mass. The donating investigator also reports transgenic mice have increased dermatological stiffness and toughness. Transgenic mice have a characteristic coat with few guard hairs compared to wildtype littermates. These mice may be useful in studies of bone formation and development, dermatology, and acromegaly. | ||
| 000191 | B6.SM-Hbad/J | Repository-Cryopreserved |
| 003253 | B6;129P-Hbb-b1tm1Unc Hbb-b2tm1Unc/J | Repository-Cryopreserved |
| Homozygous mice die perinatally. Heterozygous mice show "characteristics typical of severe thalassemia" and are fertile. | ||
| 003250 | B6;129P2-Hbbtm2Unc/J | Repository-Cryopreserved |
| Heterozygotes show the same aberrant splicing as their human counterparts and produce reduced amounts of the mouse beta globin chains and no human beta globin. Heterozygotes exhibit moderate thalassemia (anemia, splenomegaly, abnormal hematologic indices). Homozygotes are not viable. | ||
| 002474 | B6;129S4-Klf1tm1Sho/J | Repository-Cryopreserved |
| Homozygotes die at embryonic day 15 due to severe anemia during erythropoiesis of the fetal liver. There is a defect in beta-globin expression in these mice. This strain may serve as a model for the human disease beta-thalassemia. | ||
| 002404 | B6;CBA-Mostm1Ev/J | Repository-Cryopreserved |
| Mice homozygous for the Mostm1Ev targeted mutation are viable. Homozygous males are fertile; the littersize of homozygous females is markedly lower than that of wild type or heterozygous mice. Eggs lacking Mos undergo spontaneous parthenogenetic activation (extrusion of the second polar body and pronucleus formation without fertilization). Ovarian cysts develop in homozygous females as young as one month. Some of the ovarian cysts consist of several tissue types, including possible thyroid tissue, similar to about 10% of all benign cystic teratomas in human beings. | ||
| 002662 | C.Cg-Fechm1Pas/J | Repository-Cryopreserved |
| Homozygous mutants are recognizable by the intense yellow color of their sera, gross bilirubinemia, and, especially in albino mice, jaundice. Photosensitivity is evidenced by the appearance of inflammatory skin lesions, often becoming ulcerous, under standard mouseroom conditions (fluorescent light). Mutants do not differ from their normal littermates in body size or weight, nor are they retarded in growth. They exhibit hepatomegaly and splenomegaly, leading to enlarged abdomens after several months of age. Although mutants are not anemic at one month old, normocytic anemia develops with age. | ||
| 000996 | C57BL/6J-Hbbd3th/J | Repository-Cryopreserved |
| 000802 | WB.Cg-Hbath-J/J | Repository-Cryopreserved |
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Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Under Development
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- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
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