Search Criteria: Research Area is "Hematological Research: Hematopoietic Defects"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000664 | C57BL/6J | Level 1 |
| C57BL/6 is the most widely used inbred strain. It is commonly used as a general purpose strain and background strain for the generation of congenics carrying both spontaneous and induced mutations. Although this strain is refractory to many tumors, it is a permissive background for maximal expression of most mutations. C57BL/6J mice are used in a wide variety of research areas including cardiovascular biology, developmental biology, diabetes and obesity, genetics, immunology, neurobiology, and sensorineural research. C57BL/6J mice are also commonly used in the production of transgenic mice. Overall, C57BL/6 mice breed well, are long-lived, and have a low susceptibility to tumors. Primitive hematopoietic stem cells from C57BL/6J mice show greatly delayed senescence relative to BALB/c and DBA/2J. This is a dominant trait. Other characteristics include: 1) a high susceptibility to diet-induced obesity, type 2 diabetes, and atherosclerosis; 2) a high incidence of microphthalmia and other a
..... For more information please see the full descriiption on the strain data sheet | ||
| 007205 | 129S-Myo1eGt(ROSA)74Sor/J | Repository- Live |
| Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mice are anemic (low hemoglobin concentration, red blood cell count, hematocrit). These mice also exhibit polychromasia (abnormally high number of immature blood cells). Homozygotes occur at lower than Mendelian ratio (15%). Although homozygotes are fertile, pregnancy is occasionally lethal for homozygous females. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Myo1e-mutant mice may be useful in studying vascular development, hematopoiesis and cellular signaling during development and in adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 007846 | 129S-Pdgfrbtm1Sor/J | Repository- Live |
| One third of homozygous embryos, aged E16 to E18.5, exhibit purpura and edema with some embryos in this group dying at this stage. Homozygous embryos delivered by Caesarean section at E18.5 die within minutes. Homozygotes exhibit anemia, elevated numbers of nucleated erythrocytes, polychromasia, irregularly shaped mature erythrocytes (anisocytosis), and hemorrhaging. Glomerular capillary tufts are absent and the capsule space is filled with blood cells. No gene product (protein) is detected by Western blot analysis of total protein. A truncated transcript presumed to be due to exon skipping is detected by Northern blot analysis. This mutant mouse strain may be useful in studies of hematopoiesis, kidney development and and cellular signaling during development. | ||
| 007199 | 129S-Sgpl1Gt(ROSA)78Sor/J | Repository- Live |
| Mice homozygous for this mutant allele have reduced size and weight gains after birth and do not survive past 8 weeks of age. Homozygotes occur at a lower than Mendelian ratio (19%) from heterozygote X heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Beta-galactosidase staining pattern mimics the endogenous gene expression pattern in adult intestinal epithelial cells. Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mutant mice are anemic (low hemoglobin concentration, reduced red blood cell count, low hematocrit). Mutants exhibit polychromasia (abnormally high number of immature blood cells), kidney defects (blood urea nitrogen level abnormally high, kidney size smaller than wildtype, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells) and abnormalities in palate bone fusion. Homozygotes are infertile. Heterozygote
..... For more information please see the full descriiption on the strain data sheet | ||
| 006942 | B6.129-Cd33tm1Ajv/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 expression of the targeted gene's protein product is detected on the cell surface, as determined by flow cytometry analysis of hematopoietic cell populations in blood and lymphoid organs from homozygotes. Homozygotes exhibit a slight decrease in the mean erythrocyte count and hematocrit and an increase in the mean concentration of serum aspartate aminotransaminase. Experimentally induced peritonitis and systemic inflammation results in reduced immunological response. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, hematopoiesis and immune response. This strain was transferred from the collection of the Consortium for Functional Glycomics. | ||
| 006944 | B6.129-Mgl1tm1Hed/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 Northern blot or RT-PCR analysis. Immunohistochemical reactivity is not detected in inflamed skin. Although mutant mice exhibit slightly increased red blood cell counts, mean corpuscular hemoglobin, hematocrit and mean corpuscular volume when compared to wild-type controls, these levels are within the normal range for mice. Homozygotes have diminished antigen-induced granulation tissue formation but show normal antigen-independent granulation tissue formation. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, antigen-specific and antigen-independent cellular immune response and hematopoiesis. This strain was transferred from the collection of the Consortium for Functional Glycomics. | ||
| 006785 | B6.129P2(C)-Cd19tm1(cre)Cgn/J | Repository- Live |
| Homozygous mutant mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Homozygotes have a deficiency in the B-1 subset of B-lymphocytes along with a concomitant reduction in serum IgM. Their ability to respond to T-cell-dependent antigens is severely impaired, and they fail to form splenic germinal centers. In addition to disrupting the targeted gene, the targeting construct also introduced a cre cassette into exon 2 of the targeted gene, effectively placing cre expression under the control of the endogenous promoter. The Cd19 promoter specifically directs cre expression at the earliest stages and throughout B-lymphocyte development and differentiation. Although homozygous mutant mice are Cd19-deficient, heterozygous mice are phenotypically normal, and can be used for specific deletion of loxP-flanked (floxed) targets in B-lymphocytes.
In an attempt to offer alleles on well-characte
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| 008313 | B6.129P2-Hlxtm1Rph/J | Repository- Live |
| Homozygous null mice have an embryonic lethal phenotype. Homozygous mice on the C57BL/6 and B6;129 mixed background fail to develop past embryonic days 15.5 due to impaired fetal hematopoiesis (anemia, hypoplastic and abnormal development of the liver, hypoplastic gut). Homozygous mice on the FVB/N background survive through embryonic day 18.5 and dead homozygote newborn pups are observed. Late gestation homozygous embryos on the FVB/N background are smaller than wildtype littermates, pale, hydropic (subcutaneous fluid ballooning skin), and have impaired neural crest cell and enteric neuron migration from the stomach to intestine. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Naive CD4 T cells from heterozygotes exhibit increased responsiveness to IL-4, resulting in differentiation of more Th2 cells. This mutant mouse strain may be useful in studies of liver and gastrointe
..... For more information please see the full descriiption on the strain data sheet | ||
| 004781 | B6.129P2-Lyz2tm1(cre)Ifo/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Lyzs locus. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in deletion of the targeted gene in the myeloid cell lineage, including monocytes, mature macrophages, and granulocytes. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This strain represents an effective tool for generating myeloid cell-specific targeted mutants. | ||
| 005940 | B6.129S1-Csf2rbtm1Cgb/J | Repository- Live |
| Homozygous mice are viable and fertile with no behavioral abnormalities. In response to GM-CSF, bone marrow and splenocytes from homozygous mice fail to exhibit proliferation, enhanced survival in vitro, or synergistic interaction with M-CSF. They also fail to proliferate in response to IL-5. IL-3 binding and responses are unaffected. Cell composition in thymus, spleen, bone marrow, and lymph node is not significantly altered. Circulating eosinophils are dramatically reduced in blood with lesser reduction in bone marrow and tissues. Homozygous mice develop pulmonary peribronchovascular lymphoid infiltrates and areas resembling pulmonary alveolar proteinosis (PAP). Consistent with this, mutant mice have greatly increased surfactant protein-B and D accumulation in lung/airway tissue, no attenuation of saturated phosphatidylcholine with advancing age, and high levels of GM-CSF in bronchoaveolar lavage fluid. Homozygous mice are resistant to intradermal Leishmania major infection an
..... For more information please see the full descriiption on the strain data sheet | ||
| 008102 | B6.129S4-Ltb4r1tm1Adl/J | Repository- Live |
| Mice homozygous for this BLTR (BLT1)-deficient allele are viable and fertile. Northern blot analysis of neutrophils, macrophages, lymph nodes, lungs, and
spleens isolated from homozygous mice show absence of the normal transcript and presence of the expected larger transcript (due to the insertion of the neomycin resistance cassette in exon 2 of the targeted gene), albeit at lower levels than the wild type transcript. Homozygous disruption of this allele confers impaired leukocyte function (chemotaxis, recruitment, firm adhesion). For example, homozygotes exhibit substantially diminished recruitment of eosinophils in a model of peritonitis, effector T cells in a model of allergic pulmonary inflammation, and neutrophils in a model of rheumatoid arthritis. As the G protein-coupled receptor BLTR/BLT1 is expressed on myeloid leukocytes (including neutrophils, macrophages, eosinophils, T cell lymphomas, and effector T cells (TH1 CD4+ cells, TH2 CD4+ cells, and effecto
..... For more information please see the full descriiption on the strain data sheet | ||
| 006198 | B6.129S4-Matktm1Sor/J | Repository- Live |
| Homozygotes are viable and fertile with no behavioral abnormalities. The donating investigator reports homozygous mutants have no endogenous protein expression. Homozygous mice have an approximately 2-fold increase in the primitive hematopoietic stem cell population SPKLS (c-Kit+, Lin-, Sca-1+ in combination with side population cells). Homozygous deficiency also leads to the hyperproliferation of pre-B cells in the presence of Interleukin-7, and impaired IFN-gamma production in lymph and spleen cells upon in vivo antigen challenge. These mutant mice may be useful in studying tyrosine phosphorylation of hematopoietic cells, primitive/early hematopoietic populations, immune cell signaling, and regulation of immunological responses. | ||
| 006447 | B6.129S6(CBA)-Cebpatm1Dgt/J | Repository- Live |
| Mice carrying this C/EBPalpha "floxed" allele (C/EBPalphaF) are viable and fertile. The floxed allele functions similarly to the wildtype allele. In mice homozygous for C/EBPalphaF and expressing an interferon-inducible Cre recombinase (introduced by breeding to a cre-expressing strain; see Stock No. 003556), C/EBPalpha activity is disrupted, leading to defective myeloid cell development, increased hematopoietic stem cell repopulating activity, and significantly increased myeloblast population in the bone marrow compartment. In combination with an appropriate Cre transgenic strain, these mutant mice may be useful in studies of hematopoietic cell (e.g. myeloid and basophil progenitor cell) development and function, cancer (e.g. acute myeloid leukemia), and alveolar cell differentiation. | ||
| 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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| 006230 | B6.Cg-Cebpatm1Dgt Tg(Mx1-cre)1Cgn/J | Repository- Live |
| Mice homozygous for this C/EBPalpha "floxed" allele (C/EBPalphaF) and hemizygous for the Mx1-cre transgene are viable and fertile, and exhibit no abnormalities in the hematopoietic system. In the absence of cre expression, the C/EBPalphaF allele functions similarly to the wildtype allele. Mx1-Cre transgene expression can be induced by administration of either interferon (alpha or beta) or synthetic double-stranded RNA (such as poly I:C), leading to deletion of the "floxed" gene. Following 3-4.5 weeks of poly I:C treatment, deletion efficiency is greater than 95% in hematopoietic tissues, and C/EBPalpha protein is undetectable in bone marrow. These poly I:C-treated, mice have defective myeloid cell development, increased hematopoietic stem cell repopulating activity, and a significantly increased myeloblast population in the bone marrow compartment. These mutant mice may be useful in studies of hematopoietic cell (e.g. myeloid and basophil progenitor cell) d
..... For more information please see the full descriiption on the strain data sheet | ||
| 004201 | B6.Cg-Selplgtm1Fur/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No targeted allele product (mRNA or protein) is detected by Northern blot or immunoassay. Mutant mice exhibit mild neutrophilia. Impaired early neutrophil migration in thioglycolate-induced peritonitis is followed by a delayed recovery to nearly normal levels. Although early trauma-induced leukocyte adhesion and migration is greatly reduced and in vivo leukocyte rolling (leukocyte-endothelial cell interaction) in postcapillary venules is severely decreased, cytokine-induced/E selectin-mediated leukocyte rolling is only slightly reduced in the mutant mice. This mutant mouse strain represents a model that may be useful in studies of leukocyte adhesion and migration in the inflammatory response. | ||
| 006922 | B6.Cg-Sfpi1tm2Dgt/J | Repository- Live |
| Mice that are homozygous for this "PU.1F" conditional allele are viable and fertile. When PU.1F mice are bred to mice expressing Cre recombinase, exons 4-5 of the targeted gene are deleted in the cre-expressing tissues in the offspring. These mice may be useful in studying T cell lymphoma, AML and other cancers, as well as transcription factors, hematopoiesis, and the development of multiple cell lineages. For example, when PU.1F mice are crossed with mice expressing the interferon- or dsRNA-inducible Mx1-cre transgenic mice (see Stock No. 003556), this mutant mouse strain may be useful in studies of hematopoietic stem cells. | ||
| 006137 | B6.Cg-Tg(Cdh5-cre)7Mlia/J | Repository- Live |
| Hemizygotes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. In the differentiated endothelium transgene expression is observed as early as E7.5 and progresses to almost full penetrance by E14.5. In adult mice, uniform cre expression is observed in the endothelium of developing and quiescent vessels of all organs examined, as well as within a subset of hematopoietic cells. When bred with any mouse containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the flanked genome. These mice may be useful in studies of the cardiovascular system, including angiogenesis, and endothelial and hematopoietic cell lineages. | ||
| 006329 | B6;129-Baxtm2Sjk Bak1tm1Thsn/J | Repository- Live |
| Mice homozygous for both alleles (Baxfl and bak-) are viable and fertile with no reported abnormalities. Splenic and thymic tissues display no Bak1 protein expression. When bred to Cre recombinase expressing mice, the resulting offspring will have exons 2-4 of Bax deleted in the cre-expressing tissues (determined by promoter driving cre expression). The conditional deletion of Bax combined with the Bak1 null allele makes these mice useful in studies of apoptosis regulation, tissue homeostasis, and development in multiple cell lineages.
When bred to a strain with a Bak1 targeted null allele (Stock No. 004183) and to either a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 004126) or to a strain expressing interferon inducible Cre recombinase (
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| 007206 | B6;129S4-TiparpGt(ROSA)79Sor/J | Repository- Live |
| Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mice are anemic (low hemoglobin concentration, red blood cell count, hematocrit). These mice also exhibit polychromasia (abnormally high number of immature blood cells); kidney defects (blood urea nitrogen level abnormally high, kidney size smaller than wildtype, swollen blood filled, degraded glomeruli are often observed, increased number of vascular smooth muscle cells partially filling the glomeruli space); and abnormalities in palate bone fusion. Homozygotes occur at lower than Mendelian ratio (22%), and 32% die by age 2 week. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Tiparp-mutant mice may be useful in studying kidney development, vascular development, hematopoiesis and cellular signaling during development and in adult mice; specifically receptor tyrosine
..... For more information please see the full descriiption on the strain data sheet | ||
| 007202 | B6;129S4-Zfp826Gt(ROSA)76Sor/J | Repository- Live |
| At age E11.5 to E18.5, homozygous embryos exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At six weeks of age, mice are anemic (low hemoglobin concentration, red blood cell count, hematocrit). These mice also exhibit polychromasia (abnormally high number of immature blood cells); kidney defects (abnormally high blood urea nitrogen level, kidney size smaller than wild-type, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells in glomeruli); abnormalities in palate bone fusion and abnormal neural crest derived and thoracic skeleton development. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes occur at lower than Mendelian ratio (18%) and 8% die by age one week. Surviving homozygotes and heterozygotes are viable and fertile. These Zfp826 (BC055757)-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (R
..... For more information please see the full descriiption on the strain data sheet | ||
| 004126 | C.Cg-Cd19tm1(cre)Cgn Ighb/J | Repository- Live |
| The Cd19 promoter specifically directs expression at the earliest stages and throughout B-lymphocyte development and differentiation. A Cre cassette is inserted into the Cd19 exon 2, functionally disrupting the gene. Homozygous mice are Cd19-deficient, whereas heterozygous mice are phenotypically normal and can be used for specific deletion of floxed targets in B-lymphocytes. Mice that are homozygous deficient for Cd19 are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. A deficiency in the B-1 subset of B-lymphocytes is observed along with a concomitant reduction in serum IgM. Homozygous mice are severely impaired in their ability to respond to T-cell-dependent antigens and fail to form splenic germinal centers. | ||
| 005653 | C.Cg-Gata1tm6Sho/J | Repository- Live |
| Homozygous females and hemizygous males for the targeted mutation are viable, fertile, and normal in size. This mutation results in the complete ablation of the eosinophil lineage, even under conditions that normally stimulate eosinophil development, without affecting the development of other GATA-1 dependent lineages (erythroid, megakaryocytic, and mast cells). Expression of the endogenous gene is observed in erythroid and bone marrow cells. This mutant may be useful for in vivo studies of eosinophil function and eosinophil-related pathologies, including asthma and pulmonary physiology. | ||
| 006863 | C3Fe.B6-Mcm4chaos3/J | Repository- Live |
| Mice homozygous for this ENU-induced F345I hypomorphic allele (Chaos3) are viable, fertile, and overtly indistinguishable from normal littermates. Homozygous, but not heterozygous, mice have slightly reduced wildtype protein levels in mouse embryonic fibroblasts (MEFs). Whereas Chaos3 heterozygotes show mildly elevated (2- to 5-fold) micronucleus frequencies compared with wildtype, homozygotes have an approximate 20-fold increase with over 7% of erythrocytes containing micronuclei. MEFs from homozygous mice exhibit mild defects (cell proliferation, S phase and G2/M populations), and are highly susceptible to chromosome breakage following treatment with the DNA replication inhibitor aphidicolin. On a congenic C3HeB/FeJ background, greater than 80% of homozygous females exhibit mammary adenocarcinomas with a mean latency of 12 months, while males have no tumor incidence. These Chaos3 mice provide a novel, non-transgenic model of breast cancer, and may be useful for s
..... For more information please see the full descriiption on the strain data sheet | ||
| 008315 | FVB.129P2(Cg)-Hlxtm1Rph/J | Repository- Live |
| Homozygous null mice have an embryonic lethal phenotype. Homozygous mice on the C57BL/6 and B6;129 mixed background fail to develop past embryonic days 15.5 due to impaired fetal hematopoiesis (anemia, hypoplastic and abnormal development of the liver, hypoplastic gut). Homozygous mice on the FVB/N background survive through embryonic day 18.5 and dead homozygote newborn pups are observed. Late gestation homozygous embryos on the FVB/N background are smaller than wildtype littermates, pale, hydropic (subcutaneous fluid ballooning skin), and have impaired neural crest cell and enteric neuron migration from the stomach to intestine. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Naive CD4 T cells from heterozygotes exhibit increased responsiveness to IL-4, resulting in differentiation of more Th2 cells. This mutant mouse strain may be useful in studies of liver and gastrointe
..... For more information please see the full descriiption on the strain data sheet | ||
| 006202 | FVB/N-Tg(tetO-BCR/ABL1)2Dgt/J | Repository- Live |
| Hemizygotes are viable, fertile, normal in size, and do not display any behavioral abnormalities. Transgene expression is directed by the tetracycline-responsive element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoters , BCR-ABL1 fusion protein expression can be regulated in the appropriate tissue of the bitransgenic offspring with the tetracycline analog, doxycycline. These mice originally were designed to be bred with transgenic mice harboring a Tal1-tTA transgene (see Stock No. 006209), creating double transgenic offspring as a model for studies of the Philadelphia chromosome and inducible chronic myeloid leukemia. When bred to a strain expressing tTA in the epithelial cells of secretory organs and skin (see Stock No.
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| 006873 | STOCK Cebpbtm1Vpo/J | Repository- Live |
| Significant numbers of mice homozygous for this C/EBP-beta mutationon this mixed genetic background die perinatally due to hypoglycemia and a failure to mobilize glycogen. Homozygous males that survive to adulthood are fertile, but females are sterile, and display altered mammary duct formation. Macrophages isolated from homozygous mutant mice have impaired bactericidal activity. Surviving homozygotes exhibit fasting hypoglycemia, with reduced plasma insulin, plasma lipids, and free fatty acids (FFAs), and impaired hepatic glucose production. Further, they have a blunted response to glucagon and adrenaline primarily due to altered levels of hepatic cAMP production and reduced protein kinase A activity. Homozygous mice are resistant to obesity and have increased carbon dioxide production from increased metabolism in the brown adipose tissue and muscle. On a high-fat diet, homozygotes are protected from obesity and fatty liver due to reduced hepatic expression of lipogenic genes. Homozyg
..... For more information please see the full descriiption on the strain data sheet | ||
| 006882 | STOCK Tg(CAG-Bgeo,-AML1/ETO,-ALPP)1Lbe/J | Repository- Live |
| Mice hemizygous for this "Z/AP-AML1-ETO" transgene (coding for the translocation t(8;21) present in 15% of acute myeloid leukemias (AML)) are viable and fertile. Homozygotes die in utero presumably due to high lacZ expression. Prior to cre-mediated excision of the "floxed" STOP sequence, expression of lacZ is observed in all tissues including bone marrow progenitor cells. When bred to Cre recombinase expressing mice, the STOP sequence (and beta-geo) is removed in the resulting offspring, allowing transcription/co-expression of both the human AML1-ETO fusion protein and placental alkaline phosphatase (ALPP or PLAP) to proceed in the Cre recombinase expressing cells. While pan expression of AML1-ETO leads to embryonic lethality (E7.5), hematopoietic and endothelial expression leads to malignancy in B- and T- lymphoid cells and secondary mutations that closely resemble the association of AML1-ETO with acute myeloid leukemia in humans. These transgenic mice may
..... For more information please see the full descriiption on the strain data sheet | ||
| 006876 | STOCK Tg(CAG-Bgeo,-TEL/AML1,-EGFP)A6Lbe/J | Repository- Live |
| Mice hemizygous for this Cre-conditional TEL-AML1 (or iZ/EG-TEL-AML1) transgene are viable and fertile. Homozygotes die in utero, presumably due to high lacZ expression. Prior to Cre-mediated excision of the "floxed" STOP sequence, high expression of lacZ is observed in cells and tissues. When bred to Cre recombinase transgenic mice, the STOP sequence (and beta-geo) is removed in the resulting offspring, allowing transcription/co-expression of both the human TEL-AML1 fusion protein and EGFP in all cre-expressing cells. TEL-AML1 transcripts are not observed in adult organ tissues prior to excision of the floxed sequences. Following Cre-mediated deletion of the STOP sequence (by B6.Cg-Tg(Tek-cre)12Flv/J, Stock No. 004128), Western blot analysis reveals that EGFP levels are well correlated with TEL-AML1 transcript levels. While global expression of TEL-AML1 leads to embryonic lethality (E7.5), hematopoieti
..... For more information please see the full descriiption on the strain data sheet | ||
| 005854 | STOCK Tg(Cp-EGFP)25Gaia/J | Repository- Live |
| Mice homozygous for the Notch reporter transgene are viable, fertile, normal in size, and do not display any behavioral abnormalities. Enhanced green fluorescent protein (EGFP) expression is present in a wide variety of hemizygous cell/tissue types during development and in the adult, including enriched hematopoietic stem cell (HSC) populations. The location of EGFP expression is consistent with Notch signaling pathway elements/genes and appears to faithfully reflect canonical (CBF1-mediated) Notch activity. With respect to hematopoiesis, low expression is shown in fully differentiated cells of the peripheral lymphoid organs (blood and spleen). Isolated HSC retain their ability to differentiate. Mice expressing this Notch reporter transgene may be useful in studying HSC populations and other cell types utilizing the Notch, CBF1, or Wnt signaling pathways. As immature (double negative [DN]) thymocytes have differential expression patterns as they progress from DN1-DN4, these mice may al
..... For more information please see the full descriiption on the strain data sheet | ||
| 002674 | 129-Krastm1Tyj/J | Repository-Cryopreserved |
| Homozygous mice die at about embryonic day 12-13. They have a hypocellular fetal liver which also displays extensive cell death. They also appear to have a defect in both the hematopoietic cells and their microenvironment. | ||
| 002082 | 129S-Rb1tm1Tyj/J | Repository-Cryopreserved |
| Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. | ||
| 003082 | 129S1/SvImJ-Bcl2tm1Mpin/J | Repository-Cryopreserved |
| Heterozygous mice exhibit expression of beta-galactosidase in populations of large sensory neurons. Mice homozygous for the Bcl2tm1Mpin targeted mutation do not produce either the a or b form of the Bcl2 protein. Bcl2 is a major regulator of programmed cell death, a critical process in shaping the developing nervous system. The absence of the Bcl2 does not significantly influence the development of motor neurons before or during the main period of physiological cell death. Rather, Bcl2 exerts its influence beyond this period, subsequent to the phase where the majority of neuronal loss normally takes place. Polycystic kidney disease is less severe in this strain compared to the Bcl2tm1Sjk targeted mutation (Stock No. 002265). | ||
| 002831 | B6.129-Ahrtm1Bra/J | Repository-Cryopreserved |
| Mice homozygous for the targeted mutation are viable. Homozygotes do not respond to aryl-hydrocarbon receptor agonists. They show reduced liver weight (25% decrease) delayed extramedullary hematopoiesis, and transient hepatic microvesicular steatosis. | ||
| 002938 | B6.129-Kdrtm1Jrt/J | Repository-Cryopreserved |
| Mice homozygous for the Kdrtm1Jrt targeted mutation (formerly called Flk1) die at ~E8.5-E9.5 due to defects in hematopoietic and endothelial development. Embryos lack blood islands at E7.5 and fail to form organized blood vessels. There is severe reduction in hematopoietic progenitor cells. | ||
| 002463 | B6.129S-Itga4tm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Itga4tm1Hyn targeted mutation die during embryonic development. Homozygous mutant embryos fail to fuse the allantois with the chorion during placentation. There is a defect in the epicardium and coronary vessels results in in utero cardiac hemorrhage; also known as CD49D, VLA-4. | ||
| 005669 | B6.129S-Runx1tm1Spe/J | Repository-Cryopreserved |
| Heterozygous mice are viable, fertile, devoid of hemorrhagic lesions, and exhibit mild hematopoietic impairment. Mice that are homozygous for the targeted mutation have an embryonic lethal phenotype; animals are alive at embryonic day 11.5, but start dying at embryonic day 12.5. Embryos exhibit extensive hemorrhagic lesions in the central nervous system including the intraventricular regions and metencephalon as well as segmental bleeds at the VII-VIII cranial nerve complex, cervical, thoracic, and caudal regions. At embryonic day 10.5, symmetrical and bilateral necrosis preceding hemorrhage is observed in homozygotes. Homozygous disruption of the endogenous gene completely blocks definitive erythropoiesis, myelopoiesis, and lymphopoiesis. This mutant may be useful in leukemia studies as disruption of the human homolog of this gene is associated with many different leukemias. | ||
| 005963 | B6.129S1-Csf2rb2tm1Cgb Csf2rbtm1Clsc/J | Repository-Cryopreserved |
| Mice homozygous at both loci are viable and fertile with no behavioral abnormalities. Steady state hematopoiesis is normal. Bone marrow from homozygous mice fail to exhibit any cellular responses to GM-CSF, IL-5, or IL-3. Like the similar strain (Stock No. 005940; Csf2rbtm1Cgb), double homozygous mice exhibit eosinopenia, increased surfactant accumulation in lung tissue and pulmonary alveolar proteinosis (PAP), infection resistance, and attenuated tissue repair after injury. This mutant may be useful in studies of PAP, lung physiology and disease, surfactant homeostasis and metabolism, innate immunity, cytokine signaling, myoproliferative disease, hematopoietic cell populations requiring IL-3, GM-CSF, or IL-5 for development and function, and models of ischemic, traumatic, toxic, and inflammatory injuries. | ||
| 004757 | B6.129S2-Mybtm1Ssp/J | Repository-Cryopreserved |
| Homozygous null mice have an embryonic lethal phenotype, failing to develop past embryonic days 15.5. At embryonic day 13, homozygotes are normal in size and morphology, but have 10 fold lower hematocrit levels, due to anemia caused by diminished fetal hepatic erthropoiesis. In vitro examination of cells from the para-aortic, splanchnopleural (P-Sp) and aorta-gonad-mesonephros regions reveals defective hematopoiesis. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of fetal definitive hematopoiesis. | ||
| 002102 | B6.129S2-Rb1tm1Tyj/J | Repository-Cryopreserved |
| Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. 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. This is the case for this strain. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 008434 | B6.129S2-Seletm1Hyn/J | Repository-Cryopreserved |
| 002948 | B6.129S4-Tal1tm1Sho/J | Repository-Cryopreserved |
| Mice homozygous for the Tal1tm1Sho mutation die between embryonic day 9.5 and 10.5. There is a complete absence of blood formation; no hematopoietic cells could be identified by appearance, histology, colony assays, or RT-PCR for lineage-specific products. | ||
| 004069 | B6.129S6-Crebbptm1Dli/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Crebbp gene are embryonic lethal, dying at about embryonic day 10.5 exhibiting open neural tube defects. Heterozygous mice though viable and fertile, are subject to early growth retardation, craniofacial abnormalities and often fail to thrive. Heterozygous mice are also subject to age-dependent splenomegaly and irregular hematopoiesis. By three months of age, the abundance of all hematopoietic cell types is significantly diminished. Older mice (10-21 months) are more prone to develop hematologic malignancies than wildtype mice. | ||
| 006199 | B6.129X1-Fzd9tm1Uta/J | Repository-Cryopreserved |
| Mice homozygous for this targeted mutation are viable and fertile, with no gross anatomical abnormalities. Endogenous transcripts are absent in skeletal muscle and testis. Homozygotes exhibit abnormal B-cell development, reduced survival, lymphadenopathy secondary to accumulation of plasma cells, splenomegaly, and accelerated thymic atrophy. Mutant mice do not exhibit any obvious features of Williams-Beuren syndrome (WBS). These mice may be useful in studies of hematopoietic/lymphoid development and function (including B-cell and T-cell development), plasma cell homeostasis, and the Wnt/frizzled signaling pathway. 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. This is the case for this strain. It should be noted that the phenotype could vary from that originally published. We will modify the strain description if necessary as
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| 002306 | B6.Cg-an/BrkJ | Repository-Cryopreserved |
| 002727 | B6;129-Ahrtm1Bra/J | Repository-Cryopreserved |
| Mice homozygous for the Ahrtm1Bra targeted mutation are viable and fertile. Homozygotes do not respond to aryl-hydrocarbon receptor agonists. They show reduced liver weight (25% decrease) delayed extramedullary hematopoiesis, and transient hepatic microvesicular steatosis. | ||
| 004338 | B6;129-E2f2tm1Zubi/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable and normal in size. No gene product, mRNA or protein, was detected. At age 15 months mutant mice have a 27% survival rate due to diffuse autoimmune disease that resembles systemic lupus erythematosus (SLE). The phenotype includes splenomegaly by 8-12 weeks of age, glomerulonephritis, accumulated inflammatory infiltrates in the lung, liver, and skin abnormalities such as hair loss, skin wounds, erythema. Anti-dsDNA antibodies are detected in the serum. There are an increased number of mature CD8+ thymocytes and an abnormal accumulation of CD8+ Cd44high Cd69- T effector/memory cells that are autoreactive in peripheral lymphoid organs. E2F2 deficient mice appear to have normal negative selection of thymocytes but demonstrate defects in peripheral tolerance of T lymphoctes (especially Cd8+ T cells) leading to progressive autoimmune disease. This mutant mouse strain may be useful in studies of autoimmunity and may serve as model
..... For more information please see the full descriiption on the strain data sheet | ||
| 006099 | B6;129-Sfpi1tm1.2Dgt/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size, and do not display any gross physical or behavioral abnormalities. Endogenous protein expression is unaffected by the loxP sequences flanking an upstream regulatory region (URE). When bred to mice with a cre recombinase gene under the control of a promoter of interest, the URE of the targeted gene is deleted in the tissue of interest. Deletion of this "floxed" URE may be useful in studying T cell lymphoma, AML and other cancers, as well as transcription factors, hematopoiesis, and development of multiple cell lineages. | ||
| 003213 | B6;129S-Eportm1Liz/J | Repository-Cryopreserved |
| Mice lacking Epor died in utero at embryonic day 11 - 12.5 with severe anemia. Embryonic erythropoiesis was markedly diminished, while fetal liver hematopoiesis was blocked at the proerythroblast stage. Homozygotes are not viable. | ||
| 003807 | B6;129S-Seletm1Hyn Selltm1Hyn Selptm1Hyn/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Sele, Sell and Selp genes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities at birth. As mice mature, however, they become susceptible to mucocutaneous infections that eventually lead to death. No Sele, Sell or Selp gene products (mRNA or protein) are detected. Leukocytes from these mice exhibit a deficiency in the ability to interact with, and roll along, the venular wall endothelium. This deficiency in the crucial first step of leukocyte recruitment to surrounding tissues in response to infection or injury contributes to an elevated leukocyte count in the peripheral blood. Delays in neutrophil and eosinophil recruitment to the peritoneum in response to thioglycollate and ragweed allergen, respectively, have been observed, specifically. These mice are suitable for use in research applications studying leukocyte homeostasis, infectious diseases and inflam
..... For more information please see the full descriiption on the strain data sheet | ||
| 003806 | B6;129S-Seletm1Hyn Selltm1Hyn/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Sele and Sell genes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Sele or Sell gene products (mRNA or protein) are detected. A slightly diminished response in neutrophil recruitment to the peritoneum in response to thioglycollate is observed, as is a diminished ability to interact with the venular endothelium resulting in increased "rolling" along the vessel wall. These mice are suitable for use in research applications studying leukocyte homeostasis, infectious diseases and inflammation. | ||
| 002265 | B6;129S2-Bcl2tm1Sjk/J | Repository-Cryopreserved |
| Mice homozygous for the Bcl2tm1Sjk targeted mutation appear normal at birth; however, growth retardation is evident by one week of age with considerable heterogeneity in weight compared to normal wildtype siblings (30% to 90%). There is some pre-weaning loss. Homozygotes succumb to renal failure as a result of polycystic kidney disease. Hematopoiesis, including lymphocyte differentiation is initially normal but the thymus and spleen decrease in size due to increased apoptosis. The coat color of homozygotes turns grey with the second hair follicle cycle. | ||
| 002916 | B6;129S2-Seletm1Hyn Selptm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for both the Seletm1Hyn Selptm1Hyn mutations are viable and fertile. They are characterized by leukocytosis, spontaneous bacterial infections, dermatitis and defective leukocyte recruitment in many models of inflammation. | ||
| 002915 | B6;129S2-Seletm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Seletm1Hyn targeted mutation are viable and fertile. Homozygous mutant mice show only subtle defects in leukocyte recruitment, unless P-selectin (Selp) is also ablated or blocked with antibody. | ||
| 002430 | B6;129S4-Tal1tm1Sho/J | Repository-Cryopreserved |
| Mice homozygous for the Tal1tm1Sho mutation die between embryonic day 9.5 and 10.5. There is a complete absence of blood formation; no hematopoietic cells could be identified by appearance, histology, colony assays, or RT-PCR for lineage-specific products. | ||
| 006147 | B6;FVB-Tg(Sfpi1,-EGFP)7Dgt/J | Repository-Cryopreserved |
| Hemizygous mice are viable and fertile with no gross or behavioral abnormalities. Flow cytometry identifies enhanced green fluorescent protein (EGFP) reporter expression in a pattern similar to the endogenous gene; in bone marrow, high expression is observed in myeloid cells, and to a lesser degree in B lymphocytes and erythroid cells. Expression in spleen is consistent with B cells and natural killer cells, while no expression is observed in thymus. These mice may be useful in studies of hematopoietic cell development, transcription factor pathways, and leukemia (including erythroleukemia). | ||
| 007687 | BKa.Cg-Sox17tm1Sjm Ptprcb Thy1a/J | Repository-Cryopreserved |
| Mice that are homozygous for this targeted mutation are embryonic lethal around E13.5. No gene product (mRNA) is detected by RT-PCR of whole homozygous embryos. Embryos exhibit growth retardation, show severe posterior body patterning abnormalities, have hematopoietic defects and lack definitive hematopoietic stem cells. Heterozygous and homozygous mice express EGFP in cells expressing this gene, therefore, these mice may be useful to understand the gene's activity in various cell types. This strain may be helpful in studies of fetal hematopoietic stem cells and hematopoiesis. | ||
| 007686 | BKa.Cg-Sox17tm2Sjm Ptprcb Thy1a/J | Repository-Cryopreserved |
| These mice possess loxP sites on either side of the exon 3-5 region of the targeted gene. Mice homozygous for this allele are viable and fertile and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the gene. When the floxed allele is excised by crosses with a Tie2 (endothelial-specific receptor tyrosine kinase)-Cre mouse (Stock No. 004128) and the Sox17 targeted mutant EGFP reporter strain (Stock No. 007687), mutants are embryonic lethal around E13.5. Mutant embryos have severe hematopoietic failure and lack definitive hematopoietic stem cells.
When the floxed allele is excised by Mx1 (myxovirus (influenza virus) resistance 1)-Cre (Stock No. 003556) and the Sox17
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| 008438 | C.129S2(B6)-Seletm1Hyn Selptm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for both the Seletm1Hyn Selptm1Hyn mutations are viable and fertile. They are characterized by leukocytosis, spontaneous bacterial infections, dermatitis and defective leukocyte recruitment in many models of inflammation. 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. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 008435 | C.129S2(B6)-Seletm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Seletm1Hyn targeted mutation are viable and fertile. Homozygous mutant mice show only subtle defects in leukocyte recruitment, unless P-selectin (Selp) is also ablated or blocked with antibody. 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. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 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. | ||
| 002546 | C3Ou.129S2-Rb1tm1Tyj/J | Repository-Cryopreserved |
| Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. 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. This is the case for this strain. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 003395 | CD1-Tg(Igh-HOX11)11Idd/J | Repository-Cryopreserved |
| This transgenic strain is a good tool for developing therapies for non-Hodgkins lymphoma. Heterozygous mice appear normal and healthy at birth but die in their second year of life. More than 85% of of these mice die from mature B cell lymphoma. No homozygous TLX1 mice were identified in offspring of heterozygous matings, suggesting that homozygotes are not viable. | ||
| 002900 | FVB.129S2(B6)-Rb1tm1Tyj/J | Repository-Cryopreserved |
| Mice homozygous for this targeted mutation die in utero. Homozygous embryos are morphologically indistinguishable from normal embryos at 12.5 days post coitum, but then die between 13.5 d.p.c and 14.5 d.p.c. Defects are seen in fetal liver hematopoiesis as well as in lens and nervous system development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. 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. This is the case for this strain. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 006209 | FVB.Cg-Tg(Tal1-tTA)19Dgt/J | Repository-Cryopreserved |
| Hemizygotes are viable, fertile, normal in size, and do not display any behavioral abnormalities. Hemizygotes express tetracycline-controlled transactivator protein (tTA) in bone marrow hematopoietic stem cells (HSC) and in common myeloid progenitors (CMP)). tTA activity also is detected in lung. Little to no tTA activity is detected in thymus, lymph node, intestine or spleen. When bred to other transgenic mice carrying a gene of interest coupled to a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene in the bitransgenic offspring can be induced by withdrawal of tetracycline or doxycycline. This strain represents an effective tool for generating bitrangenic animals to study inducible gene expression in blood stem and progenitor cells.
These mice were originally designed to be bred with transgenic mice harboring a TRE-BCR-ABL1 transgene (Stock No. 006202), creating bitransgenic offspring as a mo
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| 003256 | STOCK Fgf2tm1Doe/J | Repository-Cryopreserved |
| Mice homozygous for the Fgf2tm1Doe targeted-mutant allele have low blood pressure, presumably resulting from low vascular tone, increased megakaryocyte colony stimulation activity-induced megakaryocyte colony formation; increased platelet counts, and decreased IL3-induced colony formation. Vessel layer hypertrophy following vessel injury is not altered in the absence of FGF2. Cardiac hypertrophic response to induced high blood pressure is severely blunted in the absence of FGF2. Both sexes of the mutant exhibit no discernible morphologic or behavioral defects and have a normal life span. Both sexes are fertile and fecundity is normal. | ||
| 004655 | STOCK Gata1tm2Sho/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Reduced levels of gene product (mRNA) is detected by RT-PCR analysis. Mutant mice are thrombocytopenic and anemic at birth. Adult mutant mice have enlarged spleens and exhibit thrombocytopenia due to arrested megakaryocyte maturation which results in increased megakaryocytes in spleen and bone marrow. Platelet number in adult mutant mice is only 10% of wildtype. Erythroblast and mast cell differentiation is defective as indicated by increased apoptotic rates and accumulation of progenitors. Mutant mice display an enhanced response and recovery to experimentally induced acute and chronic erythropoiesis stimulation. At 15 months of age, homozygous female and heterozygous male mutant mice begin to develop idiopathic myelofibrosis-like symptoms including: anemia, tear-drop poikilocytes, progenitor cells in the blood, collagen fibers and o
..... For more information please see the full descriiption on the strain data sheet | ||
| 003534 | STOCK Inpp5dtm1Dmt/J | Repository-Cryopreserved |
| Inpp5d (commonly called SHIP) -deficient mice are viable and fertile. However, fertility rate is 10% lower in homozygotes and lifespan is shortened in comparison to controls. Inpp5d -deficient mice exhibit dramatic chronic hyperplasia of myeloid cells resulting in splenomegaly, lymphadenopathy and myeloid infiltration of vital organs. Histological and flow studies demonstrate a substantial increase in granulocyte-macrophage/monocyte populations in bone marrow, spleen and lymph nodes. Spleens and lymph nodes are severely enlarged compared to wildtype. The difference in spleen size is apparent as early as 4 weeks of age, and by 16 weeks of age, spleens from null mice are 10 fold greater than those of wildtype mice. Neutrophils and bone marrow-derived mast cells from these mice appear to be less susceptible to apoptotic stimuli. | ||
| 006083 | STOCK Sfpi1tm1.3Dgt/J | Repository-Cryopreserved |
| Mice homozygous for this targeted deletion are viable and fertile as young animals. Mice on this stock (predominantly 129Sv) background often die between 3-8 months of age of a rapidly developing T cell lymphoma (64% penetrance) or between 6-12 months of acute myeloid lymphoma (AML) (29% penetrance). Homozygotes (termed PU.1 knockdown or UREdelta) have an 80% reduction of endogneous gene expression. This is associated with an accumulation of hematopoietic stem cell precursor cells and neutrophils in bone marrow and spleen. Bone marrow cells from homozygous mice have abnormal responses to myeloid cytokines, and malignant transformation is associated with clonal chromosomal abnormalities. Homozygous mice have abnormal B- and T-cell populations and lineage commitment. These mice may be useful in studing T cell lymphoma, AML and other cancers, transcription factors, and development of multiple cell lineages. Of note, the latency and penetrance of disease is slightly different from those
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| 002307 | WB.Cg-an/BrkJ | Repository-Cryopreserved |
(70 stocks) Back to Top
IMPORTANT NOTE: Price information is on the strain data sheet which can be viewed by clicking on the strain name.
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 003947 | B6.129P2-Epb4.2tm1Llp | Research Strain |
(1 stocks) Back to Top
How to Register Interest
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
Select the strain name to link to the strain data sheet.
New Strains Under DevelopmentThe Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
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It is VERY IMPORTANT that you register interest in strains Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.
- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
These strains are designated as: "Under Development for Distribution Colony"- Strains that will be made available through the Cryopreservation Repository.
These strains are designated as: "Under Development for Cryopreservation Repository"
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