Search Criteria: Research Area is "Cell Biology Research"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 001801 | C57BL/10ScSn-Dmdmdx/J | Level 2 |
| The X-linked dystrophin gene (Dmd) is highly expressed in muscle cells and encodes a cytoskeletal protein which localizes to the inner face of the sarcolemma. Dystrophin molecules bind to cytoskeletal F-actin and transmembrane beta-dystroglycan as part of a complex, multimolecular unit that mediates signaling between the intracellular cytoskeleton and the extracellular matrix. The structure and localization also suggest that dystrophin is important for stabilizing the plasma membrane, particularly during contraction. The mdx mutation of Dmd is recessive and heterozygous females are visually indistinguishable from wild-type mice. Females homozygous and males hemizygous for the Dmdmdx allele retain a normal lifespan and can survive up to two years. Like human patients who suffer from one of the most common neuromuscular diseases, Duchenne muscular dystrophy (DMD), the Dmdmdx mutants do not express dystrophin and therefore have been
..... For more information please see the full descriiption on the strain data sheet | ||
| 004650 | B6.129-Tlr2tm1Kir/J | Level 4 |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of isolated peritoneal macrophages. Bone marrow derived macrophages do not respond to spirochete (Borrelia burgdorferi) lipoprotein challenge, although non-lipoprotein sonicate stimulates activation. Arthritis due to B. burgdorferi infection, as assessed by rear ankle swelling, is more severe in mutant mice. Tissues of infected mutants can contain up to 100 times higher bacteria levels than those found in wildtype littermates. Elevated spirochete numbers persist 8 weeks post-infection. Homozygotes do not produce TNF-alpha or IL-6, and do not develop symptoms of illness when treated with leptospiral (Leptospira interrogans) lippolysaccharide (LPS). This mutant mouse strain may be useful in studies of host response to bacterial endotoxins such as septic shock. | ||
| 001021 | B6Smn.C3-Faslgld/J | Level 4 |
| Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasllpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. 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. The Cryaa
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| 006373 | 129-Braftm1Sva/J | Repository- Live |
| Homozygous "floxed B-raf" (B-raff/f) mice are viable and fertile with normal B-raf protein expression. When bred to mice expressing Cre recombinase under the control of a promoter of interest, exon 12 of the targeted gene is deleted in the tissue of interest. These mutant mice may be useful in neurological studies such as Ras/Raf and MEK/ERK signaling, synaptic (neural) plasticity, learning and memory. For example, when crossed to a strain expressing Cre recombinase in nervous tissue (see Stock No. 003771), this mutant mouse strain may be useful in studies of neuron development. For example, when crossed to a strain expressing interferon inducible Cre recombinase (see Stock No. 003755), this mutant mouse strain may be useful in studies of extraembryonic mammmalian development. | ||
| 006053 | 129-Gt(ROSA)26Sortm1Luo/J | Repository- Live |
| MADM-GG mice are viable with no gross behavioral or observable abnormalities. Regardless of Cre-recombination, these mice express EGFP as their N- and C-terminal coding sequences are interrupted by the beta-actin intron in-frame. High EGFP expression in every cell can be visualized in vivo and in fixed samples. These mutant mice are a control EGFP-expressing strain for use with MADM (mosaic analysis with double markers) mice (see Stock No. 006041 [MADM-GR (EGFP/Dsred2)] and Stock No. 006067 [MADM-RG (Dsred2/EGFP)]). Using the MADM system, a researcher can generate genetic mosaics in which an individual organism contains somatic cells of different genotypes. This allows the researcher to ascertain lineal relationships and pleiotropic gene function in multicellular organisms. These mice may also be useful in studies of cell differentiation and mitosis.
Mice harbor
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| 006067 | 129-Gt(ROSA)26Sortm2Luo/J | Repository- Live |
| MADM-RG mice are viable with no gross behavioral or observable abnormalities. Homozygous females produce less pups to weaning age compared to heterozygotes. These mutants are designed for MADM (mosaic analysis with double markers), and must be crossed to mice harboring a reciprocal mutation at the same locus (see Stock No. 006041 or Stock No. 006075, MADM-GR (EGFP/Dsred2)). The resulting offspring have one copy of each reciprocal mutation on homologous chromosomes ("trans-heterozygous") and must next be bred to a Cre-expressing strain for fluorescent protein expression. Prior to Cre-recombination, double mutant mice do not have colored cells: the chimeric genes do not produce functional proteins because their coding sequences are interrupted by the beta-actin intron in different reading frames. After DNA replication (G2 phase) in double mutant mice, Cre-recombinase introducti
..... For more information please see the full descriiption on the strain data sheet | ||
| 004293 | 129-Shhtm2Amc/J | Repository- Live |
| Mice that are homozygous for the Shhtm2Amc targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This conditional mutant contains two loxP sites flanking exon 2 of the targeted allele. Cre-mediated recombination excises exon 2 and some surrounding intronic sequence, generating a null allele. When the conditional mutant is crossed with a ubiquitously-expressing Cre recombinase carrier to remove Shh activity in the early embryo, the resulting phenotype resembles the Shh null mutation. These conditional mutant mice may be mated to strains expressing Cre recombinase to study the effects of temporal and tissue-specific ablation of the targeted allele. This mutant mouse strain represents a model that may be useful in studies of developmental defects resulting from disruption of Shh-dependent pathways.
When bred to a strain expressing Cre recombinase under the control of a tet
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| 006050 | 129-Sirt6tm1Fwa/J | Repository- Live |
| Homozygous neonates are smaller than their wildtype and heterozygous littermates. They develop normally until approximately 21 days of age, when they develop an acute and rapid, aging-like degenerative pathology resulting in death by postnatal day 24. Homozygous mutant mice exhibit subcutaneous fat loss, lordokyphosis (hunchbacked spine) with osteopenia (30% loss of bone mineral density), colitis, and severe lymphopenia due to increased lymphocyte apoptosis. At day 12, mice have reduced insulin-like growth factor I (IGF-1) levels in serum, and develop severe hypoglycemia. Mouse embryonic fibroblasts (MEFs) prepared from homozygous embryos exhibit reduced proliferation, defective base excision repair function, as indicated by increased sensitivity to alkylating agents and ionizing radiation, and increased chromosomal aberrations. The donating investigators report that no gene product (mRNA or protein) is detected by RT-PCR or immuoblot analysis of tissues, MEFs or embryonic stem cells f
..... For more information please see the full descriiption on the strain data sheet | ||
| 007664 | 129S-Efnb1tm1Sor/J | Repository- Live |
| These mice possess loxP sites flanking exons 2 through 5 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 2 through 5 deleted in the cre-expressing tissue(s). These Efnb1 conditional mutant mice may be useful in studying cellular signaling in embryonic development and adult mice; specifically receptor tyrosine kinases. For example, when crossed to a strain expressing Cre recombinase in epiblast-derived tissues (see Stock No. 003755), this mutant mouse strain may be useful in embryogenesis research. | ||
| 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. | ||
| 007209 | 129S-Schip1Gt(ROSA)77Sor/J | Repository- Live |
| Homozygotes occur at lower than Mendelian ratio (19%), and 20% die by age 1 week. Heterozygotes viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit abnormalities in neural crest-derived and thoracic skeleton development, and palate bone fusion. These Schip1-mutant mice may be useful in studying cellular signaling in development and 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. | ||
| 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 | ||
| 006661 | 129S.B6-Tg(KRT14-RAF1/ESR1)1Pkha/J | Repository- Live |
| Mice hemizygous for this "K14-Raf:ER" transgene are viable and fertile. Inducible expression of the human Raf1(Raf-1 [DD]):estrogen receptor (ER) fusion protein is observed in the epidermis following topical application of 4-hydroxytamoxifen (4OHT). Prolonged (4 weeks) induction of human Raf-1[DD] activity promotes the undifferentiated, proliferative phenotypic characteristics observed in epidermal cancer; including hyperplasia, increased mitotic index, decreased expression of differentiation markers and increased expression of beta-1 and beta-4 integrin subunits. Raf-1[DD]-induced skin abnormalities are entirely reversed within one month after 4OHT cessation. These mice have a similar 4OHT-inducible skin phenotype as the transgenic mice expressing human H-RasG12V (Stock No. 006403) or human Mek1R4F (Stock No. 006822), and may be useful in studies of the
..... For more information please see the full descriiption on the strain data sheet | ||
| 001649 | A.BY H2bc H2-T18f/SnJ-Dstncorn1/J | Repository- Live |
| Mice homozygous for the recessive Dstncorn1 mutation have abnormally proliferative basal corneal epithelial cells. Focal areas of corneal epithelial hyperplasia are found by one week of age, and neovascularization is found by 14 days of age when the eyes open. This neovascularization, which progresses during the first two months of age, is not found in mice homozygous for the Dstncorn-2J allele (which is a point mutation leading to a change in a single amino acid residue). In both mutants the corneal epithelial cells show increased levels and altered organizational pattern of filamentous actin. The areas of thickened cortical epithelia yield a roughened, opaque corneal surface. At 4 weeks of age in Dstncorn1 homozygotes, expression of keratin 14 and involucrin extend into the suprabasal layer in the areas of hyperplastic corneal epithelia. There is also an increase in the levels of expression of cofilin 1, lumican and kerat
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| 006102 | B10.Cg-H2k Tg(Il2/NFAT-luc)83Rinc/J | Repository- Live |
| Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator reports that homozygous females in their colony are subfertile. These transgenic mice express luciferase under the regulation of the Il2 minimal promoter and 3 binding sites for the NFAT inducible nuclear factor involved in the regulation of interleukin-2 and other cytokine expression. Luciferase activity in these transgenic mice identifies NFAT-mediated transcription. These NFAT-luc transgenic mice may be useful be useful as reporters for NFAT-mediated expression during thymocyte development and selection and in studies related to signal transduction, apoptosis, and transcriptional regulation. | ||
| 006100 | B10.Cg-H2k Tg(NFkB/Fos-luc)26Rinc/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Mutant mice have the luciferase gene driven by two copies of the NF-kappaB (NF-kB or NFkB) regulatory element. The presence of nuclear NF-kB DNA binding activity (as detected by electrophoretic mobility shift assay [EMSA]) is consistent with luciferase reporter activity; these reporter mice identify NF-kB transcriptional activity in any tissue. These transgenic mice may be useful in studies of immunology, cellular signaling, signal transduction, apoptosis, and transcription factor function. | ||
| 000578 | B6 x STOCK Tyrc-ch Bmp5se +/+ Myo6sv/J | Repository- Live |
| Mice homozygous for the Snell's waltzer spontaneous mutation (Myo6sv) show to a marked degree the typical circling, head-tossing, deafness, and hyperactivity of other mutant mice of this type. Homozygous mutant mice are recognizable by the age of 1 week. The abnormalities of the inner ear consist of degeneration of the entire neuroepithelium comprising the organ of Corti, the saccular and utricular maculae, and the cristae of all three semicircular canals. Although viability of homozygotes is nearly normal, breeding ability is reduced and males are more reliable breeders than females.
Specific cytoskeletal components are critical for specific cellular structures. The microvilli of intestinal brush border cells in Myo6sv homozygotes are shorter than normal. While myosin 6 is not critical for the development of hair cell stereocilia, it is essential for their maintenance. At birth the stereocilia appear nearly normal with only occasional stereocil
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| 008149 | B6(Cg)-Snord116tm1.1Uta/J | Repository- Live |
| Mice homozygous for this Snord116del (1-loxP or knockout) allele are viable and fertile. As the Snord116 gene cluster is imprinted and expressed only from the paternal allele, mice with paternal inheritance of the deletion lack expression of the targeted Snord116 small nucleolar RNAs (snoRNAs) gene cluster in brain tissues. Similarly, paternal transmission of the mutant allele is required to obtain the mutant phenotype in offspring. Affected heterozygotes (paternal deleted/maternal wildtype) recapitulate a subset of Prader-Willi syndrome (PWS) characteristics, including early-onset postnatal growth retardation, delayed sexual maturation, increased anxiety, motor learning deficit and hyperphagia (but not obesity). Other reported abnormalities include altered metabolic fuel usage, prolonged meal time, and increased levels of circulating ghrelin. These Snord116del mice may be useful in studying growth and feeding regulation, mechanisms of obesity, and pa
..... 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. | ||
| 005319 | B6.129-Cdh1tm2Kem/J | Repository- Live |
| These mice possess loxP sites flanking exons 6 to 10 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. | ||
| 006945 | B6.129-Chst3tm1Tmu/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 analysis of total spleen RNA. Protein activity is not detected in spleen, lung peripheral lymph nodes, mesenteric lymph nodes or Peyer's patches. At 5 to 6 weeks of age, homozygotes have a reduced number (approximately 68% of wildtype levels) of naive T cells in the spleen. Chondroitin sulfate D is not detected in the brains of adult homozygotes or in the telencephalon and cartilage of homozygote embryos aged 12.5 and 15.5 embryonic days. Brain development is not impaired in mutant mice. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function. This strain was transferred from the collection of the Consortium for Functional Glycomics. | ||
| 006910 | B6.129-Crkltm1Hkp/J | Repository- Live |
| While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die in utero. Immunoblots from homozygous tissues show no protein expression from the targeted gene. The prenatal lethality exhibited by homozygotes on this C57BL/6J congenic background (and also on a 129Sv genetic background) likely results from heart, liver, and placental defects. Please note that homozygous mutants on a mixed/outbred genetic background (129/Sv X Black Swiss) are viable and fertile. These mutant mice may be useful in studying the role of Crkl tyrosine-phosphorylation in Bcr/Abl (Philadelphia chromosome) chronic myelogenous leukemia (CML), acute lymphoblastic leukemia (ALL), Digeorge Syndrome (DGS) and Velocardiofacial Syndrome. | ||
| 006939 | B6.129-Fut1tm1Sdo/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. Alpha(1,2)fucosylated glycans are not detected in the epididymis of homozygotes. Fucosylated glycolipids (fucosyl GA1) are not detected in the pancreatic acinar glands of homozygotes. Homozygotes exhibit delayed maturation of nerve fibers in the glomerular layer of the olfactory bulb due to absence of cell surface carbohydrate, blood group H carbohydrate, expression in primary sensory neurons. The Donating Investigator reports that the beta-galatosidase is expressed. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, and olfactory nerve pathway development. This strain was transferred from the collection of the Consortium for Functional Glycomics. | ||
| 006080 | B6.129-Gt(ROSA)26Sortm2Luo/J | Repository- Live |
| MADM-RG mice are viable with no gross behavioral or observable abnormalities. Homozygous females produce less pups to weaning age compared to heterozygotes. These mutants are designed for MADM (mosaic analysis with double markers), and must be crossed to mice harboring a reciprocal mutation at the same locus (see Stock No. 006041 or Stock No. 006075, MADM-GR (EGFP/Dsred2)). The resulting offspring have one copy of each reciprocal mutation on homologous chromosomes ("trans-heterozygous") and must next be bred to a cre-expressing strain for fluorescent protein expression. Prior to Cre recombination, double mutant mice do not have colored cells: the chimeric genes do not produce functional proteins because their coding sequences are interrupted by the beta-actin intron in different reading frames. After DNA replication (G2 phase) in double mutant mice, Cre recombinase int
..... For more information please see the full descriiption on the strain data sheet | ||
| 006075 | B6.129-Gt(ROSA)26Sortm3Luo/J | Repository- Live |
| MADM-GR mice are viable with no gross behavioral or observable abnormalities. Homozygous mice have low fertility, while heterozygous mice have no reported fertility defects. These mutants are designed for MADM (mosaic analysis with double markers), and must be crossed to mice harboring a reciprocal mutation at the same locus (see Stock No. 006067 or Stock No. 006080, MADM-RG (Dsred2/EGFP)). The resulting offspring have one copy of each reciprocal mutation on homologous chromosomes ("trans-heterozygous") and must next be bred to a Cre-expressing strain for fluorescent protein expression. Prior to Cre-recombination, double mutant mice do not have colored cells: the chimeric genes do not produce functional proteins because their coding sequences are interrupted by the beta-actin intron in different reading frames. After DNA replication (G2 phase) in double mutant mice, Cre-recom
..... For more information please see the full descriiption on the strain data sheet | ||
| 006860 | B6.129-Ins2Akita Bdkrb2tm1Jfh/SmiJ | Repository- Live |
| Mice homozygous for the targeted mutation and heterozygous for the Ins2Akita spontaneous mutation are viable and fertile. Similar to mice only heterozygous for the Ins2Akita mutation, the double mutant mice are severely diabetic: their body weights are 70% of wildtype, they consume over 3-fold the normal amount of food, and their urinary output is approximately 20-fold more than that of wildtype mice. Double mutant mice have markedly enlarged kidneys. Urinary albumin excretion in double mutants is almost 4-fold that of either single mutant, and double mutants experience more severe nephropathy than mice that are heterozygous for the Akita mutation alone. Megsin and nephrin expression is markedly increased in double mutant mice when compared to wildtype or to mice with either single mutation alone. By 12 months of age, double mutant mice experience hair loss due to a reduction in hair follicle numbers and thinning of the dermis. Double mutants
..... For more information please see the full descriiption on the strain data sheet | ||
| 006335 | B6.129-Mgat5tm1Jwd/J | Repository- Live |
| No gene product (protein) is detected by Western blot analysis and enzyme activity is undetectable. Beta-galactosidase activity mimics endogenous gene expression patterns. Homozygotes exhibit abnormal increased leukocyte infiltration in kidney tissue, which is indicative of kidney autoimmune glomerulonephritis. Induced experimental autoimmune encephalomyelitis (EAE) and induced delayed-type hypersensitivity (DTH) responses are increased in homozygotes. Cultured splenocytes isolated from homozygotes produce 2 fold more IFN-gamma and 2 fold less IL4. Mutant mice exhibit delayed tumor progression when bred with oncomice (for example, when crossed to a polyomavirus middle T antigen expressing transgenic strain). Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator reports that homozygous females are not fertile. This mutant mouse strain may be useful in studies of glycosidi
..... For more information please see the full descriiption on the strain data sheet | ||
| 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. | ||
| 008233 | B6.129-Nrgntm1Kph/J | Repository- Live |
| Homozygous neurogranin-deficient (Ng-/-) mice are viable and fertile (although the donating investigator reports that homozygous females do not nurse their pups as well as wildtype or heterozygous mothers). Homozygotes have no mRNA or protein from the targeted gene observed in brain tissues. Expression of lacZ is observed in a manner consistent with the endogenous gene. Ng-/- mice exhibit impaired spatial learning, altered hippocampal short- and long-term plasticity (including long-term potentiation induction), and decreased activated CaMKII. Heterozygotes show similar, yet milder, effects. These neurogranin- (Ng or RC3)-mutant mice may be useful for neurological studies involving memory and learning, neuronal signaling pathways (including calmodulin, alpha-CaMKII, protein kinase A, protein kinase C, MAPK, and CREB), attention deficit-hyperactivity disorder (ADHD), and schizophrenia. | ||
| 006497 | B6.129-Skiltm2Spw/J | Repository- Live |
| Mice homozygous for this targeted mutation (called "Snoex1" in the primary reference) are viable and fertile with no reported gross morphological defects. Although the deletion of exon 1 leads to complete absence of the mature full-length protein in immunoblots of brain and embryonic tissues, a truncated 3'-end RNA species is derived from downstream coding sequence. Homozygotes exhibit T cell proliferation/activation defects, which can be rescued by treatment with anti-TGF-beta antibodies or exogenous interleukin-2. Homozygous deletion also results in increased sensitivity to TGF-beta and altered growth properties of cultured mouse embryo fibroblasts (MEFs). These mutant mice may be useful in studies of T cell activation, T cell receptor stimulation and TGF-beta signaling. | ||
| 004912 | B6.129P2-Akt1tm1Mbb/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and do not display any gross behavioral abnormalities. Homozygotes exhibit lower fertility. Female homozygotes do not nurse well; up to 50% perinatal mortality can occur. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of mouse embryonic fibroblasts. Homozygotes are only 80% of wildtype body weight at birth, and remain small. This mutant mouse strain may be useful in related to organismal growth. | ||
| 005530 | B6.129S-Ddit3tm1Dron/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 or protein) is detected by Northern or Western blot analysis of toxin challenged mouse embryonic fibroblasts (MEFs). MEFs and renal proximal tubular epithelial cells have decreased apoptosis in response to endoplasmic reticulum stress induced by the toxin, tunicamycin. Pancreatic islets cells are more resistant to nitric oxide induced apoptosis. MEFs exhibit a delayed onset of unfolded protein response (UPR) target gene expression when treated with tunicamycin. This mutant mouse strain may be useful in studies of apoptosis and pathogenesis due to endoplasmic reticulum stress. | ||
| 005960 | B6.129S-Pecam1Gt(VICTR20)12Lex/J | Repository- Live |
| Mice that are homozygous for the gene-trapped allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by immunofluorescence in aorta endothelium from homozygotes, and endothelial nitric oxide synthase isoform (eNOS) is not detected in cell to cell junctions between aorta endothelial cells in these mice. Isolated skeletal muscle arterioles from homozygous mutant mice exhibit reduced vessel dilation and no significant change in wall shear stress responses when intraluminar flow is increased. This mutant mouse strain may be useful in studies of cellular adhesion, vascular integrity and physiology. | ||
| 005763 | B6.129S1-Nod2tm1Flv/J | Repository- Live |
| Homozygous mice are viable and fertile with normal lymphoid and myeloid cellularity and no intestinal inflammation up to 6 months of age. Homozygotes do not express the targeted gene in spleen or intestinal crypts. Null mice, as well as antigen presenting cells derived from them, lack the protective immunity (IgG1, interleukin-6, and NF-kappaB-related responses) normally afforded by endogenous protein recognition of its ligand, bacterial muramyl dipeptide (MDP). Mice homozygous for the mutation have increased susceptibility to oral (intragastric) bacterial challenge and diminished cryptdins. This mouse may be useful in studies of Crohn's disease and other inflammatory bowel diseases, innate immunity, signal transduction, and bacterial susceptibility. | ||
| 006144 | B6.129S2(C)-Itgaetm1Cmp/J | Repository- Live |
| Mice that are homozygous for this targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No endogenous gene expression is detected in intraepithelial lymphocytes by FACS analysis or on TGF-beta1-treated splenocytes by immunoprecipitation. Homozygous null mice exhibit reduced numbers of intestinal intraepithelial lymphocytes and lamina propria lymphocytes. These mice may be useful in studies of the immune system, including T cell function. 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 become available. | ||
| 005977 | B6.129S2(C)-Stat6tm1Gru/J | Repository- Live |
| Homozygous mice are viable and fertile with no behavioral abnormalities. Homozygotes do not express the endogenous protein in thymus and peripheral lymphoid organs. In contrast to controls, IL-4 treated lymphocytes show no induction of MHC class II or IL-4 receptor genes and have severly impaired proliferative responses. Further, homozygous mice have a defective IgE response. While T-helper 1 (Th1) cell differentiation is unimpaired in homozygous splenocytes, Th2 cell differentiation is almost completely abrogated despite IL-4 or IL-13 incubation. Myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) is more severe in homozygous mice compared to wildtype. This mouse may be useful in studies of Th2 cell differentiation, Th2-mediated diseases, asthma, cytokine/chemokine function, signal transduction and transcription factors, and diseases of the central nervous system such as multiple sclerosis. | ||
| 006141 | B6.129S2-Thbs1tm1Hyn/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile, with an approximate 20% decrease in embryo/neonate viability and a mild and variable lordotic curvature of the spine apparent from birth. Homozygous mice have an abnormal, but no full length transcript in multiple tissues. Western analysis confirmed the absence of the protein in platelets. Homozygotes exhibit an increase in the number of circulating white blood cells. During the first four to ten weeks of life, homozygotes exhibit patches of acute and organizing pneumonia. At later time points, there is considerable hyperplasia of the various epithelial cell lineages. Mutant mice also have an increased number of retinal endothelial cells and inappropriate remodeling and maturation of retinal vasculature following injury. On the FVB/N background, spontaneous tumor growth and vasculature are significantly increased compared to wildtype. Mutant mice may be useful in studies of inflammatory responses in the lungs, eye, and
..... For more information please see the full descriiption on the strain data sheet | ||
| 002781 | B6.129S4-Cdkn1btm1Mlf/J | Repository- Live |
| Mice deficient in p27kip are viable and larger than normal littermates, with increased cellularity of all tissues. The thymus and spleen are particularly enlarged. Nullizygous adult mice have a shortened lifespan due to the growth of benign intermediate lobe pituitary tumors. Female mice are infertile, with a follicular phase ovulatory block. Large doses of exogenous gonadotropin induce ovulation, but both implantation and intrauterine embryonic development is impaired. The mice demonstrate haploid-insufficient susceptibility to the development of adenomas in the pituitary, intestine and lung adenomas following exposure to gamma irradiation or chemical carcinogens. | ||
| 006087 | B6.129S4-Cxcl10tm1Adl/J | Repository- Live |
| Homozygous mice are viable, fertile, and have no overt morphological or developmental abnormalities. No endogenous gene expression is observed in bone marrow-derived macrophages before or after IFN-gamma stimulation. Homozygous mice have defective T cell responses, including impaired proliferation and IFN-gamma secretion following antigenic challenge (129Sv background). In experimental models of T helper-1 (Th1)-mediated immune responses, homozygous-deletion leads to diminished immune function; contact hypersensitivity is reduced (129Sv background) and diminished threshold for disease expression in experimental autoimmune encephalomyelitis (EAE, human model of multiple sclerosis) (C57BL/6 background). After injection with a neurotropic coronavirus MHV, null mice (on a B6;129Sv background) exhibit impaired viral clearance, decreased CD4+/CD8+ infiltration into the brain, and are protected from viral-induced demyelination. Similarly, homozygous mice (on a C57BL/6 ba
..... For more information please see the full descriiption on the strain data sheet | ||
| 007671 | B6.129S4-Fgfr1tm5.1Sor/J | Repository- Live |
| These mice possess loxP sites on either side of exon 4 of the targeted gene. Exon 4 is the first exon found in all reported Fgfr1 splice variants. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 4 and the neomycin selection cassette deleted in the cre-expressing tissue(s). This mutant mouse strain may be useful in studies of fibroblast growth factor (Fgf) cellular signaling during embryonic development. | ||
| 003991 | B6.129S4-Itgamtm1Myd/J | Repository- Live |
| Mice that are homozygous for the Itgamtm1Myd targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No Itgam protein is detected in homozygous mutant neutrophils. Homozygous null animals have a diminished ability to clear thioglycollate-induced neutrophils, have reduced mast cell numbers in the dorsal skin and peritoneal wall/cavity, and are less susceptible to cerebral ischemia/reperfusion injury. Neutrophils from these animals are deficient at spreading, phagocytosing complement-opsonized particles, and in several Fc-mediated functions. They also exhibit impaired oxidative burst and a diminished responsiveness in LPS- and taxol-mediated gene expression. | ||
| 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. | ||
| 007669 | B6.129S4-Pdgfratm11(EGFP)Sor/J | Repository- Live |
| Mice homozygous for this knock-in targeted mutation have an embryonic lethal phenotype, with half of the embryos failing to survive past embryonic day 12.5 and the remainder failing to survive beyond embryonic day 15.5. These mice express the H2B-eGFP fusion gene from the endogenous Pdgfra locus. Fluorescence is detectable at embryonic day 4.5 in polar trophectoderm cells and at embryonic day 6.5 in the extraembryonic ectoderm. Expression of H2BGFP mimick the expression pattern of the endogenous gene. Homozygotes exhibit abnormal placenta development and placenta vasculature. This mutant mouse strain may be useful in studies of 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). | ||
| 008154 | B6.129S4-Pparatm1Gonz/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. An altered response to a group of compounds (peroxisome proliferators) that induce peroxisome proliferation and hepatocarcinogenesis is observed. No peroxisome proliferation response is detected when these mice are challenged with classical peroxisome proliferators. Typically, such a response includes hepatomegaly, peroxisome proliferation and transcriptional activation of a set of target enzyme genes. Accumulation of lipid droplets observed in liver tissue suggests that Ppara is involved in maintaining the homeostasis of hepatic lipid metabolism. Homozygotes exhibit increased gonadal adipose tissue stores, abnormal epidermal development and delayed wound healing. This mutant mouse strain may be useful in studies of lipid metabolism, cell proliferation, diabetes, obesity, and wound healing. | ||
| 005897 | B6.129S4-Ppardtm1Rev/J | Repository- Live |
| These mice possess loxP sites on either side of exon 4 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice with a cre recombinase gene under the control of a promoter of interest, exon 4 of the targeted gene is deleted in the tissue of interest, leading to premature termination of the translation product upstream of the DNA binding domain. This strain may be useful in generating tissue-specific mutants of the floxed allele for use in studies including embryo development, adipocyte physiology, fat metabolism and storage, inflammation, and cancer. | ||
| 006440 | B6.129S4-Ptentm1Hwu/J | Repository- Live |
| These mice possess loxP sites flanking exon 5 of the targeted gene. Mice homozygous for the"floxed" allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. 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 as published results become available. | ||
| 008236 | B6.129S4-Seletm1Dmil/J | Repository- Live |
| Mice homozygous for this E-selectin mutant allele (E-/-) are viable and fertile with normal circulating leukocyte and platelet profiles. While several transcripts are generated from the mutant locus (due to transcription from the endogenous promoter and/or bidirectional transcription initiated from the pgk promoter in the neo-resistance cassette), these frame-shifted transcripts are non-functional with several predicted stop codons. In contrast to wildtype mice, no protein product is detected in several tissues isolated from LPS-injected homozygous mice. Homozygous mice exhibit abnormal responses to inflammatory stimuli. E-selectin deficiency results in endostatin unresponsiveness (as shown in corneal angiogenesis (mixed B6;129 genetic background) and aortic explant (C57BL/6 congenic background) experiments). These E-selectin mutant mice may be useful in studying inflammation, leukocyte rolling, leukocyte-endothelial adhesion, angiogenesis, and cancer.
Of note, E-sel
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| 008076 | B6.129S4-Traf1tm1Tsi/J | Repository- Live |
| Mice homozygous for the TRAF1 mutant allele (TRAF1-/-) are viable and fertile. No protein expression from the targeted gene is observed in CD40-stimulated splenocytes isolated from homozygous mice. Homozygous mice on a C57BL/6 congenic background (B6-TRAF1-/-) have abnormal memory T cell survival and impaired influenza virus CD8 T cell responses. Activated B6-TRAF1-/- T cells accumulate increased levels of proapoptotic BH3-only family member Bim, particularly the most toxic isoform, Bims. The donating investigator reports that B6-TRAF1 mutant mice may be difficult to breed and gain more weight than BALB/c-TRAF1 mutant mice. Homozygous mice on a BALB/c congenic background (BALB/c-TRAF1-/-) exhibit acute liver injury and elevated serum liver enzymes following intratracheal TNF-alpha treatment. Furthermore, activated TRAF1-/- T cells have significantly increased expression of Th2 cytokines (IL-4, IL-5 and IL-13) that el
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| 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. | ||
| 006941 | B6.129S7-B4galt1tm1Shur/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Ninety percent of homozygotes die soon after birth or within two to three weeks of birth. Surviving homozygotes are initially smaller than wild-type or heterozygotes and exhibit abnormal skin and coat, but assume a normal growth rate and appearance at three to four weeks of age. No gene product (mRNA) is detected by RT-PCR analysis of homozygous tissues. Neither the long or short isoform is expressed. Beta 1,4-galactosyltransferase enzyme activity is undetectable except for residual activity in brain and testis. Galactose residues are absent from testis. Heterozygotes have an intermediate enzyme activity level. Surviving homozygotes exhibit puffy faces (hypothyroid myxedema), thin skin, decreased density of hair follicles, reduction in subdermal adipose tissue, delayed spermatogenesis and incomplete lung development. Histological an
..... For more information please see the full descriiption on the strain data sheet | ||
| 006943 | B6.129S7-B4galt1tm2Shur/J | Repository- Live |
| These mice carry a mutant allele that has a point mutation in the first translation initiation codon in exon 1, which initiates translation of the long isoform of beta 1,4-galactosyltransferase. The second translation initiation codon in exon 1 is not affected. These mice express only the shorter isoform of beta 1,4-galactosyltransferase. No long isoform protein is detected in mammary tissue by Western blot analysis. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Total Beta 1,4-galactosyltransferase activity is reduced to 72% of wildtype levels in mammary gland epithelial cells while activity on mammary epithelial cell surfaces is diminished by over 60%. Sperm and testis exhibit near wildtype levels of enzyme activity and glycoprotein galactosylation. The short isoform is expressed ectopically in sperm. Although able to undergo normal acrosomal exocytosis induced by calcium ionoph
..... For more information please see the full descriiption on the strain data sheet | ||
| 005257 | B6.129S7-Itgaltm1Bll/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 (protein) is detected by flow cytometry analysis of isolated neutrophils. Homozygotes exhibit peripheral leukocytosis due to an increased number of neutrophils. Isolated neutrophils do not exhibit increased adhesion to purified ICAM-1 or to endothelial cells. Neutrophil extravasation in response to TNF-alpha is diminished in mutant mice. Isolated neutrophils show decreased attachment strength to endothelial cells as revealed by shear stress detatchment tests. This mutant mouse strain may be useful in studies of leukocyte adhesion deficiency type I (LADI), and neutrophil adhesion and extravasation. | ||
| 002128 | B6.129S7-Itgb2tm1Bay/J | Repository- Live |
| Mice homozygous for the Itgb2tm1Bay mutation are viable and fertile. Homozygous mutant mice show an increased neutrophil count, and a decreased inflammatory response to peritonitis. Responses to delayed-type hypersensitivity and rejection of transplanted tissue are impaired. PLEASE NOTE: The Itgb2tm1Bay allele is not a null mutation; it is a hypomorphic mutation which results in the expression of very low levels of Itgb2 protein. This strain serves as a model for the moderate form of human CD18 deficiency. | ||
| 003819 | B6.129S7-Per2tm1Brd/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display gross physical or behavioral abnormalities. A mutant transcript, if translated, would generate a protein with an 87 amino acid deletion. When maintained in constant darkness, two phenotypic components are exhibited: a shortened circadian period and a loss of persistent circadian rhythmicity. When housed under constant light, homozygotes exhibit normal activity rhythm but a period length of less than 24 hours. Female homozygotes, 9-12 months of age, exhibit low reproductive success and produce small litters when compared to wildtype. This mutant mouse strain may be useful in studies related to the regulation of the sleep-wake cycle. | ||
| 006606 | B6.129X1-Camkk1tm1Tch/J | Repository- Live |
| Homozygotes are viable and fertile. Immunoblots using antibodies against both carboxy- and amino-terminal peptide sequences confirms the absence of wildtype protein in brain tissue. These CaMKKalpha-deficient mice exhibit deficits in context fear during both conditioning and long-term follow-up testing. This is accompanied by impaired activation of other kinases and substrates downstream in the Ca2+/calmodulin kinase (CaMK) cascade. Homozygous mice have normal long-term spatial memory formation, cued fear conditioning, long-term potentiation and anxiety-like behavior levels. These mutant mice may be useful in neurological studies involving the CaMK cascade, neuronal gene transcription, synaptic plasticity, contextual fear and long-term memory consolidation. | ||
| 007181 | B6.129X1-Notch1tm2Rko/GridJ | Repository- Live |
| Mice homozygous for this "floxed" Notch1 allele (fN1) are viable and fertile. These mice possess loxP sites on either side of exon 1 of the targeted gene. When bred to mice with a Cre recombinase gene, exon 1 of the targeted gene is deleted in the cre expressing tissue(s). These conditional knockout mice may be useful in generating tissue-specific mutants for studying the development of a wide range of tissues: for example, when crossed to a strain expressing Cre recombinase primarily in the nervous system (see Stock No. 003771), this mutant strain may be useful in studies of apoptosis in neural development.
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 modi
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| 005085 | B6.Cg-Cd44tm1Hbg/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 or protein) is detected. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. 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 f
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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 | ||
| 006366 | B6.Cg-Dicer1tm1Bdh/J | Repository- Live |
| These mice contain loxP sites on either side of exon 23. Homozygous mice are viable and fertile with no gross phenotypic or behavioral abnormalities. Expression of the targeted allele is indistinguishable from wild-type despite the frt-flanked neomycin cassette. Cre-mediated recombination (resulting in deletion of exon 23) in the germline leads to developmental arrest at embryonic day 7.5 (E7.5). Tissue specific deletion has been shown to result in loss of microRNA (miRNA) processing. Mutant mice can be used to generate cell/tissue-specific deletions of the endogenous gene for applications in embryonic development, translation, protein processing and miRNA/siRNA regulation of gene expression. For example, when crossed to a strain expressing Cre recombinase in mesenchyme (see Stock No. 005584), this mutant mouse strain may be useful in studies of limb morphogenesis. In an attempt to offer alleles on well-charac
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| 004993 | B6.Cg-F2rl1tm1Mslb/J | Repository- Live |
| Homozygous mice are viable and fertile with no spontaneous abnormal phenotype. No endogenous gene expression is observed in liver, airway epithelium, smooth muscle, or vasculature of the lungs. Ovalbumin-induced allergic inflammation of the airway is significantly diminished in mutant mice, showing reduced eosinophil, neutrophil, and lymphocyte infiltration into bronchoalveolar lavage fluid. IgE levels in serum of ovalbumin sensitized homoyzgous mice are reduced 4-fold compared to wild-type. This targeted mutant mouse may be useful in studies of asthma, allergic inflammation of the airway, inflammatory bowel disease, injury/trauma, G protein-coupled receptors, signal transduction, and a wide variety of immunological or inflammatory diseases. | ||
| 004088 | B6.Cg-Foxp3sf/J | Repository- Live |
| Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. Phenotypes associated with these mice include runting, scaly, crusty skin on the eyelids, ears and tails, dermal thickening, squinted eyes, cachexia, reddening and swelling of the genital papilla, and small testicles that are retained in the abdominal cavity. This disorder, which parallels X-linked autoimmunity-allergic disregulation syndrome (XLAAD) in humans, results in Coombs' test-positive anemia, hypergammaglobulinemia, a small, thin thymus, and lymphohistiocytic proliferation in the skin and lymphoid organs, with splenomegaly, lymphadenomegaly, and hepatomegaly. Foxp3sf/Y males generally die by 16-25 days of age. Transgenic expression of Foxp3 prevents scurfy disease in Foxp3sf/Y mice. Neonatal thymectomy of scurfy males ameliorates disease and increases lifespan; athymic nude Foxp3sf/Y mice do not develop scurfy
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| 006908 | B6.Cg-Ikbketm1Tman/J | Repository- Live |
| Homozygous IKKepsilon mutant mice are viable and fertile. Homozygous deletion results in a complete loss of the endogenous kinase function in lung, spleen, and embryonic fibroblasts. These mice have increased susceptibility to viral infection due to defective inteferon (IFN) signaling. These IKKepsilon mutant mice may be useful in immunological studies involving IFN signaling and host responses to infection. | ||
| 006580 | B6.Cg-Ins2Akita Ldlrtm1Her/J | Repository- Live |
| Mice homozygous for the Akita spontaneous mutation die postnatally, typically by 12 weeks of age. Independently, heterozygous Akita mutant mice are a model of insulin dependent diabetes mellitus (IDDM) with severe hyperglycemia (see the datasheet for Stock No. 003548 for additional information). LDLR-null homozygotes have elevated serum cholesterol levels (200-400 mg/dl) which can escalate to very high levels (> 2000 mg/dl) when the mice are fed a high fat diet. LDLR-deficient mice also are predisposed to develop atherosclerosis. These double mutant mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, hypercholesterolemia, and diabetes-related macrovascular complications. | ||
| 006337 | B6.Cg-Lgals1tm1Rob/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical abnormalities. No gene product (mRNA or protein) is detected by in situ hybridization of dorsal root ganglia and facial motorneuron nucleus and Western blot analysis of adult muscle tissue. Neonate mice homozygous for the mutation have abnormal axon targeting to the caudal region of the olfactory bulb. Mutant mice have fewer neural progenitor cells in the subventricular zone of the forebrain, although the number of apoptotic cells are not affected. Homozygotes exhibit hypoalgesia with a diminished nocifensive withdraw response to thermal testing. Immunohistological analysis of dorsal root ganglia from homozygotes reveals abnormal proportions of axon subpopulations and a larger number of myelinated axons. Mutant mice have a longer recovery of motorneuron function after experimental nerve injury. This mutant mouse strain represents a model that may be useful in stu
..... For more information please see the full descriiption on the strain data sheet | ||
| 006354 | B6.Cg-Lgals3tm1Poi Lgals1tm1Rob/J | Repository- Live |
| Mice that are homozygous for both of the targeted mutations are viable, fertile, normal in size and do not display any gross physical abnormalities. No gene product (protein) from either gene is detected by immunohistological analysis of skin from 16.5 day (post coitum) embyros. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and functions. This strain was transferred from the collection of the Consortium for Functional Glycomics. | ||
| 006338 | B6.Cg-Lgals3tm1Poi/J | Repository- Live |
| Homozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavoiral abnormalities. No gene product (mRNA or protein) is detected by in situ hybridization of tibia bones sections from embryonic day 16.4 mice or by immunohistological staining of fetal skin. Homozygotes have an impaired acute inflammation response. Initial inflammatory infiltrate cell recruitment is normal, but four days after intraperitoneal injection of thioglycollate, mutant mice have a four-fold lower number of recruited granulocytes. Mutant mice have impaired chondrocyte differentiation during long bone development. Fewer hypertrophic chondrocytes but more empty lacunae and condensed chondrocytes are found in the chondrovascular junction. Chondrocytes, cartilage matrix and lacunae are morphologically abnormal. Carbon tetrachloride-induced liver fibrosis results in reduced collagen deposition when compared to wildtype controls. Mutant mice also display defective myofibroblast
..... For more information please see the full descriiption on the strain data sheet | ||
| 007745 | B6.Cg-Mirn155tm1.1Rsky/J | Repository- Live |
| Mice homozygous for this loss-of-function/reporter allele (bic/mir-155-/-) are viable and fertile. The lacZ reporter allows the detection of bic promoter transcriptional activity using fluorescence activated cell sorting (FACS). In homozygotes, miR-155 expression is undetectable in activated splenic B cells. In heterozygotes, approximately 60% of germinal center (GC) B cells express the lacZ reporter whereas the vast majority of the non-GC B cells do not. Homozygous mice exhibit a reduced fraction of GC B cells in the gut-associated lymphoid tissue (GALT; including Peyer's patches (PPs) and mesenteric lymph nodes (mLNs)). In addition, bic/miR-155-/- B cells exhibit deficient tumor necrosis factor (TNF) and lymphotoxin-a (LT-a) cytokine production. Homozygous mice show impaired T cell-dependent antibody responses, and their T cells show a TH2 cytokine bias (an increased percentage of interleukin-4 (IL-4) producing cells and a decreas
..... For more information please see the full descriiption on the strain data sheet | ||
| 006124 | B6.Cg-Myo6sv-2J/J | Repository- Live |
| 006097 | B6.Cg-Nfkb1tm1Bal/J | Repository- Live |
| Mice homozygous for the Nfkb1tm1Bal targeted mutation are viable and fertile. Homozygous mutant mice exhibit defective B cell responses, defective responses to infection, and also defects in basal and specific antibody production. These mice may be useful in studies of inflammation and immune responses and signal transduction. 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. | ||
| 005089 | B6.Cg-Qkqk-2J/J | Repository- Live |
| Qkqk-2J homozygotes display rapid tremors by approximately 2 weeks of age. Histological examination at 3 weeks of age reveals holes in the striatum of the cortex and cerebellum and in the myelin of the spinal cord. Vision and hearing appear normal. | ||
| 004369 | B6.Cg-Rag1tm1Mom Ins2Akita/J | Repository- Live |
| Mice homozygous for the Rag1 targeted mutation and heterozygous for the Akita spontaneous display the diabetes phenotype in the absence of B and T cells and unlike single Akita mice, double mutants do not reject allografts. Mice heterozygous for only the Akita spontaneous mutation are viable and fertile. (Homozygotes typically die by 12 weeks of age from extreme hyperglycemia.) Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. The diabetic phenotype is more severe and progressive in heterozygous males than in females. Obesity and insulitis do not accompany diabetes. This double mutant strain is ideally suited for use in allogeneic or xenogeneic islet or stem cell transplantation protocols because the mice are severely immunocompromised and spontaneously develop diabetes at a young age. | ||
| 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. | ||
| 003780 | B6.Cg-Sgshmps3a/PstJ | Repository- Live |
| Mice homozygous for the Sgshmps3a mutation have only 3-4% of the wild type level of sulfamidase activity. This results in extensive lysosomal accumulation of heparin sulfate most prominently in neuronal tissue and liver and, to a lesser degree, in the spleen. GM2 ganglioside accumulation is also found. The outward phenotype of scruffy coat, hunched posture, and reduced activity is usually seen by 6 to 7 months of age. Corneal opacity is also found at approximately 7 months of age. Death occurs between 7 and 10 months of age, on average, and autopsy reveals brain lesions, hepatosplenomegaly and a distended bladder containing turbid urine. The homozygotes have thicker skullcaps, vertebral deformation, thickening of the urinary bladder wall, and bladder blockage that leads to severe bladder distention as they age. Sgshmps3a /Sgshmps3a mice provide a model for the human disease mucopolysaccharidosis 3A (MPSIIIA), also known as S
..... For more information please see the full descriiption on the strain data sheet | ||
| 004132 | B6.Cg-Terctm1Rdp/J | Repository- Live |
| Early generation mice that are homozygous null for the Terc gene are phenotypically normal. No Terc transcript or telomerase activity is detected. If null mice are maintained as homozygotes, progressive adverse effects on the reproductive and hematopoietic systems are observed. By the fifth generation of homozygous intercrossing, fertility is significantly diminished. Testes size and weight is reduced by ~80%. Germ cells exhibit decreased rates in proliferation and increased rates of apoptosis resulting in a general state of germ cell depletion. Females exhibit smaller ovaries and diminished uterine horns. The proliferative capacity of hematopoietic cells derived from bone marrow and spleen is significantly compromised. Progressive generations of interbreeding the null mice results in progressive telomere shortening (4.8 +/- 2.4 kb per generation). Cells from the fourth generation onward possess chromosome ends lacking detectable telomere repeats, aneuploidy, and chromoso
..... For more information please see the full descriiption on the strain data sheet | ||
| 006200 | B6.Cg-Tnks2tm1.1Yjc/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of activated spleen lymphocytes. While neither telomere shortening nor chromosomal abnormalities (even across multiple generations) are observed, homozygous mice have significantly decreased body weight. These mutant mice may be useful in studies of both telomerase function and telomerase-independent pathways which affect development and metabolism. | ||
| 005317 | B6.Cg-Tg(BAT-lacZ)3Picc/J | Repository- Live |
| Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These "BAT-GAL" transgenic mice are a reporter strain that express beta-galactosidase in the presence of activated beta-catenin. The transgene expresses the lacZ gene under the control of a regulatory sequence consisting of seven consensus LEF/TCF-binding motifs upstream of the Xenopus siamois gene minimal promoter. Transgenic mice display beta-galactosidase activity beginning at embryonic day 6.0 in the posterior side of the proximal epiblast. Beta-galactosidase expression is detectable in the posterior primitive streak and node at gastrulation, and progresses to the paraxial mesoderm and notochord. Beta-galactosidase activity in developing and adult nervous tissue mimics the pattern of Wnt signaling. When bred to other mutant strains, this reporter strain may be useful for identifying mutations that affect the Wnt-signalling pa
..... For more information please see the full descriiption on the strain data sheet | ||
| 008111 | B6.Cg-Tg(CAG-Ub*G76V/GFP)1Dant/J | Repository- Live |
| Hemizygous transgenic mice are viable and fertile; they contain a green fluorescent protein (GFP) fused to a constitutively active degradation signal (UbG76V). Transgenic transcripts are detected in all tissues examined; however the G76V substitution leads to its ubiquitination and proteasomal degradation, rather than expression of the GFP fluorescent protein.
Following administration of proteasome inhibitors, UbG76V accumulates and GFP-derived fluorescence is readily apparent, evidence of an impaired ubiquitin/proteasome system. Both of the ubiquitin/proteasome system reporter founder lines, UbG76V-GFP/1 (Stock No. 008111) and UbG76V-GFP/2 (Stock No. 008112), may be useful for monitoring the role of ubiquitin/proteasome-dependent proteolysis in diverse disorders, and in efficacy trials for monitoring the effect of compounds on th
..... For more information please see the full descriiption on the strain data sheet | ||
| 008112 | B6.Cg-Tg(CAG-Ub*G76V/GFP)2Dant/J | Repository- Live |
| Hemizygous transgenic mice are viable and fertile; they contain the green fluorescent protein (GFP) fused to a constitutively active degradation signal (UbG76V). Transgenic transcripts are detected in all tissues examined; however no GFP protein expression is detected due to the G76V substitution which leads to its ubiquitination and proteasomal degradation. Following administration of proteasome inhibitors, UbG76V accumulates and GFP-derived fluorescence is readily apparent, evidence of an impaired ubiquitin/proteasome system. This strain and UbG76V-GFP/1 (Stock No. 008111) have similar expression patterns, but this line (UbG76V-GFP/2) shows lower transgene expression and is not reported to display background fluorescence. These strains may be useful for monitoring ubiquitin/proteasome-dependent proteolysis in diverse disorders, and in efficacy trials for monitoring the effect of compou
..... For more information please see the full descriiption on the strain data sheet | ||
| 007574 | B6.Cg-Tg(Camk2a-Crebbp*)1364Tabe/J | Repository- Live |
| Mice hemizygous for this "CaMKIIα-FLAG-CBPΔ1" transgene are viable and fertile. Expression of this FLAG-epitope tagged, dominant negative truncation of the CREB-binding protein (FLAG-CBPΔ1) is spatially directed to neurons in the forebrain (hippocampus, amygdala, striatum, and cortex) and temporally directed to postnatal development by the CaMKIIα promoter. This dominant negative mutant form of CBP (designed to interrupt transcription factors utilizing CBP as a coactivator for the expression of their target genes) is expressed from the transgene at 95% of endogenous CBP levels in the hippocampus and 84% of endogenous CBP levels in the cortex. Hemizygous mice exhibit hippocampus-dependent memory deficits (such as reduced long-term potentiation, defective spatial learning, and impaired contextual fear conditioning) with none of the developmental impairments observed in CBP-deficient mutant models. These CaMKIIα-FLAG-CBPΔ1 transgenic mice may be useful
..... For more information please see the full descriiption on the strain data sheet | ||
| 006229 | B6.Cg-Tg(DRE-lacZ)2Gswz/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Following adult or in utero exposure with xenobiotic ligands (including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls (PCBs)), lacZ expression is induced in tissues targeted by the toxic compounds; for example, embryonic tissues expressing beta-galactosidase following TCDD treatment in utero include hard and soft palates, genital tubercle, certain facial regions, shoulder, and other tissues). These mice may be useful in studies of toxicology, teratogenic and xenobiotic processes, Per-Arnt-Sim transcription factors, cleft-palate, and as a reporter strain to indicate the temporal and spatial context of transcriptionally active aryl hydrocarbon receptors following agonist exposure in vivo. | ||
| 006069 | B6.Cg-Tg(HIST1H2BB/EGFP)1Pa/J | Repository- Live |
| Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express an "H2B-EGFP" fusion protein (coding sequence for the human HIST1H2BB gene [histone 1 H2bb] followed C-terminally by Enhanced Green Fluorescent Protein gene [EGFP, BD Biosciences]) under the control of the chicken beta actin promoter/enhancer coupled with the cytomegalovirus (CMV) immediate-early enhancer. Nucleosomes and chromatin in all cells fluoresce. Fluorescence is detectable during all phases of mitosis. The donating investigator reports occasional silencing of the transgene when transmitted through the female germline. This mutant mouse strain may be useful for in vivo subcellular high-resolution and 3-dimensional studies of dividing cells.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from
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| 006098 | B6.Cg-Tg(Il2/NFAT-luc)83Rinc/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Homozygous females are subfertile. These transgenic mice express luciferase under the regulation of the Il2 minimal promoter and 3 binding sites for NFAT, an inducible nuclear factor involved in the regulation of interleukin-2 and other cytokine expression. Luciferase activity in these transgenic mice identifies NFAT-mediated transcription. These mice may be useful as reporters for NFAT-mediated expression during thymocyte development and selection and in studies related to signal transduction, apoptosis, and transcriptional regulation. | ||
| 007940 | B6.Cg-Tg(Thy1-CFP/COX8A)C1Lich/J | Repository- Live |
| These transgenic mice express Cyan Fluorescent Protein (CFP) under the control of the mouse thymus cell antigen 1, theta, Thy1, promoter. CFP is specifically localized to the mitochondria by a human cytochrome c oxidase, subunit 8A (ubiquitous), targeting signal fused to the N-terminus. Fluorescence is detected in many neuronal populations including retinal cells and in all motor axons. Coronal brain sections reveal a fluorescence pattern showing somatosensory cortex barrel morphology. Neuronal, mitochondrial and neuromuscular junction morphology appears normal in transgenic mice. Axonal mitochondrial density is similar to wildtype. Homozygotes 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 mitochondrial transport.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different fro
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| 002711 | B6;129-Gabrb3tm1Geh/J | Repository- Live |
| The gamma-Aminobutyric acid type A receptors mediate the majority of rapid inhibitory synaptic transmission in the CNS. The beta3 subunit is an essential component of these receptors in many brain regions, especially during development, and is implicated in several pathophysiologic processes. The majority of mice homozygous for the Gabrb3tm1Geh mutation (or beta3-/-) die at birth with ~60% displaying cleft palate and the remaining ~35% die for unidentified reasons. Homozygous females that survive are fertile but do not care for their pups. Survivors have frequent myoclonus and occasional epileptic seizures, are hypersensitive to external stimuli and handling, have a lack of coordination and display altered responses to certain anesthesias. In addition, the observed behavioral deficits (especially regarding social behaviors) indicate that mutant mice may be a useful model of autism spectrum disorders. Of note, several strains bearing gamma-aminobutyric acid (GABA-A)
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| 006911 | B6;129-Gt(ROSA)26Sortm1(rtTA*M2)Jae Col1a1tm2(tetO-Pou5f1)Jae/J | Repository- Live |
| Mice heterozygous for both targeted mutations (R26-rtTA and Cola1a::tetO-Oct4) are viable and fertile. These "Oct-4/rtTA" mice express rtTA-M2, an optimized form of reverse tetracycline-controlled transactivator (rtTA) protein, in multiple tissues. In the absence of the tetracycline analog doxycycline (dox), Oct4 (Pou5f1) expression from the Col1a1 locus is not detected. Following dox administration, high Oct4 expression is induced in liver, bone marrow, stomach, intestine, and skin, with lower levels in the heart, lungs, kidney, spleen, and thymus; no expression was detected in the brain and testes. Dox-inducd activation of Oct4 results in dysplasia in epithelial tissues. These mutant mice may be useful for studies of tumorigenesis and pluripotent cells. | ||
| 006904 | B6;129-Msctm1Eno/J | Repository- Live |
| Mice homozygous for this MyoR mutant allele are viable and fertile with no obvious abnormalities. These mice may be useful in studying muscle development, specifically craniofacial muscles. For example, when these mice are bred with capsulin-mutant mice, the resulting double mutant offspring have significant abnormalities in craniofacial (and other) muscle development and MyoD-family transcription factor gene expression. 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 become available. | ||
| 008041 | B6;129-Sirt1tm1Ygu/J | Repository- Live |
| Mice homozygous for this targeted allele (SirT1co/co) are viable and fertile. A loxP-flanked neomycin cassette just upstream of exon 4 and a third loxP site downstream of exon 4 were inserted to create this targeted mutant Sirt1 allele. The floxed mutation does not affect SIRT1 protein expression in MEFs or mammary gland tissue in homozygotes. When bred to mice that express Cre recombinase, the resulting offspring have exon 4 (encoding an evolutionarily conserved Sir2 motif) deleted in cre-expressing tissue(s); (the donating investigator reports only one recombination event: complete removal of the neomycin cassette and exon 4, leaving a single loxp). These SirT1co/co mice may be useful in generating conditional mutants for studying transcriptional regulation and the role of estrogen, insulin growth factor-1 (IGF-1), and transcription factors (including NF-kappaB) in mammary gland development, mammary cancer, apoptosis, and metabolic di
..... For more information please see the full descriiption on the strain data sheet | ||
| 007608 | B6;129-Smad1tm1Sor/J | Repository- Live |
| Homozygotes for the Smad1tm1Sor (also called Smad1C) allele have an embryonic lethal phenotype and do not survive past ED9.5. These mice carry a mutation (the C-terminal SSVS motif was changed to AAVA) in exon 7, which effects transcriptional activity. Homozygous embryos display posterior truncation, abnormal turning, allantois malformations (failure of the allantois to connect to the chorionic plate), anterior truncation of the head with only one brachial arch, and enlarged pericardium. At ED7.5 homozygous embryos do not have any detectable primordial germ cells. Western blot analysis of ED9.5 homozygotes showed that protein levels were not affected. Heterozygotes for this mutant allele 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 homeostasis and BMP and MAPK signaling pathways during development and in the adult. | ||
| 007613 | B6;129-Smad1tm2Sor/J | Repository- Live |
| Homozygotes for the Smad1tm2Sor (also called Smad1L) allele are viable and fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mice carry a mutation in exon 3, which effects MAPK-mediated phosphorylation of the protein. Western blot analysis of MEFs from homozygotes showed that similar protein levels compared to wildtype. Homozygous embryos have fewer primordial germ cells than wildtype controls. Homozygous mice display abnormal gastric mucosa cell population ratios with fewer zymogenic cells and more parietal cells. The cytoskeleton of MEFs from homozygotes exhibit a loss of adhesion zippers, decreased stress fibers, and an accumulation of actin in the cortical regions with an increase in beta-catenin immunostaining localized to the cell membranes. This mutant mouse strain may be useful in studies of stomach development, gastic mucosal homeostasis and BMP and MAPK signaling pathways during development and in the adult. | ||
| 006251 | B6;129-Tor1atm1Wtd/J | Repository- Live |
| Homozygous mutant mice have a perinatal lethal phenotype. They fail to feed or vocalize at birth, and typically die within 48 hours. No protein is detected by immunoblot analysis in tissues (liver, brain, spinal cord, mouse embryonic fibroblasts (MEFs)) from homozygous mutant animals. Microscopic and ultrastructural examination of central nervous system neurons from embryonic day 18 homozygous embryos reveals abnormalities including dysmorphic ventral horn neuron nuclei, vesicles in the neuronal nuclear envelope and enlarged endoplasmic reticulum. Neurons within homozygotes appear normal when migrating, but develop nuclear membrane abnormalities upon maturation.
In contrast to homozygous mutant mice, heterozygotes are viable, fertile, normal in size, and do not manifest any gross physical or behavioral abnormalities. Torsin A (TOR1A) protein levels in heterozygous mice are approximately 50% of wildtype levels. This mutant mouse strain may be useful in studies of torsion dystonia 1
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| 006495 | B6;129-Trp53bp1tm1Jc/J | Repository- Live |
| Homozygous "53BP1"-deficient mice are viable and fertile, but exhibit retarded growth and generate reduced litter sizes. Protein from the targeted gene is not detected in the testes (by immunoblot) or in mouse embryonic fibroblasts (MEFs) (by immunofluorescence). Homozygotes are immunocompromised, hypersensitive to whole-body irradiation, and develop thymic lymphomas with higher frequency (8%) compared to wildtype by 4-7 months of age. MEFs from homozygous mutant mice have a defective DNA damage response with impaired Chk2 activation. These mutant mice may be useful in studies of the immune system, cancer, tumor suppression, and DNA damage response pathways. | ||
| 006958 | B6;129S-Nkd1tm1Kwha/J | Repository- Live |
| Mice homozygous for this nkd1lacZ mutant allele are viable and fertile with slightly reduced mean litter sizes. Northern blot of lung tissue, as well as western blot of embryonic tissue, confirms that the deleted exons (encoding the Dvl-binding domain) are not expressed in homozygous mutants. However, the endogenous promoter directs expression of the internal ribosome entry site-β-galactosidase (IRES-lacZ) fusion gene in a manner that closely mimics the patterns of the endogenous gene mRNAs. Because the naked cuticle (NKD) genes are considered targets for Wnt/β-catenin signaling, these nkd1lacZ mutant mice (as well as the similar nkd2lacZ mutant strain; Stock No. 006960) may be useful as a reporter for Wnt/β-catenin-dependent transcriptional activity during embryonic development or in adult mice. | ||
| 006960 | B6;129S-Nkd2tm1Kwha/J | Repository- Live |
| Mice homozygous for this nkd2lacZ mutant allele are viable and fertile with slightly reduced mean litter sizes. RT-PCR analysis of homozygous brain tissue confirms that the deleted exons (encoding the Dvl-binding domain) are not expressed in homozygous mutants. However, the endogenous promoter directs expression of the internal ribosome entry site-β-galactosidase (IRES-lacZ) fusion gene in a manner that closely mimics the patterns of the endogenous gene mRNAs. Because the naked cuticle (NKD) genes are considered targets for Wnt/β-catenin signaling, these nkd2lacZ mutant mice (as well as the similar nkd1lacZ mutant strain; Stock No. 006958) may be useful as a reporter for Wnt/β-catenin-dependent transcriptional activity during embryonic development or in adult mice. | ||
| 005217 | B6;129S1-Tlr3tm1Flv/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. Northern blot analysis detects a truncated gene product (mRNA), which is not functional. Unlike wildtype macrophages, macrophages derived from these animals fail to produce inflammatory cytokines, IFN-alpha or IFN-beta when challenged with poly(I:C), polyinosine-polycytidylic acid, a synthetic dsRNA analog. Splenocytes isolated from homozygotes do not respond to viral dsRNA and have diminished IL-6 production. Mice homozygous for the mutation are resistant to poly(I:C) induced shock and produce lower levels of IL-12. This mutant mouse strain may be useful in studies of the toll-like receptor pathway of innate immune response. | ||
| 003263 | B6;129S2-Cdkn1atm1Tyj/J | Repository- Live |
| Homozygotes are viable and fertile. p21, the product of the Cdkn1a gene, belongs to a family of regulators, known as cyclin-dependent kinase inhibitors, which modulate progression through the cell cycle. Following serum restimulation, expression of p21 is superinducible by cycloheximide in wild-type but not in p53-deficient cells. p53 appears to play a critical role in p21 induction following DNA damage. p21 can be regulated independently of p53 during normal tissue development, following serum stimulation, and during cellular differentiation. | ||
| 007204 | B6;129S4-2610005L07RikGt(ROSA)73Sor/J | Repository- Live |
| Mice homozygous for this mutant allele (called BC058969 in the primary publication) are viable and fertile, with greater than 50% embryonic lethality observed in homozygous embryos. Homozygotes occur at a lower than Mendelian ratio (9%) from heterozygote x heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects (sternum and calvarial bones). Notably, 100% incidence of calvarial bones defects is reported. Additionally, homozygotes are reported to have low β-galactosidase activity; in situ hybridization or other sensitive methods may be necessary to detect expression of the lacZ-neo reporter fusion gene. These BC058969-mutant (2610005L07Rik-mutant) mice may be useful in studying cellular signal
..... For more information please see the full descriiption on the strain data sheet | ||
| 007200 | B6;129S4-Arid5bGt(ROSA)75Sor/J | Repository- Live |
| Mice homozygous for this mutant allele have reduced size and weight gains after birth, occur at lower than Mendelian ratio (16%) and 46% die within 3 weeks of age. Homozygotes are fertile when they survive to adulthood. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit kidney defects (abnormally high blood urea nitrogen level, mutant kidney size smaller than wildtype, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells in glomeruli), and abnormalities in palate bone fusion. These Arid5b-mutant mice may be useful in studying cellular signaling in development and 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. | ||
| 007201 | B6;129S4-Plekha1Gt(ROSA)82Sor/J | Repository- Live |
| 25% of homozygotes die by 2 weeks of age. Homozygous males are infertile and, after 3 weeks of age, exhibit higher than normal (wildtype) weight gain. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Plekha1-mutant mice may be useful in studying cellular signaling in development and 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. | ||
| 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 | ||
| 007203 | B6;129S4-Zfand5Gt(ROSA)72Sor/J | Repository- Live |
| Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Histological examination of E18.5 homozygous embryos reveals thin blood vessel walls, hemorrhages and lung edema. There are fewer vascular smooth muscle cells (vSMCs) in blood vessels as indicated by immunohistochemistry for desmin and alpha-smooth muscle actin. Skeletal defects are observed in 20% of animals in the sternum and calvarial bones. Homozygotes die a few hours after birth due to difficulty breathing and bruising is visible beneath the skin. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Zfand5-mutant mice may be useful in studying cellular signaling in development and 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. | ||
| 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 | ||
| 006208 | B6;129S6-Pdzk1tm1Dls/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile. Liver tissue from homozygous mutant mice lacks endogenous protein expression. Homozygotes, but not heterozygotes, have significantly decreased (~85-95%) hepatic high density lipoprotein (HDL) receptor scavenger receptor B-I (SR-BI) levels. This decrease is further exacerbated following diet supplementation with the PPAR-alpha activator fenofibrate. These mice may be useful in studies of cardiovascular health and atherosclerosis, lipid metabolism, SR-B1 regulation, kidney function, as well as kidney transporter (e.g. urate transporter) regulation and liver organic anion transport. | ||
| 006614 | B6;CB-Tg(Thy1-CFP/COX8A)C1Lich/J | Repository- Live |
| These transgenic mice express Cyan Fluorescent Protein (CFP) under the control of the mouse thymus cell antigen 1, theta, Thy1, promoter. CFP is specifically localized to the mitochondria by a human cytochrome c oxidase, subunit 8A (ubiquitous), targeting signal fused to the N-terminus. Fluorescence is detected in many neuronal populations including retinal cells and in all motor axons. Coronal brain sections reveal a fluorescence pattern showing somatosensory cortex barrel morphology. Neuronal, mitochondrial and neuromuscular junction morphology appears normal in transgenic mice. Axonal mitochondrial density is similar to wildtype. Homozygotes 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 mitochondrial transport. | ||
| 006617 | B6;CB-Tg(Thy1-CFP/COX8A)S2Lich/J | Repository- Live |
| These transgenic mice express Cyan Fluorescent Protein (CFP) under the control of the mouse thymus cell antigen 1, theta, Thy1, promoter. CFP is specifically localized to the mitochondria by a human cytochrome c oxidase, subunit 8A (ubiquitous), targeting signal fused to the N-terminus. Fluorescence is detected in many neuronal populations including retinal ganglion cells, bipolar cells, amacrine cell and photoreceptors. Neuronal, mitochondrial and neuromuscular junction morphology appears normal in transgenic mice. Axonal mitochondrial density is similar to wildtype. Homozygotes 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 mitochondrial transport in adult motor neurons. | ||
| 004200 | B6;CBACa Aw-J/A-Npr2cn-2J/J | Repository- Live |
| Mice carrying the Npr2cn-2J display mutation short thick femurs, round heads, disorganized growth plates, and relatively normal vertebrae; A one month old female exhibited the same phenotype as above but also had splayed ribs. | ||
| 006302 | B6;SJL-Slc6a3tm1.1(cre)Bkmn/J | Repository- Live |
| Mice homozygous for this dopamine transporter IRES-cre (DATIREScre or DAT-cre) mutant allele are viable and fertile. Cre recombinase activity is observed as early as embryonic day 15, and co-localizes with endogenous gene expression in adult dopaminergic cell groups (substantia nigra (SN) and ventral tegmental area (VTA), as well as in the retrorubral field). Lower Cre recombinase activity is detected in adult olfactory bulb glomeruli, mimicking the known lower Slc6a3 (or DAT) expression in this tissue. Although the pattern and intensity of DAT immunostaining in the SN, VTA and striatum do not differ between wildtype and mutant mice, striatum DAT protein levels are moderately reduced (17%) in heterozygotes and significantly reduced (47%) in homozygotes. This decrease in DAT protein levels in homozygous mutant striatum is associated with significantly increased neuropeptide PDyn (but not D1, D2, or PPE) mRNA levels compared to wildtype. Increases in these mRNA l
..... For more information please see the full descriiption on the strain data sheet | ||
| 001756 | B6C3Fe a/a-Cacng2stg/J | Repository- Live |
| Mice homozygous for the spontaneous mutation stargazer (Cacng2stg) are first recognizable at 14 days of age by their smaller body size and slightly ataxic gait. Female stargazer homozygous mutant mice are fertile, but most of the males are unable to breed. The mutation is named for the abnormal head movements resembling choreiform head tossing that is characteristic of these mice. The behavioral symptoms progressively worsen with age, but both males and females will live to over one year of age. Electrocorticographical recordings of stargazer mice reveal frequent, prolonged, generalized spike-wave cortical discharges with behavioral arrest. The abnormal brain wave patterns are similar to those seen in human beings with absence epilepsy. Waggler homozygotes (Cacng2stg-wag) manifest a less severe phenotype than stargazer homozygotes, but do display an ataxic gait and occasional seizures. In general, young stargazer mice are more healthy than waggler ho
..... For more information please see the full descriiption on the strain data sheet | ||
| 000501 | B6CBACa Aw-J/A-Aifm1Hq/J | Repository- Live |
| Harlequin mice exhibit paucity of fur resulting in near baldness in hemizygous males and homozygous females. Heterozygous females have a patchy absence of hair that is not always obvious, since the degree of hair loss is notably less than 50%. Homozygotes and hemizygous males weigh less than heterozygous or wild type controls. Ataxia is noticeable by 5 months and progresses as the mice age. Initially the ataxia manifests itself as a side-to-side, unsteady gait with a lateral tremor visible at rest. A delayed cerebellar cortical atrophy has been characterized in these mutants, with an apoptotic loss of granule cells beginning at 4 months of age and a necrotic loss of Purkinje cells occurring subsequently. The granule cells re-enter the cell cycle, but the Purkinje cells do not, supporting the postulate that inappropriate cell cycle re-entry of terminally differentiated neurons can induce apoptosis. Cell loss is greater in the caudal lobules of the cerebellum and is extensive by 9 to 11
..... For more information please see the full descriiption on the strain data sheet | ||
| 003922 | BALB/cByJ-Clcn1adr-mto2J jgl/J | Repository- Live |
| Mice homozygous for the jagged tail-like (jgl) mutation are easily characterized by their kinked tails that are recognizable by 10 days of age. Full body X-rays revealed exostosis of the vertebrae near the tail tip and in the phalanges of all 4 feet and abnormal vertebral bodies were also reported in two 5 month old homozygotes. Both female and male reproductive organs are smaller than normal with the males showing severe atrophy of the seminipherous tubules and hyperplasia of Leydig cells. Although most homozygotes are not fertile, a few have produced litters. Homozygotes also have atrophic spleens, particularly the white pulp. | ||
| 004333 | C.129P2(B6)-Il10tm1Cgn/J | Repository- Live |
| Mice homozygous for the Il10tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a
..... For more information please see the full | ||