Search Criteria: Research Area is "Research Tools: Cardiovascular Research"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002052 | B6.129P2-Apoetm1Unc/J | Level 2 |
| Mice homozygous for the Apoetm1Unc mutation show a marked increase in total plasma cholesterol levels that are unaffected by age or sex. Fatty streaks in the proximal aorta are found at 3 months of age. The lesions increase with age and progress to lesions with less lipid but more elongated cells, typical of a more advanced stage of pre-atherosclerotic lesion. Moderately increased triglyceride levels have been reported in mice with this mutation on a mixed C57BL/6 x 129 genetic background. Aged apoE-deficient mice (>17 months) have been shown to develop xanthomatous lesions in the brain consisting mostly of crystalline cholesterol clefts, lipid globules, and foam cells. Smaller xanthomas were seen in the choroid plexus and ventral fornix. Additional studies indicate that apoE-deficient mice have altered responses to stress, impaired spatial learning and memory, altered long term potentiation, and synaptic damage. | ||
| 003291 | C57BL/6-Tg(CAG-EGFP)1Osb/J | Level 4 |
| This transgenic mouse line with an "enhanced" GFP (EGFP) cDNA under the control of a chicken beta-actin promoter and cytomegalovirus enhancer makes all of the tissues, with the exception of erythrocytes and hair, appear green under excitation light. Note that the donating investigator reports that mice homozygous for this transgene die within the first two weeks following birth.
Of note, it has been the experience at The Jackson Laboratory that Stock No. 006567 (C57BL/6-Tg(CAG-EGFP)131Osb/LeySopJ) demonstrates the highest proportion of GFP expressing cell populations in bone marrow, thymus, spleen and peripheral blood when compared to Stock No. 003291 (C57BL/6-Tg(CAG-EGFP)1Osb/J) and Stock No. 007075 (CByJ.B6-Tg(CAG-EGFP)1Osb/J).
View the pdf document on For more information please see the full phenotype on the strain data sheet | ||
| 007853 | 129S/SvEv-Tg(Alb1-Ren)2Unc/CofJ | Repository- Live |
| Mice heterozygous for the RenTgMK transgene are viable and fertile. The RenTgMK transgene contains a liver-specific albumin promoter/enhancer controlling the expression of a synthetic renin gene (engineered to allow efficient cleavage and secretion of the prorenin transgene product by the liver). This, and because the transgene was targeted to the apolipoprotein locus on Chromosome 9, results in active renin secretion from the liver independently of renal or other homeostatic cardiovascular control mechanisms (i.e. genetically clamped). RenTgMK heterozygotes have high ectopic levels of active mouse renin in the liver and elevated plasma levels of prorenin and active renin. Heterozygous mice display significantly elevated blood pressure, enhanced thirst, high urine output, proteinuria, and kidney damage. Because active renin overexpression results in increased circulating levels of angiotensin II (Ang II), heterozygotes also exhibit cardiac hypertrophy and 50% male mortality between 6-8 ..... For more information please see the full phenotype on the strain data sheet | ||
| 001673 | AXB1/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001681 | AXB10/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001683 | AXB12/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001826 | AXB13/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB13/PgnJ and AXB14/PgnJ are considered ?sister strains? being identical throughout much of the genome but differing in large regions of Chromosomes 11, 12, 13, and in small regions of a few other Chromosomes. Because these two strains are "near congenics" a nomenclature change has been made to update AXB14/PgnJ to AXB13a/PgnJ. In general, 'sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a ?near congenic? for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their suscepti ..... | ||
| 001685 | AXB15/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001687 | AXB19/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB18/Pgn, AXB19/Pgn, and AXB20/Pgn were found to be highly similar in their overall genomes, but with particular Chromosomes differing between them. Two of these "sister" strains were renamed. AXB19/Pgn was designated the primary strain since it has the best traceable history, and therefore its name remained unchanged. AXB18/Pgn was renamed AXB19a/Pgn and AXB20/Pgn was renamed AXB19b/Pgn. In general, the "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalu ..... For more information please see the full phenotype on the strain data sheet | ||
| 001686 | AXB19a/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB18/Pgn, AXB19/Pgn, and AXB20/Pgn were found to be highly similar in their overall genomes, but with particular Chromosomes differing between them. Two of these "sister" strains were renamed. AXB19/Pgn was designated the primary strain since it has the best traceable history, and therefore its name remained unchanged. AXB18/Pgn was renamed AXB19a/Pgn and AXB20/Pgn was renamed AXB19b/Pgn. In general, the "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalu ..... For more information please see the full phenotype on the strain data sheet | ||
| 001688 | AXB19b/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB18/Pgn, AXB19/Pgn, and AXB20/Pgn were found to be highly similar in their overall genomes, but with particular Chromosomes differing between them. Two of these "sister" strains were renamed. AXB19/Pgn was designated the primary strain since it has the best traceable history, and therefore its name remained unchanged. AXB18/Pgn was renamed AXB19a/Pgn and AXB20/Pgn was renamed AXB19b/Pgn. In general, the "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalu ..... For more information please see the full phenotype on the strain data sheet | ||
| 001674 | AXB2/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001690 | AXB23/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001691 | AXB24/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001676 | AXB4/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001677 | AXB5/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001678 | AXB6/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001679 | AXB8/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 008355 | B6.129(Cg)-Slc6a4tm1Kpl/J | Repository- Live |
| Mice that are homozygous for the serotonin transporter targeted mutation (SERT-/- or 5-HTT-/-) are viable and fertile with a superficially unremarkable behavioral phenotype through early adulthood. Serotonin uptake is completely absent in homozygous mice. SERT-deficiency is pleiotropic (many different phenotypic traits). Homozygotes and, to a lesser extent, heterozygotes exhibit diminished responses to serotonin receptor agonists and other classes of drugs (including MDMA, SSRIs, 8-OH-DPAT, and DOI). SERT-mutant mice are also reported to have increased anxiety-like behaviors, altered neuroendocrine and sympathoadrenal responses to even minor stress, diminished aggression, altered emotional learning, substantially increased rapid eye movement (REM) sleep time, reduced brain excitability, increased body temperature, increased colonic motility, reduced spinal reflex to injury, reduced bladder response to stretching, blood pressure responses, diminished bone and muscl ..... For more information please see the full phenotype on the strain data sheet | ||
| 008195 | B6.129-Adipoqtm1Chan/J | Repository- Live |
| Homozygous mice are viable and fertile, with absence of targeted allele expression confirmed in adipose tissue (mRNA) and plasma (adiponectin protein). While homozygous mice have normal glucose tolerance and insulin resistance, beta-oxidation activity is significantly increased in muscle and liver. Homozygotes also have endothelial dysfunction (increased leukocyte rolling and leukocyte adhesion), are protected from DSS-induced colitis, and are more susceptible to myocardial ischemia/reperfusion. When fed a high fat diet, obese homozygotes are significantly heavier with increased insulin levels and altered insulin resistance. These adiponectin-deficient (Adipoq-/- or Adipo-/-) mice may be useful in studying obesity, diabetes, insulin resistance, metabolism, inflammation, leukocyte-endothelium interactions, and colitis. | ||
| 006952 | B6.129-Akt2tm1.1Mbb Ldlrtm1Her/J | Repository- Live |
| Independently, homozygous Akt2 mutant mice develop insulin resistance and diabetes, while LDLR homozygotes are predisposed to atherosclerosis. Double mutant mice that are heterozygous for the Akt2 allele and homozygous for the LDLR mutation are viable and fertile. These double mutant mice may be useful in studies of diabetes, metabolism, hyperglycemia, and atherosclerosis. | ||
| 009106 | B6.129-Cyp27a1tm1Elt/J | Repository- Live |
| These mice harbor a targeted mutation of the Cyp27a1 (cytochrome P450, family 27, subfamily a, polypeptide 1) locus that abolishes endogenous gene expression. Homozygous mice (also called Cyp27a1-/-, cyp27-/-, or sterol 27-hydroxylase-deficient mice) are viable and fertile, with no RNA or protein expression from the targeted gene detected in liver tissue. Both formation of bile acids and excretion of fecal bile acids are decreased in homozygous mice. Compensatory up-regulation of hepatic enzymes that convert cholesterol to bile acids (bile acid synthesis) is also observed. Cyp27a1-/- mice exhibit a dramatic increase in cytochrome P450 3A (Cyp3a11) which catalyzes side-chain hydroxylations of bile acid intermediates subsequently facilitating their excretion in the bile and urine. Homozygous mice also have increased expression of other nuclear xenobiotic receptor PXR (pregnane X receptor) target genes. | ||
| 004584 | B6.129-Ppargtm2Rev/J | Repository- Live |
| These mice possess loxP sites on either side of exons 1 and 2 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 a strain expressing Cre recombinase in adipose tissue (see Stock No. 005069 for example), this mutant mouse strain may be useful in studies of insulin resistance. | ||
| 009666 | B6.129-Ppargc1atm2Brsp/J | Repository- Live |
| These mice possess loxP sites on either side of exons 3-5 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 3-5 deleted in the cre-expressing tissue(s). When bred to a strain expressing Cre recombinase specifically in the liver (see Stock No. 003574 for example), this mutant mouse strain may be useful in studies of hepatic heme biosynthesis and porphyrias. When bred to a strain expressing Cre recombinase specifically in skeletal muscle, this mutant mouse strain may be useful in studies of neuromuscular junction physiology and muscular dystrophy. | ||
| 011029 | B6.129-Rpl22tm1.1Psam/J | Repository- Live |
| Mice homozygous for this RiboTag allele are viable and fertile, with a targeted mutation of the ribosomal protein L22 (Rpl22) locus harboring a loxP-flanked wildtype C-terminal exon 4 followed by an identical C-terminal exon 4 that is tagged with three copies of the hemagglutinin (HA) epitope before the stop codon. Prior to exposure to Cre recombinase, RiboTag mice express the wildtype RPL22 protein (15 kDa). When the RiboTag mice are bred to cre-expressing mice, offspring will have the floxed wildtype exon 4 deleted in the cre-expressing tissue and subsequent use of the downstream HA epitope-tagged exon 4 as the terminal exon. The 23 kDa HA epitope-tagged ribosomal protein (RPL22HA) is incorporated into actively translating polyribosomes. These RiboTag mice allow Cre-mediated HA epitope tagging of ribosomes from user-defined cell types and/or immunoprecipitation of ribosomes bound to mRNA from those specific cell types. | ||
| 011008 | B6.129P2(Cg)-Gt(ROSA)26Sortm1(tTA)Roos/J | Repository- Live |
| Mice heterozygous for the ROSA:LNL:tTA conditional mutation of the Gt(ROSA)26Sor locus are viable and fertile, with a loxP-flanked STOP cassette preventing transcription of a downstream optimized/modified tetracycline-controlled transactivator protein ("mtTA"). Applying both Cre-lox and Tet-Off technologies, these ROSA:LNL:tTA mutant mice may be useful to generate compound mutant mice in which expression of a tetracycline-responsive promoter element (TRE; also called tet-operator or tetO)-driven gene of interest can be both directed to the cell types defined by the chosen Cre recombinase expression, as well as turned off by the addition of tetracycline (or its analog doxycycline (dox)). | ||
| 013224 | B6.129P2-Abl1tm2.1Goff/J | Repository- Live |
| These Abl1flox/flox mutant mice posses loxP sites flanking exons 5-6 of the c-abl concogene 1, non-receptor tyrosine kinase gene, Abl1. Mice that are homozygous for this allele are viable, fertile, and normal in size. When these Abl1flox/flox mutant mice are bred to mice that express Cre recombinase, the resulting offspring will have exons 5-6 deleted in the cre-expressing tissue. This strain may be useful for studying the growth, development, and physiology of cardiac tissue. | ||
| 009654 | B6.129P2-Sod3tm1Mrkl/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size, but reproductive performance is inconsistent for homozygous X homozygous crosses. No gene product (EC-SOD protein) activity is detected by gel-exclusion chromatography analysis of plasma and no protein is detected by Western blot analysis of blood vessels. EC-SOD activity is not detected in brain. When exposed to >99% oxygen conditions, homozygotes have a shorter survival time than wild-type controls and exhibit a more severe lung edema at death. Homozygotes are more sensitive to induced transient focal cerebral ischemia, which results in greater total infarct volume and more severe hemiparesis. Alloxan-induced diabetes causes increased initial hyperglycemia with delayed recovery of glycemic control. Extracellular superoxide radical concentration is doubled and normal age-related loss of endothelial cells is increased in the cornea. Mutant mice are more susceptible to LPS-induced inflammation of ..... For more information please see the full phenotype on the strain data sheet | ||
| 016222 | B6.129S(Cg)-Id2tm1.1(cre/ERT2)Blh/ZhuJ | Repository- Live |
| The Id2-CreERT2 knockin allele was designed to both abolish inhibitor of DNA binding 2 (Id2) gene function and express CreERT2 fusion protein from the Id2 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible and can be observed following tamoxifen administration. As such, when Id2-CreERT2 knockin mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Id2-expressing cells of the offspring.
No mRNA or protein expression from the Id2-CreERT2 allele is observed. The donating investigator reports that homozygous mice are runted with defective lung alveolarization. Other organ systems have not been evaluated. However, Id2-CreERT2 homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (including postnatal lethality and defects of the immune system, digestive tract, ..... | ||
| 009125 | B6.129S1(Cg)-Lmnatm1Stw/BkknJ | Repository- Live |
| Mice heterozygotes for this lamin A/C mutation are viable and fertile. The targeted allele does not express both full-length transcripts or stable lamin A/C protein. Homozygotes (Lmna -/- mice) exhibit severely retarded postnatal growth beginning as early as 2 weeks of age and abnormal movement/gait by 3-4 weeks of age that progresses to distinct scoliosis/kyphosis and death around 8 weeks of age. Lmna -/- mice also have tissue-specific alterations of nuclear envelope integrity and mislocalization of the inner nuclear membrane protein emerin. In skeletal and cardiac muscle, this results in rapid myopathic onset closely resembling Emery-Dreifuss muscular dystrophy (EDMD). These mice are a model for the autosomal variant of EDMD and may be useful in studying the role of lamins, inner nuclear membrane proteins, nuclear envelope integrity, and chromatin domain anchoring sites in EDMD.
In an attempt to offer alleles on well-characterized or multiple genetic background ..... | ||
| 009387 | B6.129S1-Osr1tm1Jian/J | Repository- Live |
| The Osr1tm1Jian (Odd1-LacZ) mutation abolishes endogenous gene function and expresses a β-galactosidase fusion protein (fused in-frame with the N-terminal 16 amino acid residues of the endogenous protein). Under control of the upstream promoter/enhancer elements, lacZ expression is directed to the same tissues as the wild-type gene (for example, β-galactosidase expression during embryogenesis is detected at E7.5 in the intermediate mesoderm, is expanded to the gut endoderm, lung bud mesenchyme and myocardial cells by E9.5, and is activated in developing branchial arches and limb buds by E10.5). Almost all (`95%) of homozygous mice die in utero between E11.5-E12.5 from circulation distress; exhibiting malformed atrial septum, dilated atria with hypoplastic venous valves, and blood backflow from the heart into systemic veins. Homozygotes also exhibit complete agenesis of adrenal glands, metanephric kidneys, gonads, and defects in pericard ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 phenotype on the strain data sheet | ||
| 007668 | B6.129S4(Cg)-Arntltm1Weit/J | Repository- Live |
| Mice homozygous for this conditional (floxed) allele possess loxP sites flanking exon 8 of the targeted gene and are viable and fertile, with circadian behavioral rhythms indistinguishable from wildtype littermates. When bred to mice that express Cre recombinase, the resulting offspring will have the exon encoding the ARNTL (BMAL1) basic helix-loop-helix (bHLH) domain deleted in the cre-expressing tissue(s). These Bmal1-floxed mutant mice may be useful in generating conditional mutations (whole-mouse or tissue-specific) to study the role of circadian clock/circadian rhythm in physiological and behavioral regulation.
For example, when crossed to a strain expressing Cre recombinase in the retina (see Stock No. 005105), this mutant mouse strain may be useful in studies of the circadian clock of the retina. | ||
| 011009 | B6.129S4-Mtortm1.2Koz/J | Repository- Live |
| Mice homozygous for this mTORfl allele are viable and fertile, with loxP sites flanking exons 1-5 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have the sequences encoding the putative transcription start site and the coding sequence through coding exon 5 deleted in the cre-expressing tissue(s). These mTORfl mutant mice may be useful in generating conditional mutations for studying mTOR and mTOR complex signaling; including regulation of cell growth, cell proliferation/differentiation, cell survival, cancer, tumor cell motility and metastasis, the RTK-PI3K-mTOR signaling axis, stem cell development, cytokine signaling, and T cell lineage commitment.
For example, when bred to a strain expressing Cre recombinase in adult striated muscle fibers and embryonic striated muscle cells of the somites and heart (see Stock No. 006149 for example), ..... | ||
| 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 ..... | ||
| 006243 | B6.129S4-Timp1tm1Pds/J | Repository- Live |
| Homozygous females and hemizygous males (the gene is X-linked) are viable and fertile. No endogenous transcript is detected in lung tissue from affected mice by Northern blot analysis.. Homozygous mice have increased resistance to corneal and pulmonary infection with P. aeruginosa, and have altered immune, hematopoietic, and vascular permeability in bleomycin-induced lung injury trials. Homozygotes also show increased and continued progression of aneurysm formation compared with wild-type mice in induced thoracic aortic aneurysm (TAA) models. Mice with this X-linked targeted mutation may be useful in studies of cornea and pulmonary infection, pulmonary injury and aneurysm, as well as of P. aeruginosa resistance in individuals with unresolved, antibiotic-resistant pulmonary infections, such as those often observed in cystic fibrosis patients.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genet ..... | ||
| 007611 | B6.129S6(SJL)-Cdh2tm1Glr/J | Repository- Live |
| These mice possess loxP sites on either side of exon 1 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 exon 1 deleted in the cre-expressing tissue(s). When bred to a strain with inducible Cre recombinase expression in cardiac cells (see Stock No. 005657 for example), this mutant mouse strain may be useful in studies of myocardium physiology. | ||
| 006878 | B6.129S6-Taglntm2(cre)Yec/J | Repository- Live |
| Mice homozygous for this SM22alpha-CreKI allele are viable and fertile. These mice have a Cre-recombinase gene inserted into the endogenous transgelin (SM22alpha) locus. The donating investigator reports that this mutation results in a loss of function of the targeted gene. Cre recombinase activity is shown in adult smooth muscle cells (such as arteries, veins, and visceral organs) and cardiac myocytes, but activity is not observed in the same embryonic tissues. It has been the experience of The Jackson Laboratory that optimal breeding is achieved by mating heterozygous females to homozygous males as female mortality post gestation has been noted in our colony. These SM22alpha-CreKI mice may be useful for Cre-lox technology applications in studying smooth muscle and cardiac gene function, as well as cardiovascular disease. | ||
| 012565 | B6.129S7(129S4)-Ift20tm1.1Gjp/J | Repository- Live |
| These Ift20flox mice harbor loxP sites flanking exons 2-3 (encoding the first 71 codons including the start codon) of the intraflagellar transport 20 homolog (Chlamydomonas) locus. The primary cilium is a microtubule-based antenna-like structure that emanates from the surface of virtually all cells in the mammalian body. The primary cilium functions as a sensory organelle (mechano-, chemo-, photo-receptor) that receives signals from other cells/the environment, and transmits these signals to the nucleus to elicit a cellular response. Most types of eukaryotic cilia and flagella are assembled and maintained by the process of intraflagellar transport (IFT). During IFT, large protein complexes (IFT particles) are transported along the ciliary microtubules under the ciliary membrane. IFT particle proteins organize into at least three distinct complexes called complex A, complex B and the Golgi IFT complex. The unique role of Ift20 in both complex B as well as the Golgi IFT ..... For more information please see the full phenotype on the strain data sheet | ||
| 008039 | B6.129S7-Gja1tm1Dlg/J | Repository- Live |
| Mice homozygous for this Cx43flox conditional allele are viable and fertile, with loxP sites flanking exon 2 of the targeted gene. Presence of the loxP sites has no reported affect on expression of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have exon 2 deleted in the cre-expressing tissue(s). These Cx43flox mutant mice may be useful in generating conditional mutations for studying the role of connexin and gap junctions in various tissues and systems, including the cardiovascular system. | ||
| 006883 | B6.129S7-Ldlrtm1Her Sod2tm1Leb/J | Repository- Live |
| Independently, mice that are homozygous for this MnSOD mutation (Sod2tm1Leb) allele exhibit postnatal lethality and exhibit anemia, degeneration of neurons in the basal ganglia and brainstem, progressive motor disturbances, and myocardial injury. Individual LDLR homozygous mutants are predisposed to atherosclerosis. When mutant mice are homozygous for both alleles, they die in utero. Mice heterozygous for the Sod2 mutation and homozygous for the LDLR are viable and fertile. The mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, and hypercholesterolemia, and oxidative stress. | ||
| 014632 | B6.Cg-Fbn1Tsk/J | Repository- Live |
| The Fbn1Tsk allele contains a 30 to 40kb genomic tandem duplication resulting in a larger than normal in-frame transcript. Homozygotes are embryonic lethal, failing to survive past somite formation (7-8 days of gestation). Heterozygotes are viable and fertile, exhibiting excessive growth and hyperplasia of connective tissue, cartilage, tendon sheaths and bone. Skin tightness, due to hyperplasic thickening of subcutaneous loose connective tissue and abnormal organization and distribution of skin microfibrillar arrays, develops by the first week after birth. Although the size of the skeleton is increased, body weight remains normal. Mutant mice exhibit polyuria during the light cycle. Collagens and glycosaminoglycans accumulate in the skin, heart, lungs and bladder. Hypertrophy is also observed in the enlarged heart (aortic adventitia). Mutant mice have enlarged thoracic size and lungs with abnormal alveolar walls, irregular shaped alveoli, and increased lung cap ..... For more information please see the full phenotype on the strain data sheet | ||
| 006965 | B6.Cg-Gt(ROSA)26Sortm1(rtTA*M2)Jae/J | Repository- Live |
| Homozygotes are viable, fertile, normal in size and do not display any behavioral abnormalities. These targeted mutant mice have widespread expression of an optimized form of reverse tetracycline-controlled transactivator (rtTA-M2) protein. This R26-M2rtTA strain may be useful for doxycycline-inducible studies which utilize rtTA/tet-O (tet-on/TRE) models. | ||
| 016231 | B6.Cg-Msh2tm2.1Rak/J | Repository- Live |
| The Msh2LoxP allele has loxP sites flanking exon 12 of the mutS homolog 2 (E. coli) [Msh2] gene. Homozygous Msh2LoxP mice are viable and fertile with no observed abnormalities. When bred to mice that express Cre recombinase, the resulting offspring will have the sequences encoding a portion of the essential ATPase domain of MSH2 protein deleted in the cre-expressing tissue(s). These Msh2LoxP mice may be useful in generating tissue-specific MSH2 deletions for studying DNA mismatch repair (single-nucleotide and insertion/deletion mismatches), as well as tumor development.
For example, when Msh2LoxP mice are bred to a strain expressing Cre recombinase in embryonic tissues (EIIA-Cre; see Stock Nos. 003314 or 003724), the resulting mice with pan deletion of MSH2 exhibit high inciden ..... | ||
| 006881 | B6.Cg-Tg(Aqp2-cre)1Dek/J | Repository- Live |
| Mice hemizygous for this AQP2-Cre transgene are viable and fertile. Transgenic cre activity, directed by the mouse aquaporin 2 promoter, is observed in kidney cells (collecting duct) and testes (sperm). When bred with mice containing a loxP-flanked sequence of interest, cre-mediated recombination will result in deletion of the flanked sequence. In such breedings, maternal inheritance of the transgene is recommended for kidney-specific recombinase activity as males express cre in sperm as well as kidney tissues. These AQP2-Cre mice may be used to generate conditional mutations in the renal collecting duct for studying nephrology, physiology, metabolism, or type II diabetes. In addition, cre expression in sperm may be useful in generating conditional mutations in multiple or all tissues in the resulting offspring. | ||
| 006137 | B6.Cg-Tg(Cdh5-cre)7Mlia/J | Repository- Live |
| Hemizygotes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. In the differentiated endothelium transgene expression is observed as early as E7.5 and progresses to almost full penetrance by E14.5. In adult mice, uniform cre expression is observed in the endothelium of developing and quiescent vessels of all organs examined, as well as within a subset of hematopoietic cells. When bred with any mouse containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the flanked genome. These mice may be useful in studies of the cardiovascular system, including angiogenesis, and endothelial and hematopoietic cell lineages. | ||
| 007742 | B6.Cg-Tg(Myh11-cre,-EGFP)2Mik/J | Repository- Live |
| Mice hemizygous for the smMHC/Cre/eGFP transgene (smMHCCre/eGFP) are viable and fertile, with the smooth muscle myosin heavy chain (smMHC or Myh11) promoter directing bicistronic Cre and EGFP protein expression to smooth muscle cells during development as well as in the adult mouse. Hemizygotes from founder line SMCG2 (SM2Cre/GFP) display intense EGFP fluorescence restricted to vascular and nonvascular smooth muscle, with strong concordance between cre expression and EGFP fluorescence (verifying the use of fluorescence as a marker for conditional gene recombination). When bred with mice containing a loxP-flanked sequence of interest, the resulting offspring can have Cre-mediated recombination of the flanked sequence in smooth muscle. Homozygotes are viable and fertile, with smaller litter sizes and a higher incidence of perinatal mortality. These smMHC/Cre/eGFP transgenic mice may be useful in studies utilizing "Cre-lox" technology or fluoresc ..... For more information please see the full phenotype on the strain data sheet | ||
| 008205 | B6.Cg-Tg(NPHS2-cre)295Lbh/J | Repository- Live |
| Podocin-Cre mice (mice harboring the p2.5P-Cre transgene) are viable and fertile, with expression of Cre recombinase directed to podocytes within kidney glomeruli by the human podocin (NPHS2) promoter/enhancer region. Cre-recombinase activity is reported in podocytes during late capillary loop stage of glomerular development and persists in podocytes of mature glomeruli, with no evidence for cre expression detected in other tissues examined. Embryonic Cre-recombinase activity is also reported as early as 8.5 dpc. When bred with mice containing a loxP-flanked sequence, Cre-mediated recombination will result in deletion of the sequence. These Podocin-Cre mice (mice harboring the p2.5P-Cre transgene) may be useful in generating conditional knockouts for studying the role of podocyte nephrobiology in renal disorders. | ||
| 008468 | B6.Cg-Tg(tetO-DTA)1Gfi/J | Repository- Live |
| These tet-DTA transgenic mice express diphtheria toxin A (DTA) under the control of a tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator) and a cytomegalovirus minimal promoter. When bred with another mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), tissue diphtheria toxin A expression can be regulated with the tetracycline analog doxycycline (dox) in the resulting double mutant offspring. These tet-DTA mice may be useful in generating bi-transgenic mutant mice for the reversible, inducible deletion of specific groups of cells.
For example, when bred to a strain expressing tTA in cardiac myocytes (see Stock No. 003170 for example), this mutant mouse strain may be useful in studies of human cardiomyopathies. When bred to a strain expressing tTA in pancreatic beta cells (see Stock N ..... | ||
| 005657 | B6.FVB(129)-Tg(Myh6-cre/Esr1*)1Jmk/J | Repository- Live |
| The alpha-MHC-MerCreMer transgene has the mouse Myh6 promoter (myosin, heavy polypeptide 6, cardiac muscle, alpha; alpha-MHC) directing expression of a tamoxifen-inducible Cre recombinase (MerCreMer) to juvenile and adult cardiac myocytes. Mice homozygous for the alpha-MHC-MerCreMer transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre recombinase expression in heart tissue is confirmed by western blot. Southern blot confirmed heart cell specificity compared to brain, kidney, lung, liver, and skeletal muscle. Insertion of this transgene and its protein show no changes in echocardiography, heart mass or pathology, or hypertrophy marker genes compared to nontransgenic littermates. Of note, the MerCreMer double fusion protein has substantially greater Cre recombinase activity with less promiscuity compared with the CreMer single fusion protein. When alpha-MHC-MerCreMer transgenic mice are bred with mice containing For more information please see the full phenotype on the strain data sheet | ||
| 006475 | B6.FVB(129S4)-Tg(Ckmm-cre)5Khn/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice have the Cre recombinase gene driven by the muscle creatine kinase (MCK or Ckm) promoter. Cre activity is observed in skeletal and cardiac muscle. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in skeletal and cardiac muscle deletion of the flanked genome. | ||
| 011038 | B6.FVB-Tg(Myh6-cre)2182Mds/J | Repository- Live |
| The cardiac-specific murine alpha myosin-heavy chain (Myh6, myosin, heavy polypeptide 6, cardiac muscle, alpha) promoter drives expression of cre in this transgenic strain. Breeding this mouse with another carrying loxP-flanked sequences results in the deletion of the flanked sequences in the offspring. The promoter induces greater than 90% recombination in cardiac muscle cells. No recombination is observed in liver, lung, skeletal muscle (quadriceps), and spleen, or in extraneous cell types in the heart. | ||
| 013781 | B6.FVB-Tg(Myh6/NFAT-luc)1Jmol/J | Repository- Live |
| These nuclear factor of activated T cell (NFAT)-luciferase transgenic mice display detectable luciferase activity in most tissues surveyed at 3 weeks of age, with highest expression occurring in brain, kidney, and heart - each of which are sites of considerable calcineurin (Ppp3ca, protein phosphatase 3, catalytic subunit, alpha isoform) protein expression. NFAT-luciferase activity peaks during developmental maturation of the heart, whereas the adult heart shows relatively lower activity. In the adult heart, NFAT-luciferase activity is upregulated in a delayed, but sustained manner throughout 8 weeks of pathological cardiac hypertrophy induced by pressure-overload, or more dramatically following myocardial infarction-induced heart failure. This strain may be useful in studies of cardiac hypertrophy and calcineurin/NFAT coupling. | ||
| 009336 | B6;129P2-Map1lc3btm1Mrab/J | Repository- Live |
| Homozygous (LC3β-/-) mice are viable and fertile, harboring an IRES Tau-lacZ/floxed PGK-neo allele that disrupts exons III-IV of the targeted gene. No LC3β protein expression from the targeted locus is detected in developing head and trunk tissues at embryonic day (E)14.5 or E18.5. No lacZ expression is reported. While homozygotes have a mild survival advantage in the absence of feeding (suggesting compensatory increase(s) in other autophagy proteins), no other overt phenotype is reported. LC3β-/- mouse embryonic fibroblasts (MEFs) exhibit reduced fibronectin synthesis but retain normal levels of fibronectin protein. These LC3β-mutant mice may be useful in studying the role of murine light chain RNA-binding proteins in fibronectin regulation as well as starvation and autophagy. | ||
| 014181 | B6;129S-Prkd1tm1Eno/J | Repository- Live |
| These mice possess loxP sites flanking exons 12 through 14 of the targeted gene, which encode part of the catalytic domain. 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 12 through 14 deleted in the cre-expressing tissue(s).
When bred to a strain with Cre recombinase expression in cardiomyocytes (see Stock No. 011038 for example), this mutant mouse strain may be useful in studies of cardiac response and remodeling due to pathological stress. | ||
| 009389 | B6;129S1-Bambitm1Jian/J | Repository- Live |
| Mice homozygous for this Bambiflox allele are viable and fertile, with loxP sites flanking exon 1 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have the sequences encoding the endogenous signal peptide deleted in the cre-expressing tissue(s); this is expected to produce a null allele. These mutant mice may be useful in generating conditional mutations for studying the role of Bambi in developmental biology and the TGF-beta pathway. | ||
| 006028 | B6;129S6-Epha2tm1Jrui/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile with no overt developmental or behavioral abnormalities. The Jackson Laboratory is distributing these mice on their original C57BL/6;129S6 mixed background. The published phenotype of these mutant mice is described below. In mutant mice of a mixed BALB/c, C57BL/6, and 129S6 background, murine pulmonary microvascular endothelial cells (MPMEC) isolated from homozygotes express no endogenous protein. MPMEC show impaired ephrin-A1-induced vascular assembly and defective migration both in vitro and in vivo. In addition, MPMEC from homozygous mice exhibit decreased angiogenesis and fail to activate Rac1 in response to ephrin-A1 in vivo. Mutant mice crossed to BALB/c for 7 generations are protected from tumor progression, angiogenesis and metastasis following metastatic mammary adenocarcinoma cell transplantation. These mutant mice may be useful in studies of postnatal angiogenesis (endothelial cell migra ..... | ||
| 005993 | B6;129S6-Pcsk9tm1Jdh/J | Repository- Live |
| Homozygous mice are viable and fertile with no behavioral abnormalities. No expression of the endogenous RNA or protein is observed in liver. Homozygotes have reduced plasma cholesterol levels; apolipoprotein B (apoB)-containing low-density liproprotein (LDL) is nearly undetectable and apolipoprotein E (apoE)-containing high density liproprotein (HDL) levels are reduced 30%. Homozygotes show increased hepatic LDL-receptor (LDLR) protein (but not RNA) expression. Homogygous mice also have accelerated clearance of circulating cholesterol. Lovastatin addition to the diet of homozygous mice results in further increased hepatic LDLR and LDL clearance from the blood. Heterozygous mice have intermediate plasma cholesterol and LDL clearance. This mouse may be useful in studies of lipid homeostasis, cholesterol metabolism, apolipoprotein function, and statin treatment for hypercholesterolemia. | ||
| 011039 | B6;129S7-Map3k7tm1Mds/J | Repository- Live |
| These mice carry a floxed allele of Map3k7 (mitogen-activated protein kinase kinase kinase 7). When bred to mice expressing cre recombinase, exon 1 of the targeted gene is deleted in the cre-expressing tissues of the offspring. This strain may be useful in studies of Wolff-Parkinson-White syndrome, electrophysiological and biochemical properties of the heart.
For example, when crossed to a strain expressing Cre recombinase in cardiac muscle cells (see Stock No. 011038), this mutant mouse strain may be useful in studies of cell metabolism. | ||
| 010803 | B6;FVB-Tg(Adipoq-cre)1Evdr/J | Repository- Live |
| Mice hemizygous for this Adipoq-Cre BAC transgene are viable and fertile, with expression of a Cre recombinase directed to adipose tissue by the promoter/regulatory regions of the mouse adiponectin (Adipoq) locus on the BAC transgene. Transcription/translation from the BAC Adipoq locus is disabled, and Cre recombinase expression levels are similar to that of endogenous Adipoq expression. These mice express Cre recombinase effectively in white adipose tissue (WAT) and brown adipose tissue (BAT), but not in macrophages (including adipose-tissue resident macrophages, alveolar macrophages, or thioglycollate-stimulated peritoneal macrophages). The donating investigator reports highly efficient Cre recombinase activity, with no ectopic expression. The phenotype of homozygous mice was not determined by the donating investigator. These Adipoq-Cre BAC transgenic mice may be useful in generating conditional mutations for studying adipose tissue function and storage, obesity, ..... For more information please see the full phenotype on the strain data sheet | ||
| 008850 | B6;SJL-Tg(Mt1-LDLR)93-4Reh/AgnJ | Repository- Live |
| Mice hemizygous for this MMT-I-hLDLR transgene (hLDLRTg mice) are viable and fertile, with human low density lipoprotein receptor (hLDLR) expression controlled by the mouse metallothionein 1 gene (Mt1) promoter sequences. The donating investigator reports that homozygous mice are not viable. Expression of hLDLR mRNA is highest in liver, moderate in kidney, small intestine, and heart, and lowest in brain and pancreas. Treatment with cadmium sulfate (CdSO4) stimulates transcription from the metallothionein promoter and results in higher levels of hLDLR expression. This overexpression of functional LDLR in transgenic mice results in greatly increased clearance of LDLR ligands (LDL, apoprotein B-100 and apoprotein E) from plasma when compared to wild-type mice. These hLDLRTg mice may be useful for studying the role of apolipoproteins and their receptors, lipid transport and lipoprotein metabolism in a wide variety of disease (including atherosclerosis, Alzheimer's disease, and hepat ..... For more information please see the full phenotype on the strain data sheet | ||
| 001692 | BXA1/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin.The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001699 | BXA11/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001700 | BXA12/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001701 | BXA13/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001702 | BXA14/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. In 2004 a phenotype of small body size was found to be segregating in this colony after recovery from cryopreservation. It appears that this phenotype is segregating recessively in this strain and is present in the cryopreserved bank stock. The expressed phenotype is small size relative to littermates and mice with this diminished body size often catch up to their littermantes in body size af ..... For more information please see the full phenotype on the strain data sheet | ||
| 001703 | BXA16/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001693 | BXA2/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001710 | BXA24/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001711 | BXA25/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001999 | BXA26/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001694 | BXA4/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001696 | BXA7/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001697 | BXA8/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. BXA17/Pgn was found to be a replica of BXA8/Pgn. BXA17/Pgn was lost in 1989 or 1990. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 008603 | C.129P2(B6)-Gt(ROSA)26Sortm1(tTA)Roos/J | Repository- Live |
| Mice heterozygous for the ROSA:LNL:tTA conditional mutation of the Gt(ROSA)26Sor locus are viable and fertile, with a loxP-flanked STOP cassette preventing transcription of a downstream optimized/modified tetracycline-controlled transactivator protein ("mtTA"). Applying both Cre-lox and Tet-Off technologies, these ROSA:LNL:tTA mutant mice may be useful to generate compound mutant mice in which expression of a tetracycline-responsive promoter element (TRE; also called tet-operator or tetO)-driven gene of interest can be both directed to the cell types defined by the chosen Cre recombinase expression, as well as turned off by the addition of tetracycline (or its analog doxycycline (dox)).
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 describe ..... | ||
| 007900 | C57BL/6-Gt(ROSA)26Sortm1(HBEGF)Awai/J | Repository- Live |
| Mice homozygous for this iDTR mutation are viable and fertile. These mice have the simian Diphtheria Toxin Receptor (DTR; from simian Hbegf) inserted into the Gt(ROSA)26Sor (ROSA26) locus. Widespread expression of DTR is blocked by an upstream loxP-flanked STOP sequence. When bred to Cre recombinase-expressing mice, the STOP sequence is deleted in tissues where Cre is present, permitting DTR expression. Cells expressing DTR are rendered susceptible to ablation following Diphtheria toxin administration.
For example, when bred to a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 006785), this mutant mouse strain may be useful in studies of lymphocyte cell ablation. When crossed to a strain expressing Cre recombinase in oocytes (see Stock No. 011062), this mutant mouse strain ma ..... | ||
| 012343 | C57BL/6-Gt(ROSA)26Sortm7(Pik3ca*,EGFP)Rsky/J | Repository- Live |
| Mice homozygous for the R26StopFLP110* conditional allele (also called P110*-transgene) are viable and fertile, with a loxP-flanked Neo-STOP cassette preventing transcription of the downstream bicistronic sequences (P110* [a constitutively active form of the mouse catalytic P110α subunit of phosphatidylinositol 3-kinase] and EGFP). When bred to mice that express Cre recombinase, offspring will have the STOP cassette deleted and subsequent expression of the P110* signal molecule and EGFP fluorescence in the cre-expressing cells. Expression of P110* leads to constitutively active PIK3 heterodimer activity; resulting in the generation of downstream effectors that mediate signal transduction cascades that control cell survival and cell cycle progression (growth, and proliferation). Of note, breeding these mice to an FLP-expressing strain will result in removal of the frt-flanked IRES-EGFP cassette. | ||
| 012352 | C57BL/6-Gt(ROSA)26Sortm8(Map2k1*,EGFP)Rsky/J | Repository- Live |
| Mice homozygous for the R26StopFLMEK1DD conditional allele are viable and fertile, with a loxP-flanked Neo-STOP cassette preventing transcription of the downstream bicistronic sequences (MEK1DD [a mutant form of rat MAPKK1 rendered constitutively active by two serine->aspartic acid substitutions (S218D/S222D) within the catalytic domain] and EGFP). When bred to mice that express Cre recombinase, offspring will have the STOP cassette deleted and subsequent expression of the MEK1DD signal molecule and EGFP fluorescence in the cre-expressing cells. Expression of MEK1DD leads to constitutive activity of MAP Kinase signal transduction pathways that mediate various cellular activities, including gene expression, mitosis, differentiation, proliferation, cell survival, and cell cycle progression. Of note, breeding these mice to an FLP-expressing strain will result in removal of the frt-flanked IRES-EGFP cassette. | ||
| 012361 | C57BL/6-Gt(ROSA)26Sortm9(Rac1*,EGFP)Rsky/J | Repository- Live |
| Mice homozygous for the R26StopFLRACDA conditional allele are viable and fertile, with a loxP-flanked Neo-STOP cassette preventing transcription of the downstream bicistronic sequences (RACDA [RacG12V; a mutant form of Rac1 rendered constitutively active by a glycine->valine substitution at amino acid 12] and EGFP). When bred to mice that express Cre recombinase, offspring will have the STOP cassette deleted and subsequent expression of the RACDA signal molecule and EGFP fluorescence in the cre-expressing cells. Expression of RACDA leads to constitutive activity of Rac1-dependent signal transduction; which is associated with gene expression, proliferation, cell survival, cell cycle progression, cytoskeletal reorganization, and Rho- and CDC42-pathways. Of note, breeding these mice to an FLP-expressing strain will result in removal of the frt-flanked IRES-EGFP cassette. | ||
| 008535 | C57BL/6-Tg(Pf4-cre)Q3Rsko/J | Repository- Live |
| These transgenic mice express a codon-improved Cre recombinase (iCre) under the control of the mouse Pf4 (platelet factor 4), or Cxcl4, promoter. Cre recombinase expression is detected in the majority of megakaryocytes. Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The BAC clone used to generate this strain also contains 4 other genes: Cxcl5, Cxcl7, Cxcl15 and Cxcl3. The additional copy of these chemokine genes in the BAC has no effect on blood count of the mutant mice. This strain represents an effective tool for generating megakaryocyte lineage-restricted specific-targeted mutants. | ||
| 013729 | C57BL/6-Tg(tetO-EDN1,-lacZ)9Mhus/J | Repository- Live |
| These ET+ transgenic mice express the human endothelin (EDN1 or ET-1) gene and a β-galactosidase (lacZ) reporter, both regulated by the bidirectional tetracycline operator, tetO. Homozygous mice are viable, fertile, and normal in size. ET-1 is a vasoconstrictor expressed in endothelial cells, and is a key mediator in vascular tone and renal homeostatsis. When mated to a mutant strain expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), LacZ and ET-1 expression may be regulated with the tetracycline analog doxycycline (DOX) in the double mutant offspring.
When bred to a strain expressing tTA driven by α-myosin heavy chain (α-MHC) cardiomyocyte specific (see Stock No. 003170) overexpression of lacZ and ET-1 results in left ventricular dilation, contractile dysfunction, ca ..... | ||
| 008040 | CBy.B6-Gt(ROSA)26Sortm1(HBEGF)Awai/J | Repository- Live |
| Mice homozygous for this iDTR mutation are viable and fertile. These mice have the simian Diphtheria Toxin Receptor (DTR; from simian Hbegf) inserted into the Gt(ROSA)26Sor (ROSA26) locus. Widespread expression of DTR is blocked by an upstream loxP-flanked STOP sequence. When bred to Cre recombinase-expressing mice, the STOP sequence is deleted in tissues where Cre is present, permitting DTR expression. Cells expressing DTR are rendered susceptible to ablation following Diphtheria toxin administration.
For example, when bred to a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 006785), this mutant mouse strain may be useful in studies of lymphocyte cell ablation. When crossed to a strain expressing Cre recombinase in the pituitary and, at lower levels, in the testes (see Stock No. > ..... | ||
| 007075 | CByJ.B6-Tg(CAG-EGFP)1Osb/J | Repository- Live |
| This transgenic mouse line with an "enhanced" GFP (EGFP) cDNA under the control of a chicken beta-actin promoter and cytomegalovirus enhancer makes all of the tissues, with the exception of erythrocytes and hair, appear green under excitation light. Note that mice homozygous for this transgene die within the first two weeks following birth.
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. Of note, it has been the experience at The Jackson Laboratory that Stock No. 006567 (C57BL/6-Tg(CAG-EGFP)131Osb/LeySopJ) demonstrates the highest proportion of GFP expr ..... | ||
| 013585 | FVB-Tg(Cdh5-tTA)D5Lbjn/J | Repository- Live |
| These transgenic mice express tetracycline regulated transactivator under the direction of the mouse Cdh5, cadherin 5, promoter. When these VE-Cadherin-tTA mice are bred with mice carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE, TetRE or tetO), expression of that gene in blood vessel endothelial cells may be conditionally inactivated with administration of the tetracycline in the double mutant offspring. Tetracycline was used by the Donating Investigator in the original publication Proc Natl Acad Sci 2005;102:128-33. When crossed with a strain carrying a tetracycline-responsive promoter driven lacZ transgene, beta-galactosidase is expression is observed in VEGFR-2, CD31 expressing cells in the blood vessels of bi-transgenic day 13.5 aged embryos. Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 016571 | FVB-Tg(Myh6/tetO-Gata6)2Jmol/J | Repository- Live |
| These Gata6 transgenic mice contain the GATA binding protein 6 (Gata6) sequence regulated by a tetracycline operator (tetO), driven by myosin, heavy polypeptide 6, cardiac muscle, alpha (Myh6 or α-MHC) promoter/enhancer elements. Hemizygotes are viable, fertile, and normal in size. α-MHC limits overexpression of GATA6 to the heart. GATA6 is a zinc-finger-containing transcription factor expressed in mesoderm and endoderm derived tissues such as heart, liver, lung, gonad, and gut. Along with GATA4, GATA6 is necessary for the development of the embryonic heart and cardiac hypertrophy in the adult heart. When mated to a mutant strain expressing tetracycline-controlled transactivator protein (tTA), expression of GATA6 protein may be regulated with tetracycline or its analog doxycycline (dox) in the double mutant offspring. When bred to mice expressing tTA driven by the α-MHC promoter, double transgenic an ..... For more information please see the full phenotype on the strain data sheet | ||
| 014155 | FVB-Tg(Myh6/tetO-Itpr1)22.3Jmol/J | Repository- Live |
| In this transgenic strain, a conditional Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha )/tetO promoter drives expression of a recombinant mouse "IP3 sponge". The IP3 binding domain encoded by amino acid residues 224-604 of mouse type 1 IP3R (Itpr1 (inositol 1,4,5-triphosphate receptor 1); also called mIP3R1) is fused to glutathione S-transferase (GST). This enables expression of high affinity IP3 chelator fusion protein when the strain is crossed with a driver strain encoding tetracycline transactivator (tTA). | ||
| 014153 | FVB-Tg(Myh6/tetO-Itpr2)3.11Jmol/J | Repository- Live |
| These transgenic animals carry the mouse Itpr2 (inositol 1,4,5-triphosphate receptor 2) gene driven by a conditional Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha)-tetO cardiac-specific promoter.
When crossed with a driver strain encoding the tetracycline transactivator (tTA), a 12-fold increase in protein expression is observed. Overexpression in the heart generates mild baseline cardiac hypertrophy at 3 months of age, but no greater signs of heart disease past 10 months of age. Increased hypertrophic response occurs following pathological/physiological stimuli. | ||
| 014154 | FVB-Tg(Myh6/tetO-Itpr2)4.9Jmol/J | Repository- Live |
| These transgenic animals carry the mouse Itpr2 (inositol 1,4,5-triphosphate receptor 2) driven by a conditional Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha)-tetO cardiac-specific promoter.
When crossed with a driver strain encoding the tetracycline transactivator (tTA), a 5-fold increase in protein expression is observed. No phenotype is observed at baseline, but increased hypertrophic response occurs following certain types of stumuli. Administration of doxycline (Dox) causes near complete extinguishment of ITPR2 expression. | ||
| 013778 | FVB-Tg(tetO-Cacnb2)1Jmol/J | Repository- Live |
| Expression of Cacnb2 (calcium channel, voltage-dependent, beta 2 subunit) is regulated by a tetracycline operator (tetO); also called tetracycline-responsive element (TRE, TetRE) or tet-operator) in this transgenic strain. When mated to a mutant strain expressing tetracycline-controlled transactivator protein (tTA), expression of CACNB2 protein may be regulated with tetracycline or its analog doxycycline (dox) in the double mutant offspring. When crossed with a Myh6-tTA strain (e.g. Stock No. 003170), double transgenic mice show increased Ca2+ influx through cardiac L-type Ca2+ channels resulting in Ca2+ overload, myocyte disorganization, interstitial fibrosis, and cell death. Compound mutant animals show a 7.4-fold increase in CACNB2 expression. This strain may be useful in studies of cardiomyopathy. | ||
| 013780 | FVB-Tg(tetO-Cib1)1Jmol/J | Repository- Live |
| Expression of Cib1 (calcium and integrin binding 1 (calmyrin)) is regulated by a tetracycline operator (tetO); also called tetracycline-responsive element (TRE, TetRE) or tet-operator) in this transgenic strain. When mated to a mutant strain expressing tetracycline-controlled transactivator protein (tTA), expression of CIB1 protein may be regulated with tetracycline or its analog doxycycline (dox) in the double mutant offspring. When crossed with a Myh6-tTA strain (e.g. Stock No. 003170), double transgenic mice show enhanced cardiac hypertrophy in response to pressure overload or calcineurin signalling. This strain may be useful in studies of cardiac hypertrophy. | ||
| 012387 | FVB-Tg(tetO-Ppargc1a)1Dpk/J | Repository- Live |
| These transgenic mice express Ppargc1a (peroxisome proliferative activated receptor, gamma, coactivator 1 alpha) and a myc-his tag regulated by the tetracycline operator (tetO; also called tetracycline-responsive element (TRE, TetRE) or tet-operator). When mated to a mutant strain expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), tissue Ppargc1a expression may be regulated with the tetracycline analog doxycycline (dox) in the double mutant offspring. This strain may be useful for studies of metabolism, cardiomyopathy, and mitochodrial function. | ||
| 006206 | FVB.129S6-Gt(ROSA)26Sortm2(HIF1A/luc)Kael/J | Repository- Live |
| Mice heterozygous for this "ODD-luc" knock-in are viable and fertile with no gross phenotypic or behavioral abnormalities. These mice have the C-terminal portion of the hypoxia-inducible factor 1 alpha (HIF1A) oxygen-dependent degradation domain (ODD) fused to the firefly luciferase (luc) gene. This region of the ODD also contains a proline residue (amino acid 564) that, when hydroxylated, will serve as a binding site for von Hippel-Lindau tumor suppressor protein (pVHL). Under normal oxygen concentrations, prolyl hydroxylation by egg-laying-defective nine (EGLN) proteins leads to pVHL-dependent polyubiquitylation and proteasomal degradation (thus, little or no luciferase fluorescence). Under hypoxia, proline hydroxylation is impaired and ubiquitination is attenuated, resulting in stabilization of the fusion protein and high levels of luciferase fluorescence in the hypoxic tissue(s). These "ODD-Luc" bioluminescent reporter mice may be useful in researching transcriptional ..... For more information please see the full phenotype on the strain data sheet | ||
| 003516 | FVB.Cg-Tg(CAG-EGFP)B5Nagy/J | Repository- Live |
| This transgenic strain expresses an Enhanced Green Fluorescent Protein (Clontech) driven by chicken beta-actin promoter and CMV intermediate early enhancer. Mice, and cells derived from them, are distinguished from wildtype on the basis of fluorescence. The transgene is expressed in all nucleated embryonic tissues. Cells and tissues with increased hemoglobin content exhibit reduced fluorescence as development progresses. In newborn and adult mice, the entire organ system expresses EGFP. Though widespread, expression levels vary between different organs. This strain can be used as a source of fluorescently marked cells or tissues. Animals from stock 003516 homozygous for Tg(CAG-EGFP)B5Nagy allele have displayed an increased incidence of lymphoma compared to animals hemizygous for this allele. Lymphoma in homozygous breeders for stock 003516 has been observed as early as 4 months of age. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles ..... | ||
| 002856 | FVB/N-Tg(TIE2-lacZ)182Sato/J | Repository- Live |
| Transgenic mice carry a beta-galactosidase reporter gene under the control of the murine Tek (Tie2) promoter. LacZ is expressed specifically in vascular endothelial cells in embryonic and adult mice. The transgenic line may be useful when crossed with tumor producing strains and the transgene used to visualize neovascularization during tumorigenesis. | ||
| 008407 | STOCK Epas1tm1Mcs/J | Repository- Live |
| The Hif-2α 2-loxP allele, also called Hif-2&alphafl or Epas12lox, contains loxP sites flanking exon 2 of the endothelial PAS domain protein 1 locus (Epas1 or Hif-2α). Homozygous mice are 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 deleted in the cre-expressing tissue(s).
For example, when bred to a strain with inducible Cre recombinase expression in cardiac cells (see Stock No. 005657 for example), this mutant mouse strain may be useful in studies of erythropoiesis. When bred to a strain with tamoxifen inducible widespread Cre recombinase expression(see Stock No. 008085 for example), this mutant mouse strain may be useful in studie ..... | ||
| 010698 | STOCK Fgf2tm2Doe/J | Repository- Live |
| Mice homozygous for the Fgf2lmw-ko (Fgf2lmw or FGF2 LMWKO) allele are viable and fertile with no reported abnormalities in endothelial cell migration and proliferation. As the targeted allele disrupts expression of the fibroblast growth factor 2 low molecular weight (Fgf2 lmw) isoform, the 18 kDa isoform is not expressed (as demonstrated in brain, aorta, lung, and endothelial cells from homozygous mice). The Fgf2 high molecular weight (hmw) isoforms (20.5 and 21 kDa) are still expressed in the nucleus from the targeted allele. Homozygous mice have significantly reduced bone mineral density and fewer mineralized nodules, coincident with increased expression of the Wnt antagonist secreted frizzled receptor 1 (sFRP-1) in bone tissue. Homozygous deficiency of the Fgf2 lmw isoform is associated with significantly impaired recovery in postischemic cardiac/contractile function after ischemia-reperfusion (I-R) injury. | ||
| 010720 | STOCK Fgf2tm3Doe/J | Repository- Live |
| Mice homozygous for the Fgf2hmw-ko (Fgf2hmw or FGF2 HMWKO) allele are viable and fertile with no histological, immunohistochemical, or morphometric abnormalities in myocardial architecture or blood vessel and cardiac capillary density. As the targeted allele disrupts expression of the two Fgf2 high molecular weight (Fgf2 hmw) isoforms, the 20.5 and 21 kDa isoforms are not expressed (as demonstrated in heart, liver, and brain tissues from homozygous mice). The Fgf2 low molecular weight (lmw) isoform (18 kDa) is still expressed in the cytoplasm and nucleus from the targeted allele. Homozygous deficiency of the Fgf2 hmw isoforms is associated with significant improvement in postischemic cardiac/contractile function after ischemia-reperfusion (I-R) injury. | ||
| 008194 | STOCK Gata4tm1.1Sad/J | Repository- Live |
| Mice homozygous for this Gata4loxP conditional allele are viable and fertile, with loxP sites flanking exons 3-5 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (coding for both zinc finger DNA-binding domains and the nuclear localization signal essential for GATA4 function) deleted in the cre-expressing tissue(s). These GATA binding protein 4 conditional mice may be useful in generating conditional mutations for studying GATA4 function during organogenesis (such as cardiogenesis) or in adult mice.
For example, when crossed to a strain expressing Cre recombinase in cardiac myocytes (see Stock No. 009074), this mutant mouse strain may be useful in studies of cardiac hypertrophy, stress-compensation and myocyte viability. When bred to a strain expressing Cre recombinase in heart muscle (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 013731 | STOCK Gt(ROSA)26Sortm1(CAG-Brainbow2.1)Cle/J | Repository- Live |
| Mice homozygous for the R26R-Confetti conditional allele are viable and fertile, with a CAG promoter, loxP site, and STOP cassette preventing transcription of the downstream Brainbow 2.1 sequences. The Brainbow 2.1 region contains two loxP-flanked dimers, each uniquely positioned in head-to-tail tandem. One dimer has nuclear-localized green fluorescent protein (hrGFPII) and a reverse-oriented cytoplasmic yellow fluorescent protein (mYFP). The other dimer has cytoplasmic red fluorescent protein (tdimer2(12)) and a reverse-oriented membrane-tethered cyan fluorescent protein (mCerulean). The Brainbow2.1 region may be written as loxP-STOP-loxP-GFP-PFY-Pxol-loxP-RFP-PFC-Pxol to show the transcriptional direction of each part. When bred to mice that express Cre recombinase, the resulting offspring may have a recombination event that stochastically places one of the four fluorescent proteins into position directly downstream of the CAG promote ..... For more information please see the full phenotype on the strain data sheet | ||
| 006331 | STOCK Gt(ROSA)26Sortm1(DTA)Jpmb/J | Repository- Live |
| Homozygous "ROSA26-eGFP-DTA" mice are viable, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator reports that some homozygous males are subfertile. Mutant mice display widespread expression of EGFP, but DTA transcription is prevented by a strong transcriptional stop sequence. When bred to mice that express Cre recombinase under the control of a promoter of interest, the loxP-flanked EGFP and stop sequence are removed, and DTA expression is activated, resulting in the specific ablation of cre-expressing cells. This strain may be useful on its own as a fluorescent reporter or in combination with cre-expressing mice to produce conditional deletions of specific groups of cells. Transgenic mice also may have applications in toxicology and protein synthesis research.
For example, when crossed to a strain expressing Cre recombinase in the midbrain and dorsal spinal cord (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 008600 | STOCK Gt(ROSA)26Sortm1(tTA)Roos/J | Repository- Live |
| Mice heterozygous for the ROSA:LNL:tTA conditional mutation of the Gt(ROSA)26Sor locus are viable and fertile, with a loxP-flanked STOP cassette preventing transcription of a downstream optimized/modified tetracycline-controlled transactivator protein ("mtTA"). Applying both Cre-lox and Tet-Off technologies, these ROSA:LNL:tTA mutant mice may be useful to generate compound mutant mice in which expression of a tetracycline-responsive promoter element (TRE; also called tet-operator or tetO)-driven gene of interest can be both directed to the cell types defined by the chosen Cre recombinase expression, as well as turned off by the addition of tetracycline (or its analog doxycycline (dox)). | ||
| 012266 | STOCK Gt(ROSA)26Sortm5(ACTB-tTA)Luo/J | Repository- Live |
| Mice homozygous for this ROSA26-ZtTA (or ZtTA) conditional allele are viable and fertile, although the donating investigator reports that heterozygous mice are more healthy and fertile than homozygous mice. This ROSA26-ZtTA (or ZtTA) conditional allele is designed with a loxP-flanked β-geo transcriptional STOP cassette preventing transcription of the downstream tetracycline-controlled transactivator protein (tTA). When bred to mice that express Cre recombinase, offspring will have the STOP cassette deleted and subsequent expression of the tTA in the cre-expressing cells. The donating investigator reports that the CMV enhancer/chicken beta-actin core promoter (pCA) allows stronger and persistent expression of the downstream tTA (especially in adult cells) compared to the endogenous Gt(ROSA)26Sor locus alone. Applying both Cre-lox and Tet-Off technologies, these ZtTA mutant mice may be useful to generate compound mutant mice in which expression of a tetracyclin ..... For more information please see the full phenotype on the strain data sheet | ||
| 006770 | STOCK Rag1tm1Mom Tg(TIE2GFP)287Sato/J | Repository- Live |
| To generate this double mutant strain, B6.Cg-Tg(TIE2GFP)287Sato/1J (Stock No. 004659) was crossed to C.129S7(B6)-Rag1tm1Mom/J (Stock No. 003145). This mutant mouse strain may be useful in studies examining angiogenesis in transplanted tissues. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described for each single mutant. We will modify the strain description if necessary as published results become available. | ||
| 010911 | STOCK Wt1tm1(EGFP/cre)Wtp/J | Repository- Live |
| Homozygous mice die between embryonic day (E)13.5 and birth with defects of heart, kidney, gonads, and multiple other organs. Heterozygous (Wt1GFPCre/+) mice are viable and fertile. The Wt1GFPCre "knock-in" allele both abolishes Wt1 gene function and expresses an enhanced green fluorescent protein-Cre recombinase fusion protein (EGFPCre) from the Wt1 promoter/enhancer elements. In heart from heterozygous mice, EGFPCre expression is directed to proepicardium and epicardium from E9.5 to E15.5, and is not found in the myocardium. When bred to mice containing loxP-flanked sequences, the resulting offspring will have Cre-mediated deletion of the floxed sequences in the Wt1-expressing cells (and their descendants). As Wt1 is expressed in the developing genitourinary system and in the mesothelia overlying most visceral organs, these mutant mice may be useful as fluorescent/Cre-lox tools for lineage-tracing/marking Wt1-expressin ..... For more information please see the full phenotype on the strain data sheet | ||
| 010912 | STOCK Wt1tm2(cre/ERT2)Wtp/J | Repository- Live |
| Homozygous mice die between embryonic day (E)13.5 and birth with defects of heart, kidney, gonads, and multiple other organs. Heterozygous (Wt1CreERT2/+) mice are viable and fertile. The Wt1CreERT2 "knock-in" allele both abolishes Wt1 gene function and has expression of the CreERT2 fusion protein (CreERT2) under control of the Wt1 promoter/enhancer elements. In heart from heterozygous mice, CreERT2 expression is directed to proepicardium and epicardium from E9.5 to E15.5, and is not found in the myocardium. CreERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Wt1CreERT2 mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Wt1-expressing cells of the offspring. The donating investigator reports that Cre activity may be observed prior to tamoxifen exposure only in ..... For more information please see the full phenotype on the strain data sheet | ||
| 013749 | STOCK Tg(ACTB-EGFP,-tdTomato)11Luo/J | Repository- Live |
| Homozygous MADM-11GT mice are viable and fertile with no gross behavioral or observable abnormalities. The MADM-11GT allele has the CMV enhancer/chicken beta-actin core promoter, the N-terminal portion of a mutant enhanced green fluorescent protein (mut4-EGFP), a beta-globin intronic sequence containing an frt site and a loxP-flanked neomycin resistance gene, and the MYC-tagged C-terminal portion of a red fluorescent protein (tdTomato) all inserted into the Hipp11 locus on chromosome 11 (cytoband A1 at ~3cM between the Eif4enif1 and Drg1 loci). These MADM-11GT mutants are designed for MADM (mosaic analysis with double markers), and must be crossed to MADM-11TG mice harboring a reciprocal mutation at the same locus (see Stock No. 013751). The resulting GT/TG offspring have one copy of each reciprocal mutation on homologous chromosomes ("trans-heterozygou ..... For more information please see the full phenotype on the strain data sheet | ||
| 014092 | STOCK Tg(ACTB-tTA2,-MAPT/lacZ)1Luo/J | Repository- Live |
| Homozygous CAG-stop-tTA2 transgenic mice are viable and fertile. CAG-stop-tTA2 transgenic mice harbor the ii-CAG-stop-tTA2-IRES-tau-lacZ-ii transgene; designed with a loxP-flanked transcriptional STOP cassette preventing transcription of the downstream modified tetracycline-regulated transactivator (tTA2). The ii-CAG-stop-tTA2-IRES-tau-lacZ-ii transgene is flanked by two copies of the chicken β-globin HS4 insulator on each side to preserve expression fidelity (see additional information below). When bred to mice that express a tamoxifen-inducible Cre recombinase (CreERT2), administration of tamoxifen to the double mutant offspring allows the CreERT2 fusion protein to enter the nucleus of the cre-expressing cells; this deletes the STOP cassette and results in expression of tTA2. The donating investigator reports that tau-lacZ fusion protein expression in the tamoxifen-treated double mutant offspring is faint. Of note, the donating investigator h ..... For more information please see the full phenotype on the strain data sheet | ||
| 013751 | STOCK Tg(ACTB-tdTomato,-EGFP)11Luo/J | Repository- Live |
| Homozygous MADM-11TG mice are viable and fertile with no gross behavioral or observable abnormalities. The MADM-11TG allele has the CMV enhancer/chicken beta-actin core promoter, the N-terminal portion of a red fluorescent protein (tdTomato), a beta-globin intronic sequence containing an frt site and a loxP-flanked neomycin resistance gene, and the C-terminal portion of a mutant enhanced green fluorescent protein (mut4-EGFP) all inserted into the Hipp11 locus on chromosome 11 (cytoband A1 at ~3cM between the Eif4enif1 and Drg1 loci). These MADM-11TG mutants are designed for MADM (mosaic analysis with double markers), and must be crossed to MADM-11GT mice harboring a reciprocal mutation at the same locus (see Stock No. 013749). The resulting TG/GT offspring have one copy of each reciprocal mutation on homologous chromosomes ("trans-heterozygous"), and mu ..... For more information please see the full phenotype on the strain data sheet | ||
| 003116 | STOCK Tg(CAG-EGFP)D4Nagy/J | Repository- Live |
| This transgenic strain carries the Enhanced Green Fluorescent Protein (Clontech) driven by chicken beta-actin promoter and CMV intermediate early enhancer. The transgene was found to have integrated on the X chromosome. Mice of this strain, and cells derived from them, can be distinguished from wildtype on the basis of fluorescence. Transgene expression is seen as early as ~embryonic day 2.75, as morula stage embryos begin to compact. Expression of EGFP is spatiotemporally widespread, though levels differ between different lineages (e.g., expression is slightly higher in the heart). As the transgene is located on the X chromosome, transgenic males will exclusively transmit the EGFP transgene to their female offspring, providing the basis for a non-invasive sexing assay based on green fluorescence. These mice may be useful for sex discrimination prior to overt sexual dimorphism (embryonic day 12.5), monitoring X-inactivation, and may be a source of fluorescently marked cells/tiss ..... For more information please see the full phenotype on the strain data sheet | ||
| 008755 | STOCK Tg(Ins2-rtTA)2Efr Tg(teto-DTA)1Gfi/J | Repository- Live |
| This strain was generated by breeding Stock No. 008168 and Stock No. 008250 together at The Jackson Laboratory. The resulting double transgenic colony was established as Stock No. 008755. The Ins2-rtTA (or RIP7-rtTA) transgene expresses the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the rat insulin 2 (Ins2) promoter. The tet-DTA (or tetO-DTA) (transgene expresses diphtheria toxin A (DTA) under the control of a tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator) and a cytomegalovirus minimal promoter. Mice harboring both of these transgenes has doxycycline-inducible expression of DTA in pancreatic beta cells; i.e. addition of the tetracycline analogue doxycycline (dox) results in ablation of pancreatic beta cells. | ||
| 009074 | STOCK Tg(Myh6-cre)1Jmk/J | Repository- Live |
| These transgenic mice express nuclear-localizing Cre recombinase under the control of the mouse Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha; alpha-MHC) promoter. Cre recombinase expression is detected in a majority of cardiac myocytes. Approximately 70% efficiency has been demonstrated when crossed with one floxed allele strain. Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Evidence suggests that this transgene is X-linked. | ||
| 005650 | STOCK Tg(Myh6-cre/Esr1*)1Jmk/J | Repository- Live |
| The alpha-MHC-MerCreMer transgene has the mouse Myh6 promoter (myosin, heavy polypeptide 6, cardiac muscle, alpha; alpha-MHC) directing expression of a tamoxifen-inducible Cre recombinase (MerCreMer) to juvenile and adult cardiac myocytes. Mice homozygous for the alpha-MHC-MerCreMer transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre recombinase expression in heart tissue is confirmed by western blot. Southern blot confirmed heart cell specificity compared to brain, kidney, lung, liver, and skeletal muscle. Insertion of this transgene and its protein show no changes in echocardiography, heart mass or pathology, or hypertrophy marker genes compared to nontransgenic littermates. Of note, the MerCreMer double fusion protein has substantially greater Cre recombinase activity with less promiscuity compared with the CreMer single fusion protein. When alpha-MHC-MerCreMer transgenic mice are bred with mice containing For more information please see the full phenotype on the strain data sheet | ||
| 003658 | STOCK Tg(TIE2GFP)287Sato/J | Repository- Live |
| This strain expresses Green Fluorescent Protein (GFP) under the direction of the endothelial-specific receptor tyrosine kinase (Tek, formerly, Tie2) promoter. Endothelial cells expressing GFP can be visualized via fluorescent microscopy or purified by FACS. | ||
| 005493 | STOCK Tg(Tek-rtTA,TRE-lacZ)1425Tpr/J | Repository- Live |
| Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice harbor co-injected transgenic constructs. The reverse tetracycline-controlled transactivator (rtTA) protein is expressed under the direction of the endothelial-specific receptor tyrosine kinase enhancer/promoter (Tek). The second transgenic construct expresses a nuclear-localizing beta-galactosidase gene (lacZ) under the control of a tetracycline-responsive element (TRE). In the presence of tetracycline or a tetracycline analog (such as doxycycline), selective expression of lacZ is observed in the nuclei of vascular endothelium in a wide variety of tissues (aorta, heart, brain, lung, kidney, liver, spleen, uterus, prostate, stomach, skeletal muscle, large and small intestine). Expression is observed as early as embryonic day 9.5. In the absence of tetracycline, some lacZ expression occurs in the smaller branches of ..... For more information please see the full phenotype on the strain data sheet | ||
| 012345 | STOCK Tg(tetO-tdTomato,-Syp/EGFP*)1.1Luo/J | Repository- Live |
| Hemizygous TRE-Bi-SG-T line 1.1 transgenic mice are viable and fertile, with no reported phenotypic abnormalities. The TRE-Bi-SG-T transgene has Myc-tagged tdTomato and full-length mouse synaptophysin/mut4EGFP fusion protein (Syp-GFP) expression under the control of the bi-directional tet-responsive promoter (tetO or TRE). When bred with another mouse expressing tetracycline-controlled transactivator protein (tTA) or reverse tetracycline-controlled transactivator protein (rtTA), tdTomato and Syp-GFP fusion protein expression can be regulated with the tetracycline analog doxycycline (dox) in the resulting double mutant offspring. In tTA(-dox) or rtTA(+dox)-expressing cells, tdTomato expression is directed to the entire cell, while GFP expression is directed to the synapse/synaptic vesicle. The donating investigator reports that direct GFP fluorescence and direct tdTomato fluorescence may be visualized in these mice when tTA is present/dox is absent. In addition, the three Myc epi ..... For more information please see the full phenotype on the strain data sheet | ||
| 005989 | 129;FVB-Tg(PTH-cre)4167Slib/J | Cryopreserved - Ready for recovery |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre activity is observed only in parathyroid tissue; no activity is seen in thyroid, muscle, lymph node, trachea, thymus, salivary tissues, lung, heart, liver, brain, stomach, spleen, kidney, large intestine, small intestine, and pancreas. When bred with any mouse containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in parathyroid-specific deletion of the flanked genome. These transgenic mice may be useful in generating mouse models of parathyroid-specific deletion of genes of interest, such as multiple endocrine neoplasia type 1, extracellular calcium-sensing receptor, and vitamin D receptor. | ||
| 007175 | 129S-Cyp4a14tm1Jhc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this "Cyp 4a14" mutant allele are viable and fertile. Homozygous deficiency of the targeted gene leads to spontaneous hypertension (more severe in males) that is androgen-sensitive. Homozygotes also exhibit other interrelated metabolic and regulatory effects; increased renal vascular resistance, impaired renal hemodynamics, elevated plasma androgens (5α-dihydrotestosterone (DHT) and testosterone), upregulated Cyp4a12 gene expression, and increased formation of prohypertensive 20-HETE. These "Cyp 4a14" mutant mice may be useful studying kidney function and metabolism, cardiovascular physiology, hypertension, and the relationships between blood pressure, sex hormones, and p450 ω-hydroxylases. | ||
| 007005 | 129S-Scg5tm1Led/J | Cryopreserved - Ready for recovery |
| The colony at The Jackson Laboratory Repository is on a mixed 129S genetic background and may not recapitulate the phenotype originally described.
The following text reflects the phenotype reported by the donating investigator (Dr. Iris Lindberg) on a "129Sv" genetic background (probably "Taconic Sv129" (129S6/SvEvJ)). | ||
| 008238 | 129S-Seletm1Dmil/J | Cryopreserved - Ready for recovery |
| 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 ..... | ||
| 007199 | 129S-Sgpl1Gt(ROSA)78Sor/J | Cryopreserved - Ready for recovery |
| 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 phenotype on the strain data sheet | ||
| 008523 | 129S6.Cg-Tg(NPHS2-cre)295Lbh/BroJ | Cryopreserved - Ready for recovery |
| Mice harboring the p2.5P-Cre transgene are viable and fertile, with expression of Cre recombinase directed to podocytes within kidney glomeruli by the human podocin (NPHS2) promoter/enhancer region. Cre-recombinase activity is reported in podocytes during late capillary loop stage of glomerular development and persists in podocytes of mature glomeruli, with no evidence for cre expression detected in other tissues examined. Embryonic Cre-recombinase activity is also reported as early as 8.5 dpc. When bred with mice containing a loxP-flanked sequence, Cre-mediated recombination will result in deletion of the sequence. These 2.5P-Cre transgenic mice may be useful in generating conditional knockouts for studying the role of podocyte nephrobiology in renal disorders. | ||
| 001684 | AXB13a/PgnJ | Cryopreserved - Ready for recovery |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB13/PgnJ and AXB14/PgnJ are considered "sister strains" being identical throughout much of the genome but differing in large regions of Chromosomes 11, 12, 13, and in small regions of a few other Chromosomes. Because these two strains are "near congenics" a nomenclature change has been made to update AXB14/PgnJ to AXB13a/PgnJ. In general, "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis.
The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibi ..... | ||
| 008884 | B6.129(Cg)-Pnliptm1Dyh/J | Cryopreserved - Ready for recovery |
| These mice harbor a null mutation of the Pnlip (pancreatic lipase [also called pancreatic triglyceride lipase or PTL]) gene. Homozygous (PTL-/-) mice are viable and fertile, with no protein expression from the targeted allele observed in pancreatic tissue extracts. Homozygotes exhibit mildly delayed triglyceride (also called triacylglycerol or TAG) absorption after low fat diet feeding, but significantly delayed TAG absorption on a high fat/high cholesterol diet. Homozygous mice have a significant decrease in the rate/amount of cholesterol absorption; attributed to PTL-deficiency delaying dietary fat absorption to the distal small intestine (ileum) where intestinal cholesterol uptake is less efficient. Because PLT-/- mice retain endogenous Cel (carboxyl ester lipase [also called cholesterol esterase]) expression, pancreatic extracts from PTL-/- mice retain robust TAG hydrolytic activity (albeit at lower levels than wildtype mice). This TAG hydrolytic ..... For more information please see the full phenotype on the strain data sheet | ||
| 006203 | B6.129(FVB)-Ahrtm3.1Bra/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exon 2 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. Hepatic protein expression of the conditional allele (before exon 2 excision) is equivalent to wildtype by Western blot analysis. This strain may be useful in generating tissue-specific mutants of the floxed allele for use in studies including teratogenesis and xenobiotic metabolism (including dioxin and PCB), Per-Arnt-Sim transcription factors, and fetal vascular development such as ductus venosus closure.
When bred to a strain expressing Cre recombinase in hepatocytes (see Stock No. 003574 for example), this mutant mouse strain may be useful in studies of toxicology. When bred to a strain expressing Cre recombinase in endothelial cells (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 005704 | B6.129-Fbn1tm2Rmz/J | Cryopreserved - Ready for recovery |
| Both heterozygous and homozygous "mgR" mutant mice are viable with no phenotypic abnormalities at birth. The protein expressed from this mutant allele is the same size as wild-type. Skin tissues show an intermediate reduction in transcript levels compared to wild-type and the mg-delta null allele. Thus the "mgR" mutation does not completely ablate gene function (resulting in rapid death). Instead, expression is hypomorphic and conducive to studying the clinical stages precursive to animal lethality. Homozygotes develop medial calcification, the inflammatory-fibroproliferative response, and inflammation-mediated elastolysis in the natural history of dissecting aneurysm and die between 2-6 month of age with Marfan syndrome (MFS)-like manifestations. | ||
| 008518 | B6.129-Leprtm1Mgmj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the LeprS1138 mutant allele (or s/s mice) are viable and partially fertile with a Tyr->Ser replacement at amino acid residue 1138 of the leptin receptor long form (LRb)-specific exon 18b. The mutation specifically disrupts LRb-STAT3 transcription factor signaling. The mutant protein, LRbS1138, is expressed normally on the cell surface and mediates other leptin signals normally, but fails to activate STAT3. Similar to homozygous db/db mice (which are devoid of all leptin signaling), homozygous s/s mice display hyperphagia, decreased energy expenditure, and decreased thyroid function resulting in profound obesity and dramatically increased serum leptin levels compared to wild-type. Unlike db/db mice, however, s/s mice are fertile and long bodied, have improved glucose tolerance (less hyperglycemic), are not protected from intimal hyperplasia following vessel injury, and do not exhibit elevated hypothalamic ex ..... For more information please see the full phenotype on the strain data sheet | ||
| 008385 | B6.129-Leprtm2Mgmj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the LeprLeu985 mutant allele (or l/l mice) are viable and fertile with a Tyr->Leu replacement at amino acid residue 985 of the leptin receptor long form (LRb)-specific exon 18b. The mutation specifically disrupts LRb-SHP2 and LRb-SOCS3 transcription factor signaling. The mutant protein, LRbL985, is expressed normally and mediates other leptin signals normally, but fails to recruit SHP2 or SOCS3. Homozygous male and female mice are neuroendocrinologically normal, but homozygous females may exhibit decreased feeding, body weight, adipocity, circulating leptin, circulating insulin, expression of orexigenic neuropeptides, protection from high-fat diet-induced obesity, and increased leptin sensitivity depending upon diet and genetic background. Homozygous LeprLeu985 mutant mice may be useful for studying the influence of LRb-SHP2 and LRb-SOCS3 signaling in the physiological and metabolic function of leptin; specifically b ..... For more information please see the full phenotype on the strain data sheet | ||
| 008397 | B6.129-Pcyt1atm1Irt/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exons 4 and 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 4 and 5 deleted in the cre-expressing tissue(s). When bred to a strain with inducible Cre recombinase expression in the myeloid cell lineage (see Stock No. 004781 for example), this mutant mouse strain may be useful in studies of atherosclerosis. | ||
| 006879 | B6.129-Scd2tm1Myz/J | Cryopreserved - Ready for recovery |
| While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die within 24 hours of birth. Brain tissues from homozygous mice show no expression from the targeted gene. Homozygotes exhibit neonatal lethality with 100% penetrance on this genetic background (less penetrant on 129SvEv genetic background) likely due to severe skin permeability barrier abnormalities. Null mice also have abnormal epidermal morphology and abnormal lipid homeostasis in the skin and liver. These mutant mice may be useful in studying monounsaturated fatty acid synthesis, lipid biosynthesis and metabolism, cholesterol homeostasis, and skin disease, as well as obesity and diabetes. | ||
| 006156 | B6.129-Sceltm1Hba/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable and have no overt morphological or developmental abnormalities. The donating investigator reports that fertility may be impaired in homozygous mice (limited number of litters possible). No endogenous gene expression is observed in skin or stratified squamous epithelia. These mutant mice may be useful in dermatological studies, such as cornified envelope formation, organization of the intima, as well as structural distinctions between arteries and veins, and respiratory structure and function. | ||
| 008201 | B6.129-Sepp1tm1Rfb/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for this targeted mutation are viable and fertile. No RNA or selenoprotein P (Se-P) protein expression from the targeted gene is observed in plasma. Homozygous (Sepp1-deficient) mice are viable with altered selenium metabolism rendering them intolerant of low dietary selenium intake and resulting in significantly shortened life span. Homozygotes have lower brain selenium concentrations and develop progressive neurological dysfunction (impaired movement and coordination); the progression of which is preventable (but not reversible) with dietary selenium supplement. Homozygous females are fertile but have difficulty producing and raising pups. Homozygous males have sharply reduced fertility due to flagellar structural defects ("kinked sperm") which, unlike the neurological phenotype, are not prevented with dietary selenium supplement. Sepp1-deficient mice, supplemented with dietary selenium and infected with an African Trypanosomiasis parasite, exhibit increased ..... For more information please see the full phenotype on the strain data sheet | ||
| 008235 | B6.129P2-Abcg5tm1Plo/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this adenosine triphosphate-binding cassette (ABC) half-transporter G5 mutant allele (Abcg5-/-) are viable and severely subfertile; the donating investigator reports that males have significantly reduced fertility and females are almost non-fertile. No gene product (mRNA) from the mutant allele is detected in homozygous liver extracts. The expression of beta-galactosidase (lacZ) from the targeted gene is not characterized to date (July 2008). Abcg5-deficient mice exhibit sitosterolemia (high plasma plant sterol concentrations) and macrothrombocytopenia (enlarged platelets caused by defective megakaryocyte development) associated with a near 70% reduction in total number of platelets. Specifically, when allowed ad libitum access to PicoLab Rodent Diet 5053 chow, homozygous mice exhibit strongly elevated plasma levels of β-sitosterol (37-fold) and campesterol (7.7-fold); with further increased levels upon addition of the synthetic ..... For more information please see the full phenotype on the strain data sheet | ||
| 005960 | B6.129S-Pecam1Gt(OST16303)Lex/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 012646 | B6.129S-Scpep1tm1Jomm/J | Cryopreserved - Ready for recovery |
| In these mice endogenous gene function of the serine carboxypeptidase 1 (Scpep1) gene is replaced with a β-galactosidase (lacZ) gene. Mice homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. SCPEP1 expression promotes smooth muscle cell proliferation and migration after injury to the vessel wall. Scpep1 KO mice exhibit a reduction in arterial injury-induced neointimal area as well as decreases in the area bound by the external elastic lamina after vessel wall injury. These mice may be useful for studying vascular remodeling after injury and vascular occlusive diseases. | ||
| 006221 | B6.129S1-Lyve1tm1Lhua/J | Cryopreserved - Ready for recovery |
| Homozygotes are viable and fertile, and produce normal-sized litter. No gross phenotypic or behavioral abnormalities have been reported, even in older (2 year old) mice. Homozygous mutants express neither endogenous RNA or protein in liver tissue. Lymphatic capillary vessel morphology in the liver and intestines of homozygous mice is abnormal, with vessels having distended or rounded lumens in contrast to the smaller, typically collapsed, irregular shapes observed in wildtype controls. Intradermal interstitial-lymphatic flow also is increased. Syngenic tumor cell transplants into grow more rapidly and robustly in homozygous mutant mice compared with transplants into wildtype mice, and develop porous interstitial spaces. These mutant mice may be useful in studies of structural and functional characteristics of the lymphatic system, cell-surface retention sequence (CRS) motif-containing growth factor secretion, autocrine and paracrine regulation of cell growth, as well as of cancer and t ..... For more information please see the full phenotype on the strain data sheet | ||
| 009602 | B6.129S4(Cg)-Kcnn2tm2Jpad/J | Cryopreserved - Ready for recovery |
| The SK2T mutant allele has a tetracycline-based genetic switch inserted into the 5' UTR of the targeted gene, just upstream of the translation initiation site. This genetic switch harbors both the tetracycline-controlled transactivator protein (tTA) as well as the tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator). The donating investigator reports that long term administration of tetracycline (or its analog doxycycline (dox)) does not block transcription of the downstream Kcnn2 locus. The donating investigator also reports that homozygous mice are viable but do not thrive without dox treatment. SK2-tTA heterozygotes (SK2T) exhibit approximately ten-fold overexpression of SK2 protein before dox treatment. In the absence of dox, homozygous mice exhibit enhanced SK channel-mediated restriction of glutamatergic activity in CA1 neurons, attenuated hippocampal synaptic plasticity, impaired spatial learning ..... For more information please see the full phenotype on the strain data sheet | ||
| 006490 | B6.129S4-Abcb7tm1Mdf/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable and fertile with no reported neurological or hematological abnormalities. These mutant mice have loxP sites flanking exons 9 and 10 of the endogenous gene. When bred to Cre recombinase expressing mice, exons 9 and 10 are deleted in the offspring dependent on the tissue specificity of the Cre recombinase expressing parent. The donating investigator reports that the null allele is not transmissible due to an effect on the extraembryonic tissues. This mutant may be useful in studying cytosolic Fe-S cluster assembly and metabolism, Friedreich ataxia, anemia, and hematopoiesis.
When bred to a strain expressing Cre recombinase in liver (see Stock No. 003574 for example), this mutant mouse strain may be useful in studies of hepatocyte iron metabolism.
When bred to a strain expressing Cre recombinase in epiblast derived cells (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 009105 | B6.129S4-Asgr1tm1Sau/SaubJxmJ | Cryopreserved - Ready for recovery |
| These mice harbor a targeted mutation of the asialoglycoprotein receptor 1 (Asgr1; also known as hepatic lectin-1 [HL-1]) locus that abolishes endogenous gene expression. Homozygous mice (Asgr1-/- mice) are viable and fertile, with no plasma asialoglycoprotein or platelet level abnormalities. Asgr1-/- mice have impaired hepatic clearance of asialoglycoproteins (exogenous desialylated glycoproteins). Homozygous mice also exhibit altered von Willebrand factor (vWF) levels (increased plasma vWF and reduced hepatocyte-associated vWF). Asgr1-deficiency is associated with reduced bleeding time and enhanced platelet survival. When injected with Streptococcus pneumoniae, homozygous mice have increased susceptibility to infection and mortality (severe intravascular coagulation due to impaired clearance of prothrombotic components: platelets and vWF desialylated by the bacterium's neuraminidase are not eliminated from circulation). These Asgr1 mutant mice may be useful in st ..... For more information please see the full phenotype on the strain data sheet | ||
| 009603 | B6.129S4-Kcnn3tm1Jpad/J | Cryopreserved - Ready for recovery |
| The SK3T mutant allele has a tetracycline-based genetic switch inserted into the 5' UTR of the targeted gene, just upstream of the translation initiation site. This genetic switch harbors both the tetracycline-controlled transactivator protein (tTA) as well as the tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator); allowing transcription of the downstream Kcnn3 locus to be blocked by administration of tetracycline (or its analog doxycycline (dox)). SK3-tTA homozygotes (SK3T/T) exhibit approximately three-fold overexpression of SK3 before dox treatment, and SK3 expression is effectively eliminated by addition of dox. Heterozygous mice exhibit similar expression from both their wild-type and SK3T mutant allele before dox treatment, and no SK3 expression from the mutant allele during dox treatment. In the absence of dox, homozygous mice exhibit abnormal respiratory responses to hypoxia. Homozygous ..... For more information please see the full phenotype on the strain data sheet | ||
| 006503 | B6.129S4-Lpltm1Ijg/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exon 1 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. These mice may be useful for cardiovascular studies (such as lipid metabolism and fat storage) and obesity research.
For example, when crossed to a strain expressing Cre recombinase in cardiac muscle cells (see Stock No. 011038), this mutant mouse strain may be useful in studies of cardiac lipid metabolism. | ||
| 005897 | B6.129S4-Ppardtm1Rev/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 006142 | B6.129S4-Ppargtm1Rev/J | Cryopreserved - Ready for recovery |
| All mice homozygous for this targeted mutation die after gestational day 9.5 from severe placental defects and myocardial thinning. Heterozygotes are viable and fertile. White adipose tissue from heterozygous mice display approximately half the mRNA expression compared to wildtype. Tracer-determined glucose disposal rates and hepatic glucose production show that peripheral tissues and livers from heterozygotes are more sensitive to the effects of insulin than wildtype. This mutation eliminates both DNA-binding and ligand-binding functions of the endogenous gene, concomitantly generating a lacZ reporter that faithfully recapitulates the endogenous expression pattern. Heterozygous mice or homozygous embryo-derived cells may be useful in studies of embryo and placental development, diabetes, atherosclerosis, inflammation, and for beta-galactosidase reporter function of the endogenous gene. | ||
| 006039 | B6.129S7-Efnb2tm1And/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation show growth retardation and enlargement of the heart at embryonic day 10 (E10), with 100% lethality occurring around E11. Reporter protein expression patterns are consistent with arterial, but not venous, expression of the endogenous gene; prominent lacZ signal is observed in hindbrain and somites, with lower levels in aorta and heart as early as E8.25. Expression in the yolk sac was first detected at E8.5, and is also observed in nephrogenic mesoderm and branchial arches. Homozygous embryos show defective angiogenic remodeling at the capillary plexus stage in both yolk sac and head. Endothelial vessel support cell differentiation of the yolk sac is also defective. Homozygotes lack myocardial trabecular extensions, and capillary ingrowth into the neural tube does not occur. Heterozygous mice are viable, fertile, exhibit no behavioral defects, and have identical lacZ expression patterns. These mutant mice may be useful in studying ..... For more information please see the full phenotype on the strain data sheet | ||
| 006042 | B6.129S7-Efnb2tm2And/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for this floxed 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 1 of the targeted gene is deleted in the tissue of interest. These mutant mice may be useful in studying the cellular and molecular mechanisms underlying vasculogenesis and angiogenesis, the topography of neovascularization, and adult neovascularization, including tumor angiogenesis. To test the effectiveness of this model, these mutant mice were bred to an endothelial-specific Cre-expressing transgenic mice, Tg(Tek-cre)12Flv (Stock No. 004128) . Offspring homozygous for the Cre-mediated exon 1 deletion show angiogenic remodeling defects and embryonic death identical to homozygous Efnb2tm1And mice (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 007682 | B6.129X1-Apobtm1.1Zc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this apoB38.9 allele (apoB38.9/38.9) are viable with impaired fertility, bearing a premature stop codon at residue 1767 of the targeted gene. As a result, homozygous plasma shows a truncated apoB38.9 as the sole apoB protein. Plasma from heterozygous (apoB+/38.9) mice have reduced apoB100 and apoB48 compared to wildtype, with apoB38.9 representing 20% of total circulating apoB. This apoB38.9 truncation affects both apoB100 and apoB48 metabolism in mice, and mimics human Familial Hypobetalipoproteinemia (FHBL). Homozygous and, to a lesser extent, heterozygous mice exhibit symptoms of FHBL due to impaired lipoprotein export system/VLDL secretion, including elevated hepatic triglyceride (TG), cholesterol and free fatty acids (FFA), with decreased plasma TG and cholesterol. Because plasma and liver lipid profiles range from mild to severe in populations of heterozygous apoB38.9 mice on a mixed (C57BL/6J;129X1/SvJ) genetic background, apoB+/38 ..... For more information please see the full phenotype on the strain data sheet | ||
| 006580 | B6.Cg-Ins2Akita Ldlrtm1Her/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 007942 | B6.Cg-Isl2tm1Arbr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Isl2DTA targeted mutation are viable and fertile. These mice have the diphtheria toxin (DTA) gene inserted into the Isl2 (insulin related protein 2 (islet 2)) locus. Expression of DTA in Isl2-expressing cells is blocked by an upstream loxP-flanked STOP sequence. When bred to Cre recombinase-expressing mice, the STOP sequence is deleted in tissues where Cre is present, permitting DTA expression and subsequent cell ablation.
When bred to a strain expressing Cre recombinase in motor neurons (see Stock No. 006600 for example), this mutant mouse strain may be useful in neurodevelopmental studies. These Isl2DTA mutant mice are available on a STOCK genetic background (Stock No. 007603), as well as a C57BL/6J-backcrossed background (Stock No. 007942 ..... | ||
| 006877 | B6.Cg-Ldlrtm1Her Tg(H2-K-AKR1B1)1Tj/J | Cryopreserved - Ready for recovery |
| Independently, mice hemizygous for this "huAR" transgene express human aldose reductase as a model for increased oxidative stress, while LDLR homozygotes are predisposed to atherosclerosis and hypercholesterolemia. The donating investigators report that the H2-Kd promoter functions on this H2-Kb genetic background without any loss of transgene expression. When mutant mice are hemizygous for the transgene and homozygous for the targeted allele, they may be useful in studies of diabetes, metabolism, atherosclerosis, hypercholesterolemia, and oxidative stress. | ||
| 006906 | B6.Cg-Lepob Ldlrtm1Her/J | Cryopreserved - Ready for recovery |
| Independently, the C57BL/6-Lepob homozygotes (Stock No. 000632) model the increasingly prevalent metabolic disorder seen in humans (hyperglycemia, hyperinsulinemia, and hyperlipidemia), while LDLR-deficient mice (Stock No. 002207) are predisposed to atherosclerosis. When mutant mice are homozygous for both mutant alleles, they exhibit exacerbated hyperlipidemia and extensive atherosclerotic lesions in the aorta. The mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, and hypercholesterolemia. | ||
| 012627 | B6.Cg-Stard4tm1.1Bres/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exon 3 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 exon 3 deleted in cre-expressing tissues. | ||
| 008221 | B6.Cg-Tg(IGFBP1)2Miel/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the hIGFBP-1 transgene are viable and fertile with no reported gross morphological or developmental changes. The hIGFBP-1 transgene encompasses the entire human IGFBP-1 structural gene and its regulatory sequences, allowing transgene expression of IGFBP-1 to remain responsive to normal hormonal regulation. Transgenic mice overexpress hIGFBP-1, with hIGFBP-1 mRNA expression in a tissue-specific fashion more similar to the human pattern than the murine pattern. Fasting transgenic mice have elevated total serum IGFBP-1 levels that fluctuate according to nutritional status (as they do in humans), and exhibit postprandial hyperinsulinemia with preservation of normal glucocompetence and insulin sensitivity. Transgenic mice also have significantly greater hyperinsulinemic response to glucose challenge and cardiovascular abnormalities in response to carbohydrate load and vasoconstrictors. Transgenic mice exhibit fasting hyperglycemia and hyperinsulinemia and glucose intoler ..... For more information please see the full phenotype on the strain data sheet | ||
| 009344 | B6.Cg-Tg(tetO-Ifng)184Pop/J | Cryopreserved - Ready for recovery |
| The donating investigator reports that homozygous mice are viable and fertile. These TRE/IFN-γ transgenic mice have expression of mouse interferon-gamma (IFN-γ) regulated by the tetracycline-responsive promoter (tetO [also called tetracycline-responsive element (TRE or tet-operator)] fused to the human cytomegalovirus minimal promoter). When mated to a mutant strain expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), expression of IFN-γ may be regulated with the tetracycline analog doxycycline (dox) in the double mutant offspring. Because interferon-gamma (IFN-γ) is a pleiotropic cytokine secreted by activated T-lymphocytes and natural killer cells, these line 184 TRE/IFN-γ mice may be bred to generate bi-transgenic mutant mice with conditional (inducible/reversible) expression of IFN-γ for studying antiviral responses, immune surveillance, inhibiting cellular prol ..... For more information please see the full phenotype on the strain data sheet | ||
| 002982 | B6.Cg-Tg(xstpx-lacZ)32And/J | Cryopreserved - Ready for recovery |
| This mutant, when crossed with a cre transgenic, will express lacZ in cells where cre is expressed to remove the STOP of translation section which lies between the 2 loxP sites. LacZ expression is restricted to neural and skeletal muscle tissue and heart by the chicken beta-actin promoter that is driving the reporter. | ||
| 008222 | B6.FVB-Tg(IGFBP2)1Miel/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the IGFBP-2 transgene are viable and fertile with no reported gross morphological or developmental changes. Transgenic mice overexpress human IGFBP-2 (hIGFBP-2), with hIGFBP-2 mRNA detected in a variety of organs and tissues, including adipose tissue. Overexpression of hIGFBP-2 is associated with reduced susceptibility to obesity and improved insulin sensitivity; transgenic mice are protected from glucose intolerance and increased blood pressure with age, and are also resistant to obesity and insulin resistance on a high fat diet. The phenotype of hIGFBP-2 overexpressing mice may vary between male and female mice. These IGFBP-2 transgenic mice may be useful in studying metabolic homeostasis, adipocyte biology, and the role of insulin-like growth factor binding protein in protecting against obesity- and age-associated complications (such as hypertension and diabetes).
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alle ..... | ||
| 011082 | B6;129-Edn2tm1.1Nat/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of the second exon in the Edn2 (endothelin 2) gene. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the gene. When crossed with a Sox2-Cre transgenic strain, mice homozygous for the resulting allele lack Edn2 expression. This strain may be useful in elucidating the many roles of this gene. | ||
| 011078 | B6;129-Fzd4tm2.1Nat/J | Cryopreserved - Ready for recovery |
| This strain combines a conditional knockout and an alkaline phosphatase (AP) reporter of the frizzled 4 (Fzd4; Fz4) gene. LoxP sites flank the 5' and 3' UTR's. Without recombination, homozygotes of this allele are indistinguishable from wild type mice and the AP reporter is not expressed. Following cre-mediated recombination, the coding region is excised, and the downstream AP reporter is expressed under the control of the Fzd4 promoter in a cell/tissue-specific manner. Loss of Fzd4 signaling causes defective vascular growth which leads to chronic but reversible silencing of retinal neurons. Loss of expression in all endothelial cells disrupts the blood brain barrier in the cerebellum. This strain may be useful in studies of vascular growth, remodeling, maintenance and disease. | ||
| 008678 | B6;129-Ubbtm1Rrk/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the targeted allele are viable and fertile. This polyubiquitin B (Ubb) mutation is characterized by a GFP-puror fusion protein "knock-in" allele that also abolishes endogenous gene function. Direct visualization of GFP fluorescence is observed in ovaries, testes, hypothalamus (arcuate nucleus) and cerebral cortex. Homozygotes have no Ubb mRNA observed in the various tissues tested, and are viable but sterile due to failure of germ cells to progress through meiotic prophase I and hypogonadism. Homozygotes also exhibit a complex metabolic phenotype initially characterized by dysfunction of neurons within the central nervous system accompanied by retarded perinatal growth that progresses to adult-onset obesity linked to selective hypothalamic neurodegeneration. Homozygotes also develop adult-onset hyperleptinemia (but normal levels of circulating glucose and insulin) as a consequence of increased fat content. These Ubb-mutant mice may be useful in studyin ..... For more information please see the full phenotype on the strain data sheet | ||
| 007226 | B6;129P2-Has2tm1Jam/J | Cryopreserved - Ready for recovery |
| While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die between embryonic day (E)9.5 and E10.5. Embryonic mRNA expression from the targeted gene shows only truncated transcripts of the expected length, with no full-length mRNA expression. Homozygous embryos exhibit severe cardiac and vascular abnormalities, lack hyaluronan (HA), and have yolk sac and somite deformities. Heart deformities can be rescued in explants from homozygous mice following exogenous HA or activated H-Ras treatment. These Has2 mutant mice may be useful in studying embryogenesis and development, specifically cardiac and vascular morphogenesis, as well as cell transformation. | ||
| 006470 | B6;129S-Hopxtm1Eno/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable and fertile on this mixed genetic background. Absence of the targeted protein is confirmed in heart and brain tissues from homozygotes. The lacZ expression pattern is similar to that of the endogenous gene. Homozygous heart tissues show altered serum response factor (SRF)-associated gene expression. Mice homozygous for this null allele segregate into two phenotypic classes characterized by an excess or deficiency of cardiac myocytes. These mutant mice may be useful in studying cardiac growth and development. | ||
| 007204 | B6;129S4-2610005L07RikGt(ROSA)73Sor/J | Cryopreserved - Ready for recovery |
| 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 phenotype on the strain data sheet | ||
| 006258 | B6;129S4-Apoa2tm1Bres/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile. Homozygous mice have no detectable transcripts in liver tissues and the high density lipoprotein (HDL) particle size is reduced. Homozygotes have decreased plasma levels of HDL cholesterol and free fatty acids in both fed and fasted states. In addition, the plasma concentration of fasting glucose and insulin is decreased. These mice may be useful in studies of lipid metabolism, atherosclerosis, heart disease, insulin resistance and diabetes. | ||
| 006404 | B6;129S4-Apoa4tm1Bres/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile with no protein detectable in plasma, liver, or intestinal tissues. Homozygotes have decreased plasma levels of cholesterol, free fatty acids, and high density (HDL) and very low density lipoprotein (VLDL). These mice may be useful in studies of lipid metabolism, atherosclerosis, heart disease, appetite regulation, intestinal lipid absorption, or inflammatory bowel disease. | ||
| 007208 | B6;129S4-Csrnp1Gt(ROSA)80Sor/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this mutant allele are viable and fertile, with some incidence of perinatal lethality before two weeks of age (the Donating Investigator reports 18% of homozygotes die by two weeks of age). Homozygotes have abnormalities in palate bone fusion. 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. These 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. | ||
| 009046 | B6;129S4-Hras1tm1Tyj/J | Cryopreserved - Ready for recovery |
| A G12V mutant form of protein is conditionally expressed from this gene when a floxed stop segment is excised by Cre. This oncogene is involved with the development of Costello syndrome, a neuro-cardio-facio-cutaneous developmental syndrome. | ||
| 006238 | B6;129S4-Thbs2tm1Bst/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile. Multiple analyses has confirmed the absence of protein in embryonic and adult tissue of homozygous mice. Homozygotes exhibit skin disorders (abnormal collagen fiber patterns, reduced tensile strength, increased fragility) and skin fibroblasts have attachment defects. Mice also exhibit an increase in total density/cortical thickness of the long bones, abnormally long bleeding times, and a significant increase in blood vessel density. Homozygous mice exhibit accelerated wound healing after biopsy and accelerated/increased tumor formation following chemically-induced skin carcinogenesis. Mutant mice may be useful in studies of collagen fibrillogenesis in skin and tendons, angiogenesis and vascular pathophysiology, wound healing, chemically-induced tumor progression, and as a potential model for Ehlers Danlos syndrome. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are fre ..... | ||
| 007207 | B6;129S4-Zfp640Gt(ROSA)81Sor/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Zfp640-mutant allele are viable and fertile, with abnormalities in palate bone fusion and increased weight gain observed only in males after adolescence. 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. 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 Zfp640-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. | ||
| 004670 | B6;129S6-Abcg5/Abcg8tm1Hobb/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for this targeted allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected in liver or jejunum. A 2 to 3 fold increase in fractional absorption of dietary plant sterols results in plasma sitosterol levels that are elevated 30 fold compared to wildtype levels. Biliary cholesterol levels are low, as are plasma and liver cholesterol levels. Plasma and liver cholesterol levels increase rapidly (2.4 and 18 fold, respectively) following cholesterol feeding. This mutant mouse strain represents a model that may be useful in studies related to sitosterolemia and cholesterol homeostasis. | ||
| 006208 | B6;129S6-Pdzk1tm1Dls/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 004365 | B6;129S6-Srebf1tm1Mbr/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. The targeted mutation results in a total ablation of the SREBP-1c transcript and only a slight redution in levels of the alternate SREBP-1a transcript. There is a 50% increase in level of SREBP-2 transcript and increases in transcripts of enzymes utilized in cholesterol biosynthesis. Liver cholesterol content is increased while plasma cholesterol and plasma triglycerides levels are reduced. There is a reduction of expression of all genes required for fatty acid and triglyceride synthesis. Administration of liver X receptor (LXR) agonist did not result in increased levels of SREBP-1a transcript or in liver triglycerides. This mutant mouse strain represents a model that may be useful in studies of transcriptional control of fatty acid and triglyceride biosynthesis. | ||
| 003266 | B6;129S7-Epas1tm1Rus/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Epas1tm1Rus targeted mutation develop normally until embryonic day 11.5. Beginning at embryonic day 12.5 the ratio of homozygous embryos begins to decline and by day 16.5 there are no viable mutant embryos. Overall morphological development, including the circulatory system, is normal. Of particular interest however, is a pronounced bradycardia in homozygous mutant mice. Catecholamine levels in homozygous mutant mice are also significantly lower than wildtype controls. Administration of the catecholamine precursor DOPS to pregnant females rescues approximately 40% of mutant embryos. Embryos that survive to birth appear runted, fail to nurse, and die within 24 hours of birth. These results suggest a pivotal role of EPAS1 in catecholamine homeostasis. Heterozygous mice from this strain contain a modified lacZ gene in the targeting construct. This characteristic makes this strain useful as a marker for endothelial cells. | ||
| 006044 | B6;129S7-Ephb4tm1And/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation show growth retardation and lack of blood flow by embryonic day 9.5-10 (E9.5-10), with lethality occurring around this time. Expression of lacZ occurs exclusively in embryonic vascular endothelial cells and is preferentially expressed on veins. Homozygous embryos show defective angiogenic remodeling at the capillary plexus stage in both yolk sac and head. Arrested cardiac morphogenesis and defective myocardial trabecular extensions are also observed. Heterozygous mice are viable, fertile, exhibit no behavioral defects, and have identical lacZ expression patterns. These mutant mice may be useful in studying the cellular and molecular mechanisms underlying vasculogenesis and angiogenesis, the topography of neovascularization, and adult neovascularization, including tumor angiogenesis. The developmental abnormalities in homozygous mice closely resemble those observed for mutant mice bearing a lacZ-expressing null mutation ..... | ||
| 012388 | B6;129X1-Ppargc1btm1Dpk/J | Cryopreserved - Ready for recovery |
| These mice carry a floxed allele of Ppargc1b (peroxisome proliferative activated receptor, gamma, coactivator 1 beta). When bred to mice with a cre recombinase gene under the control of a promoter of interest, exons 4-6 of the targeted gene are deleted in the tissue of interest. This strain may be useful in studies of the metabolic and functional maturation in the tissue of interest, using a conditional "knockout" strategy. | ||
| 006907 | B6;CBA-Tg(APOC3)3707Bres/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this "human apo CIII" transgene are viable and fertile. This high expressor founder line (3703) exhibits transgene expression primarily in the liver with some intestinal expression as well. Hemizygous mice have severe plasma hypertriglyceridemia and significantly increased plasma cholesterol. However, resistance to insulin-mediated glucose uptake or hyperinsulinemia are not observed. This high expressor human apo CIII transgenic strain may be useful in studying lipid metabolism, very low density lipoproteins (VLDL), hypertriglyceridemia, coronary heart disease, and/or atherosclerosis. | ||
| 010574 | B6;SJL-Tg(Gh1-rtTA)4-3Jek/J | Cryopreserved - Ready for recovery |
| The donating investigator reports that homozygous mice are viable and fertile. These GH-rtTA transgenic mice have expression of the reverse tetracycline-controlled transactivator (rtTA) protein directed to GH1-producing cells (pituitary somatotropes) by the rat growth hormone (Gh1) promoter. When mated to a mutant strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE, TetRE or tetO), expression of the target gene in GH1-producing cells may be induced with administration of the tetracycline analog doxycycline (dox) in the double mutant offspring. These GH-rtTA transgenic mice are a Tet-On tool that allows conditional, dox-inducible expression of genes in GH1-producing cells/tissues (such as pituitary somatotropes) and may be useful for studying pituitary hormone secretion and proliferation. | ||
| 010573 | B6;SJL-Tg(Prl-tTA)6-5Jek/J | Cryopreserved - Ready for recovery |
| The donating investigator claims homozygous mice are viable and fertile. These Prl-tTA transgenic mice have expression of the tetracycline-controlled transactivator (tTA) protein directed to PRL-producing cells (pituitary lactotropes/mammotropes) by the rat prolactin (Prl) promoter. The donating investigator also reports some expression in testis. When mated to a mutant strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE, TetRE or tetO), expression of the target gene in the PRL-producing cells may be conditionally abolished with administration of the tetracycline analog doxycycline (dox) in the double mutant offspring. These Prl-tTA transgenic mice are a Tet-Off tool that allows dox-conditional expression of genes in PRL-producing cells/tissues (such as pituitary lactotropes/mammotropes) and may be useful for studying pituitary hormone secretion and proliferation. | ||
| 008082 | B6;SJL-Tg(Tagln-tTA)1Mrab Tg(tetO-Mcpt1)1Mrab/J | Cryopreserved - Ready for recovery |
| Hemizygous tTA+/RVCH+ (or SM22a-tTA/TRE-RVCH-HA) mice are viable and fertile, harboring two transgenes using the Tet-Off system. The SM22a-tTA transgene has the 3 kb SM22alpha promoter directing expression of the tetracycline transactivator gene (tTA) to vascular smooth muscle cells (SMCs). The TRE-RVCH-HA transgene has the tetracycline-responsive element (TRE; also called tet-operator or tetO) controlling expression of a rat vascular chymase-hemagglutinin tag (RVCH-HA) fusion gene. In the absence of tetracycline (or its analog doxycycline (dox)), the SM22alpha promoter limits RVCH-HA fusion protein expression to vascular SMCs. This RVCH overexpression results in hypertension. Because this binary transgenic system also allows for a second level of control, i.e. addition of dox, expression of the RVCH-HA fusion protein can be completely abolished; reversing the hypertension phenotype. These SM22a-tTA/TRE-RVCH-HA bi-transgenic mice allow targeted overexpression or Tet-Off conditio ..... For more information please see the full phenotype on the strain data sheet | ||
| 013042 | B6N;129S-Acacbtm1.1Lowl/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Acc2flox allele are viable, fertile, normal in size, and have no reported physical abnormalities. The Acc2flox allele has loxP sites flanking the biotin-binding motif exon (and the preceding exon) of the targeted locus. When bred to mice that express Cre recombinase, the resulting offspring will have the floxed sequences deleted in the cre-expressing cells/tissues. The exon immediately upstream of the biotin-binding catalytic domain was included so that splicing of the remaining exons following Cre-mediated deletion would introduce a frameshift and nonsense mutation after Asp865 in any translated protein. These mutant mice may be useful to generate conditional mutations for studying malonyl-CoA (the substrate for fatty acid synthesis and the regulator of fatty acid oxidation) synthesis and other metabolic cellular signaling molecules, as well as diet-induced obesity, glucose intolerance and insulin resistance.
NOTE: W ..... | ||
| 004583 | B6SJL-Tg(ABCG5/ABCG8)14-2Hobb/J | Cryopreserved - Ready for recovery |
| These transgenic mice over-express the human ABCG5 and ABCG8 genes under the direction of their endogenous regulatory sequences. Copy number of the transgene was estimated using Southern blot analysis to compare transgenic mouse genomic DNA to human genomic DNA. These transgenic mice have approximately ten copies of the transgene. Northern blot analysis revealed the human transgene is expressed in the liver and small intestine. RT-PCR showed trace levels of transgene transcript in ovary tissue. Absorption of dietary cholesterol in transgenic mice is reduced by 50%. Mean fasting plasma cholesterol levels are significantly lower in female transgenic mice. Excretion of neutral sterols in feces is elevated to three times higher above normal in male transgenic mice and six times higher in female transgenic mice. Bile from transgenic animals is opaque as compared to the clear bile of wildtype animals. Cholesterol in the bile is elevated to levels five times higher than normal in male transge ..... For more information please see the full phenotype on the strain data sheet | ||
| 008237 | C.129S4-Seletm1Dmil/J | Cryopreserved - Ready for recovery |
| 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 ..... | ||
| 007744 | C57BL/6-Tg(APOE-DGAT2)24Far/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this LivLE6-DGAT2 transgene are viable and fertile, with human DGAT2 expression directed to the liver by the hepatic promoter/enhancer sequences from the human apolipoprotein E gene. Mice from founder line 24 (referred to as Liv-DGAT2-low) have an approximately 2-fold increase in total hepatic DGAT2 mRNA/protein expression, with no reported overexpression in kidney, brain, or skeletal muscle. As DGAT2 is one of two enzymes that catalyze the final step of triacylglycerol (TG) biosynthesis, transgenic mice develop hepatic steatosis with increased hepatic TG and insulin signaling lipid (diacylglycerol, ceramide and unsaturated Fatty AcylCoA) content. Liv-DGAT2-low mice also exhibit increased transcription of fatty acid synthesis genes (SREBP-1c, fatty acid synthase, and stearoyl CoA desaturase 1). Fasted mice show a 65% decrease in plasma TG, but are not insulin resistant (blood glucose and insulin are similar to wildtype). Liv-DGAT2-low mice challenged with a high-fat ..... For more information please see the full phenotype on the strain data sheet | ||
| 008314 | C57BL/6-Tg(HBB-cre)12Kpe/J | Cryopreserved - Ready for recovery |
| These transgenic mice express Cre recombinase under the control of the human beta hemoglobin (HBB) promoter and intron 2-enhancer fragment, and the human beta hemoglobin locus control region (LCR). Cre recombinase expression is detected in blood, brain, gonads, spleen and liver by RT-PCR analysis and in blood by RNAse protection assay analysis. During development Cre activity is restricted to erythroid tissues. The Donating Investigator reports that recombination occurs at 50-100% efficiency in erythroid/megakarycytic cell lineages beginning at onset of hematopoiesis at approximately embryonic day 7.5. When crossed with a strain containing a loxP site-flanked sequence, Cre-mediated recombination results in deletion of the flanked sequence in erythroid tissues. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This strain represents an effective tool for generating tissue speci ..... For more information please see the full phenotype on the strain data sheet | ||
| 006070 | CBy.129S6(B6)-Epha2tm1Jrui/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable, fertile, and display no overt developmental or behavioral abnormalities. In mutant mice of a mixed BALB/c, C57BL/6, and 129S6 background, murine pulmonary microvascular endothelial cells (MPMECs) isolated from homozygotes express no endogenous protein. MPMECs from Epha2-deficient mice show impaired ephrin-A1-induced vascular assembly and defective migration both in vitro and in vivo. In addition, MPMECs from homozygous Epha2 mice exhibit decreased angiogenesis and fail to activate Rac1 in response to ephrin-A1 in vivo. Mutant mice on a BALB/c background that were transplanted with metastatic mammary adenocarcinoma cells showed impaired tumor progression, angiogenesis and metastasis to the lung, compared with wildtype littermate controls. These mutant mice may be useful in studies of postnatal angiogenesis (endothelial cell migration, assembly into new tubules, and cytoskeletal regulation), or as a ..... For more information please see the full phenotype on the strain data sheet | ||
| 007683 | CByJ.129X1(Cg)-Apobtm1.1Zc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this apoB38.9 allele (apoB38.9/38.9) are viable with impaired fertility, bearing a premature stop codon at residue 1767 of the targeted gene. As a result, homozygous plasma shows a truncated apoB38.9 as the sole apoB protein. Plasma from heterozygous (apoB+/38.9) mice have reduced apoB100 and apoB48 compared to wild-type, with apoB38.9 representing 20% of total circulating apoB. This apoB38.9 truncation affects both apoB100 and apoB48 metabolism in mice, and mimics human Familial Hypobetalipoproteinemia (FHBL). Homozygous and, to a lesser extent, heterozygous mice exhibit symptoms of FHBL due to impaired lipoprotein export system/VLDL secretion, including elevated hepatic triglyceride (TG), cholesterol and free fatty acids (FFA), with decreased plasma TG and cholesterol. These BALB/cByJ-apoB38.9 mice are also heterozygous for the BALB/cByJ-derived SCAD deletion (Acadsdel-J). While BALB/cByJ inbred mice have elevated liver TG f ..... For more information please see the full phenotype on the strain data sheet | ||
| 006768 | D2.Cg-Tg(Myh6-Zfpm2)1Sho/EiJ | Cryopreserved - Ready for recovery |
| 002981 | DBA/2-Tg(xstpx-lacZ)36And/J | Cryopreserved - Ready for recovery |
| This test strain is used determine the tissue expression pattern of cre transgenic mice. The transgene is loxP-STOP-of-translation-loxP-lacZ driven by the beta-actin promoter. The lacZ is expressed only in cells where the STOP element has been removed by Cre recombinase. LacZ expression is restricted to neural and skeletal muscle tissue and heart by the chicken beta-actin promoter that is driving the reporter. | ||
| 006405 | FVB-Tg(Ckmm-cre)5Khn/J | Cryopreserved - Ready for recovery |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice have the Cre recombinase gene driven by the muscle creatine kinase (MCK or Ckm) promoter. Cre activity is observed in skeletal and cardiac muscle. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in skeletal and cardiac muscle deletion of the flanked genome. | ||
| 009438 | FVB-Tg(Myh6-SOD2,Tyr)3Pne/J | Cryopreserved - Ready for recovery |
| These transgenic mice overexpress the human superoxide dismutase 2, mitochondrial (SOD2) under the control of the mouse myosin, heavy polypeptide 6, cardiac muscle, alpha, Myh6, promoter. This transgenic insert was co-injected with the tyrosinase coat color marker, TyBS, which confers dark grey pigmentation on an albino background. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator reports that homozygotes are viable but have not been tested for fertility. Transgene expression is specific to the heart as detected by Western blot analysis. Expression is localized to mitochondria. SOD activity increased by 20-fold in heart and cardiac catalase activity is increased 2-fold. Exogenous reactive oxygen species (ROS) are reduced in cardiomyocytes isolated from transgenic mice. This mutant mouse strain may be useful in studies of diabetic cardiom ..... For more information please see the full phenotype on the strain data sheet | ||
| 011037 | FVB-Tg(Myh6-cre)2182Mds/J | Cryopreserved - Ready for recovery |
| The cardiac-specific murine alpha myosin-heavy chain (Myh6, myosin, heavy polypeptide 6, cardiac muscle, alpha) promoter drives expression of cre in this transgenic strain. Breeding this mouse with another carrying loxP-flanked sequences results in the deletion of the flanked sequences in the offspring. The promoter induces greater than 90% recombination in cardiac muscle cells. No recombination is observed in liver, lung, skeletal muscle (quadriceps), and spleen, or in extraneous cell types in the heart. | ||
| 010588 | FVB-Tg(Myh6/NFAT-luc)1Jmol/J | Cryopreserved - Ready for recovery |
| The mouse alpha myosin heavy chain cardiac promoter drives expression of nuclear factor of activated T cell (NFAT) binding sites and a luciferase reporter to detect calcineurin-NFAT signaling. In the adult heart, NFAT-luciferase activity is upregulated in association with cardiac hypertrophy induced by pressure-overload and following myocardial infarction-induced heart failure. | ||
| 010580 | FVB-Tg(Myh6/tetO-PRKCA*)1Jmk/J | Cryopreserved - Ready for recovery |
| These transgenic mice express a dominant negative form of rabbit PRKCA (protein kinase C, alpha) under the control of an inducible mouse Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha) minimal promoter. When bred with transgenic mice expressing a tetracycline transactivator or reverse transactivator protein, cardiac-specific expression of the rabbit cDNA can be controlled in the offspring by withdrawal or administration of a tetracycline analog. When crossed with a transcriptional transactivator (tTA) line in the absence of doxycycline, the mice develop a mild cardiomyopathy. | ||
| 008537 | FVB-Tg(Tek-cre)2352Rwng/J | Cryopreserved - Ready for recovery |
| These transgenic mice express the Cre recombinase under the control of the mouse Tek, endothelial-specific receptor tyrosine kinase (also known as Tie2), promoter. Cre recombinase expression is detected in most endothelial cells and blood islands of the extraembryonic mesoderm by embryonic day (ED)7.5 and in the dorsal aorta by ED8.5. Especially high levels of expression are seen in head vasculature by ED9. When crossed with reporter strains (expressing beta-galactosidase or alkaline phosphatase), recombination is detected in all blood vessels and some blood cells examined at ED11.5, which indicates that Cre activity occurs in early vascular progenitor cells, endothelial cells and some hematopoietic cells. Mice homozygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This strain represents an effective tool for generating endothelial cell specific-targeted conditional mutations. | ||
| 010578 | FVB-Tg(tetO-Dusp6)1Jmol/J | Cryopreserved - Ready for recovery |
| A tetracycline-responsive element (TRE; tetO) and mouse alpha myosin heavy chain minimal promoter regulate expression of Myc-tagged mouse Dusp6. When these transgenic mice are bred to Myh6-tTA transgenic animals, in the offspring, Dusp6 expression is upregulated in the heart. Transgene expression can be abated in the double transgenic animals with doxycycline administration. | ||
| 008685 | FVB-Tg(tetO-Kdr*)4377.5Rwng/J | Cryopreserved - Ready for recovery |
| These transgenic mice express a truncated mouse Kdr (kinase insert domain protein receptor) gene under the control of a tetracycline-responsive promoter element (TRE or tetO). The truncated gene encodes amino acids 1 through 828, which includes the cytoplasmic tyrosine kinase domain, and has a hemaglutin (HA) tag fused at the C terminus. When bred with a transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), a bitransgenic animal can be produced that has tissue-specific expression of Kdr that can be regulated with the tetracycline analog, doxycycline.
For example, when bred to a strain expressing tTA in liver (see Stock No. 003563) and a targeted mutation of Kdr (see Stock No. 002938) , this mutant mouse strain may be useful in studies of liver organogenesis. ..... | ||
| 003170 | FVB.Cg-Tg(Myh6-tTA)6Smbf/J | Cryopreserved - Ready for recovery |
| This strain expresses the tetracycline-controlled transactivator protein (tTA) under the regulatory control of the rat alpha myosin heavy chain promoter, which directs expression of tTA, specifically, in cardiac myocytes. When these Myh6-tTA (also called 2.9alphatTA or MHCAtTA) transgenic mice are mated to a second transgenic strain carrying a gene of interest coupled to a tetracycline-responsive promoter element (TRE), conditional expression of the target gene in cardiac myocytes may be controlled by the administration of tetracycline or doxycycline. | ||
| 006402 | FVB/N-Adrb3tm1Lowl/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable and fertile. No gene product (mRNA) is detected by Northern blot analysis from homozygous brown or white adipose tissue. Homozygous mice have modest increases in fat stores (female more than male). In contrast to control animals, homozygous mice are unresponsive to beta-3 adrenergic receptor (beta3-AR) agonist treatment (no effect on adenylate cyclase activity, lipolysis, or gastro-intestinal motility). These mutant mice may be useful in studies of energy balance, obesity, fat metabolism, cholesterol homeostasis, diabetes, and pharmacological screening of beta3-AR agonists for potential drug treatment. | ||
| 008716 | FVB/N-Tg(Myh6-AIP/PLN*)46Jded/J | Cryopreserved - Ready for recovery |
| SR-AIP transgenic mice carry the α-MHC-AIP4-SR transgene. Hemizygous SR-AIP mice are viable and fertile, with expression of AIP4 (a tetramer of the CaMKII autocamtide inhibitory peptide AIP) directed to the sarcoplasmic reticulum (SR) of the heart by the murine alpha-myosin heavy chain (α-MHC or Myh6) promoter and a truncated phospholamban (PLB) transmembrane domain (harboring two loss-of-function mutations to prevent direct SERCA inhibition by the fusion protein). FLAG epitope expression may be used to identify presence of the fusion protein. The SR-targeted AIP concatemer peptide binds CaMKII, preventing phosphorylation of PLB and subsequent activation of SERCA, thereby increasing diastolic intracellular calcium. Whole
heart function and diastolic relaxation are slightly impaired, and pregnancy leads to earlier onset of cardiac hypertrophy. These SR-AIP transgenic mice may be useful in studying sarcoplasmic reticulum-targeted CaMKII inhibitio ..... For more information please see the full phenotype on the strain data sheet | ||
| 012461 | FVB/N-Tg(Myh6-Cast)1Gwd/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the Myh6-Cast allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Expression of Cast is regulated by an α-myosin heavy chain (Myh6) promoter, which results in the overexpression of calpastatain, a highly specific global inhibitor of calpain 1 and calpain 2, in the heart. Overexpression of calpastatin causes diminished ubiquitination of myocardial proteins resulting in a progressive dilated cardiomyopathy characterized by accumulation of intracellular protein aggregates, formation of autophagosomes, and degeneration of sarcomeres. These Myh6-Cast mice may be useful for assessing the consequences of cardiomyocyte-specific calpain inhibition in normal, ischemic, and failing hearts, and the contribution of endogenous calpains to myocardial protein turnover. | ||
| 006875 | FVB/N-Tg(Tagln-rtTA)E1Jwst/J | Cryopreserved - Ready for recovery |
| Transgenic SM22-rtTA mice are viable and fertile. These mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the murine SM22-alpha (SM22α or transgelin) promoter. When hemizygotes are mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene in the bitransgenic offspring is inducible in smooth muscle cells with administration of the tetracycline analog, doxycycline. These SM22-rtTA mice provide a "Tet-On" tool that allows the inducible expression of genes in smooth muscle cells. | ||
| 005941 | FVB/N-Tg(tetO-Aurkb,lacZ)41Kra/J | Cryopreserved - Ready for recovery |
| Hemizygous and homozygous transgenic mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Expression of the bicistronic transgene is directed by a tetracycline-responsive regulatory element (TRE; tetO). When transgenic mice are bred with another transgenic strain expressing the tetracycline-controlled transactivator protein (tTA) under the regulation of a tissue-specific promoter, both aurora kinase B (Aurkb) and lacZ cistrons are inducibly expressed in the appropriate tissue in the bitransgenic offspring. This mouse was originally designed to be bred with Tg(Pf4-tTA)42Kra transgenic mice, which express tTA from a megakaryocyte-specific promoter. Megakaryocytes and platelet cells derived from the bitransgenic offspring show inducible and reversible beta-galactosidase expression. Further, megakaryocytes inducibly express Aurkb mRNA (but not protein) with a modest effect on megakaryocyte ploidy and no effect on platelet quant ..... | ||
| 003315 | FVB/N-Tg(tetORo1-lacZ)3Conk/J | Cryopreserved - Ready for recovery |
| Transgenic mice express both Ro1 (Receptor Activated Solely by a Synthetic Ligand (RASSL), opioid, #1) and lacZ under the regulation of tetracycline responsive elements (TRE; tetO)(see Strain Development for more information). When Ro1 is expressed in the heart (by crossing it with strain FVB.Cg-Tg(Myh6-tTA)6Smbf/J - Stock No. 003170), administration of the drug spiradoline produces a dramatic decrease in heart rate. Since Ro1 and lacZ are co-integrated and under tetracycline/doxycycline control, X-gal staining can be used to identify cells in which the tet-inducible system is working. Ro1 activates Gi-signaling in response to spiradoline, and can be used to study the effect of Gi-signaling in many tissues. In the heart, Ro1-mediated activation of Gi-signaling slows heart rate, but in other tissues it is predicted to control diverse physiological events, such as cell proliferation, se ..... For more information please see the full phenotype on the strain data sheet | ||
| 006999 | STOCK Dbttm1Geh Tg(Cebpb-tTA)5Bjd Tg(tetO-DBT)A1Geh/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Dbt (E2) targeted mutation and carrying both the LAP-tTA and TRE-E2 transgenes are viable and fertile. The E2-targeted mutation leads to absence of branched-chain keto acid dehydrogenase (BCKDH) activity and E2 protein in liver tissue, but this absence is rescued by the two transgenes: liver-directed expression of the modified human BCKDH E2 subunit from the complimentary "Tet-off" transgenes abrogates the severity of Maple Syrup Urine Disease (MSUD) phenotype observed in E2-deficient single mutant mice. Triple mutant mice are a model for intermediate MSUD (iMSUD); BCKDH activity is only 5-6% of that found in wildtype mice. This low level of BCKDH activity is sufficient to allow survival, but insufficient to normalize circulating branched chain amino acids levels. Because these mice have near normal amounts of E2 protein, but only 5-6% of normal BCKDH enzyme activity, it is probable that the c-myc tag at the carboxy-terminus of the human E2 transge ..... For more information please see the full phenotype on the strain data sheet | ||
| 009672 | STOCK Egln1tm1Kael/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exons 2 and 3 of the targeted gene. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the gene (widespread deletion of expression is embryonic lethal). This strain may be useful in studies of development and cardiovascular disease.
For example, when crossed to a strain expressing tamoxifen-inducible Cre recombinase in most tissues (see Stock No. 004682), this mutant mouse strain may be useful in studies of polycythemia and congestive heart failure. | ||
| 008196 | STOCK Gata6tm2.1Sad/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Gata6loxp conditional allele are viable and fertile, with loxP sites flanking exon 2 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (coding for the majority of the GATA6 protein) deleted in the cre-expressing tissue(s). These Gata6loxp mice may be useful in generating conditional GATA binding protein 6 mutations for studying GATA6 function in organogenesis or in adult mice.
For example, when bred to a strain expressing Cre recombinase in the villi and crypt cells of the intestine (see Stock No. 004586 for example), or when bred to a strain expressing Cre recombinase in the embryo (see Stock No. 003724, 003314 for example), this mutant mouse strain may be useful in studies of the transcrip ..... | ||
| 005994 | STOCK Mbtps1tm1Jdh/J | Cryopreserved - Ready for recovery |
| These mice carry a targeted mutation in which exon 2 of the targeted gene is flanked by loxP sites. A loxP-flanked ("floxed") neomycin resistance cassette also is inserted downstream in intron 2. Homozygotes are viable and fertile, and the floxed gene appears to function normally. When homozygotes are crossed with transgenic strains expressing Cre-recombinase, cre-mediated recombination of the loxP-flanked sequences can result in one of three genotypes: a) deletion of the neo cassette only, leaving a loxP-flanked second exon and unimpaired endogenous gene function. b) Deletion of exon 2 only, leaving a loxP-flanked neo cassette and no endogenous gene function. c) Deletion of both the neo cassette and exon 2, leaving a single loxP site and no endogenous gene function. When these floxed mutant mice are bred to mice carrying the Mx1-cre transgene (for example, Stock No. 003556), liver- ..... For more information please see the full phenotype on the strain data sheet | ||
| 006578 | STOCK Myoz2tm1Eno/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this calsarcin-1 mutant allele are viable and fertile. Immunoblot of homozygous cardiac tissue shows no endogenous protein expression. Strong lacZ expression throughout all cardiac chambers mirrors the expression pattern of the endogenous gene, and marked skeletal muscles known to contain a high proportion of type I (slow) fibers. Homozygotes have skeletal muscle abnormalities in type I (slow) fibers and calcineurin activity. Echocardiography of homozygous mice reveals abnormal heart performance. Absence of gene function activates a cardiac hypertrophic fetal gene program (despite the absence of hypertrophy) and enhanced the cardiac growth response to pressure overload. These mutant mice may be useful in studying growth and gene expression of cardiac and skeletal muscle, as well as the pathogenesis of human cardiomyopathies. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic bac ..... | ||
| 005707 | STOCK Rag1tm1Mom Tg(TIE2-lacZ)182Sato/J | Cryopreserved - Ready for recovery |
| Mice homozygous for both the targeted mutation and the transgene are viable and fertile. The transgene beta-galactosidase is well expressed, reflects endogenous Tek/Tie2 activity, and is specific to the vascular endothelium. Mice homozygous for the Rag1 mutation are immunodeficient as they lack mature B and T lymphocytes. This double mutant mouse may be useful in studies of cancer, tumor-related angiogenesis, and as a recipient of xenografted tumors. | ||
| 006473 | STOCK Smyd1tm1Dsr/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for this targeted mutation are viable and fertile. Mice homozygous for this targeted allele, however, die between embryonic day (E) 9.5 and 10.5 due to cardiomyocyte maturation defects, including an enlarged heart, single left-side ventricular chamber with tremendous extra cellular matrix expansion between the myocardial and endocardial layers, and defective Hand2 expression. No mRNA transcripts from the targeted mutant gene are detected in cardiac tissue from E9.5 homozygotes. These mutant mice may be useful in studying cardiomyocyte differentiation and cardiac morphogenesis. 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. | ||
| 003115 | STOCK Tg(CAG-EGFP)B5Nagy/J | Cryopreserved - Ready for recovery |
| This transgenic strain expresses an Enhanced Green Fluorescent Protein (Clontech) driven by chicken beta-actin promoter and CMV intermediate early enhancer. Mice, and cells derived from them, are distinguished from wildtype on the basis of fluorescence. The transgene is expressed in all nucleated embryonic tissues. Cells and tissues with increased hemoglobin content exhibit reduced fluorescence as development progresses. In newborn and adult mice, the entire organ system expresses EGFP. Though widespread, expression levels vary between different organs. This strain can be used as a source of fluorescently marked cells or tissues. | ||
| 012477 | STOCK Tg(Myh6*/tetO-GCaMP2)1Mik/J | Cryopreserved - Ready for recovery |
| This inducible calcium sensor transgene contains a conditional cardiac (cc) expressing eGFP-calmodulin fusion protein, GCaMP2. Mice homozygous for the ccGCaMP2 transgene are viable and fertile, normal in size and do not display any gross physical or behavioral abnormalities. Expression of ccGCaMP2 is regulated by a tetracycline operator (tetO), driven by an enhanced Myh6 promoter which limits GCaMP2 expression in heart. When bred with transgenic mice expressing a tetracycline transactivator (tTA) or reverse transactivator protein, cardiac-specific expression of GCaMP2 can be controlled by withdrawal or administration of tetracycline or a tetracycline analog, doxycycline, in the double mutant offspring. These mice may be useful for measurement of myocyte Ca2+ transients in the beating heart of adult and embryonic mice in vivo and in vitro. | ||
| 008168 | STOCK Tg(tetO-DTA)1Gfi/J | Cryopreserved - Ready for recovery |
| These tet-DTA transgenic mice express diphtheria toxin A (DTA) under the control of a tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator) and a cytomegalovirus minimal promoter. When bred with another mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), tissue diphtheria toxin A expression can be regulated with the tetracycline analog doxycycline (dox) in the resulting double mutant offspring. These tet-DTA mice may be useful in generating bi-transgenic mutant mice for the reversible, inducible deletion of specific groups of cells. For example, when bred to a strain expressing tTA in cardiac myocytes (see Stock No. 003170 for example), this mutant mouse strain may be useful in studies of human cardiomyopathies. | ||
| 007679 | SWR.129X1(B6)-Apobtm1.1Zc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this apoB38.9 allele (apoB38.9/38.9) are viable with impaired fertility, bearing a premature stop codon at residue 1767 of the targeted gene. As a result, homozygous plasma shows a truncated apoB38.9 as the sole apoB protein. Plasma from heterozygous (apoB+/38.9) mice have reduced apoB100 and apoB48 compared to wildtype, with apoB38.9 representing 20% of total circulating apoB. This apoB38.9 truncation affects both apoB100 and apoB48 metabolism in mice, and mimics human Familial Hypobetalipoproteinemia (FHBL). Homozygous and, to a lesser extent, heterozygous mice exhibit symptoms of FHBL due to impaired lipoprotein export system/VLDL secretion, including elevated hepatic triglyceride (TG), cholesterol and free fatty acids (FFA), with decreased plasma TG and cholesterol. Because plasma and liver lipid profiles range from mild to severe in populations of heterozygous apoB38.9 mice on a mixed (C57BL/6J;129X1/SvJ) genetic background, apoB+/38. ..... For more information please see the full phenotype on the strain data sheet | ||
| 014556 | 129S6/SvEv-Apoetm4Mae/J | Under Development - Now Accepting Orders |
| The Apoetm4Mae mutant allele was created using the same targeting vector used to generate the Apoetm1Unc mutant allele. Both alleles are functionally identical; replacing part of exon 3 and intron 3 with a neomycin resistance cassette and abolishing apoE expression. Mice homozygous for the apoE mutation (apoE-deficient mice) are viable and fertile, with defective lipoprotein metabolism. Compared to wildtype mice, apoE-deficient mice exhibit increased plasma cholesterol and triglyceride levels, along with spontaneous development of atherosclerotic plaques in the aortic root and aortic arch. Several strain-specific differences are reported between apoE-deficient mice coisogenic on a 129S6/SvEv genetic background (129S6-apoE-/-) and apoE-deficient mice congenic on a C57BL/6 genetic background (B6-apoE-/- ; see Stock No. 002052). Compared to B6-apoE-/- mice, 129S6-a ..... For more information please see the full phenotype on the strain data sheet | ||
| 013046 | 129S6/SvEv-Liastm1Mae/J | Under Development - Now Accepting Orders |
| The Liastm1Mae mutant allele has the exons 4-6 of the of the lipoic acid synthetase (Lias) gene deleted. The deleted region encodes the functionally conserved Cys motifs of the enzyme responsible for converting octanoic acid to α-lipoic acid (also called 1,2-dithiolane-3-pentanoic acid, thioctic acid, ALA, or LA) via insertion of a sulfur atom into the hydrocarbon chain of octanoic acid. Lias mRNA expression in heterozygous mice is approximately half of wildtype levels. Lias homozygous mice die in utero shortly after implantation. When heterozygous dams are fed an exogenous racemic α-lipoic acid diet (equal amounts of left- and right-handed enantiomers of the chiral α-lipoic acid molecule), embryonic lethality of homozygous embryos is not rescued. Heterozygous mice are viable and fertile, with a mild reduction of plasma antioxidant capacity. Inducing stress conditions (such as inflammation, hypercholesterolemia and hyperglycemia) is exp ..... For more information please see the full phenotype on the strain data sheet | ||
| 017309 | B6.129P2-Syktm1.2Tara/J | Under Development - Now Accepting Orders |
| In this conditional Sykb (spleen tyrosine kinase) mutant strain, exon 1 has been flanked by loxP sites. When crossed with a Cre recombinase-expressing strain, these mice are useful in eliminating tissue-specific expression of the gene. Homozygous floxed mice are fully viable and fertile.
Homozygous null mice show a variety of defects including high rates of perinatal lethality, abnormal vascular morphology, abnormal osteoclast differentiation, impaired neutrophil phagocytosis, and defects in B cell development. | ||
| 011077 | B6;129-Ubbtm2Nat/J | Under Development - Now Accepting Orders |
| A targeted insertion located 2 kb 5' of the Ubb ubiquitin b gene (the integration site of the Z/AP reporter) gives constitutive expression of a nuclear-localized beta-galactosidase/neomycin resistance protein reporter (NLS-beta-geo) in the absence of Cre-mediated recombination. Following cre-mediated recombination, the NLS-beta-geo coding region is excised and a downstream open reading frame is expressed. The downstream open reading frame codes two proteins - Norrin (NDP), and GFP with 6xMyc epitope, but the GFP coding region, which follows an IRES, is expressed at very low levels. After cre-mediated recombination in the retina, ectopic Norrin expressed from this locus can rescue the vascular defect caused by a Norrin null mutation.
For example, when crossed to a strain expressing Cre recombinase in epiblast cells (see Stock No. 008454), this mutant mouse strain may be useful in studies of retinal vascularization. ..... | ||
| 017593 | B6;129S-Sox2tm1(cre/ERT2)Hoch/J | Under Development - Now Accepting Orders |
| These Sox2-CreER knockin mice have the SRY-box containing gene 2 (Sox2) open reading frame replaced with a CreERT2 fusion gene. Sox2 is a widespread marker of pluripotent and many adult stem/progenitor cell types. Heterozygous mice are viable and fertile, while homozygous mice exhibit embryonic lethality. Following tamoxifen administration, Cre-ERT2 activity is observed in adult epithelial tissues; including testes, forestomach, glandular stomach, anus, cervix, esophagus, and lens, as well as glands associated with oral cavity, trachea, and cervix. When these mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequences in the cre-expressing cells of the offspring. Cre-ERT2 activity is also detected in blastocysts, neural progenitor cells, and embryonic stem cell cultures following tamoxifen administration. These mice may be useful for stud ..... For more information please see the full phenotype on the strain data sheet | ||
| 016901 | B6N.129S-Txniptm1.1Rlee/J | Under Development - Now Accepting Orders |
| Mice homozygous for a systemic knockout of the Txnip (thioredoxin interacting protein) gene are viable, fertile, and born at predicted Mendelian frequencies. No TXNIP protein is synthesized. Fasting blood glucose levels indicate hypoglycemia without hyperinsulinemia. Homozygous mice placed on a high-fat diet for 4 weeks show significant increases in adipogenesis and insulin sensitivity as compared to wildtype controls. | ||
| 016131 | C57BL/6J-Sec61a1m1Gek/J | Under Development - Now Accepting Orders |
| Mice homozygous for the ENU-induced missense mutation, called Sec61a1Y344H, are viable and fertile. By ~4 weeks of age, homozygous males and females maintained on a high-fat diet (~58% kcal from fat) become diabetic (hyperglycemic) with hypoinsulinemia; the result of endoplasmic reticulum (ER) stress-induced apoptosis of pancreatic β-cells. In addition to diabetes, these mice exhibit other metabolic, endocrinological, and growth abnormalities (including hyperlipidemia, hepatosteatosis, hypercholesterolemia, hypertriglyceridemia, and, in older mice, hepatic cirrhosis). Homozygous mice maintained on a chow diet (~5% kcal from fat) become diabetic by ~10 weeks of age; exhibiting hyperglycemia, hypoinsulinemia, glucose intolerance, and pancreatic β-cell loss. Heterozygous mice have an intermediate hypoinsulinemic phenotype on high-fat diet. These Sec61a1Y344H mutant mice may be useful in studying diabetes, ER protein trafficking/processing/sec ..... For more information please see the full phenotype on the strain data sheet | ||
| 017319 | FVB-Tg(Myh6-Mtpn)4Ssen/J | Under Development - Now Accepting Orders |
| 017542 | FVB-Tg(Myh6/tetO-ATP2B4)1Jmol/J | Under Development - Now Accepting Orders |
| These transgenic animals carry the human ATP2B4 (ATPase, Ca++ transporting, plasma membrane 4; also known as PMCA4b) cDNA driven by a conditional mouse Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha)-tetO cardiac-specific promoter. These mice show no overt phenotype.
When crossed with a driver strain encoding the tetracycline transactivator (tTA), heart-specific protein expression is seen in the absence of doxycycline (Dox). Immunolocalization studies in the hearts of double transgenic mice show mostly sarcolemmal and T-tubular expression, a pattern that was essentially the same for the endogenous mouse gene, albeit at substantially lower levels. Administration of Dox inhibits expression. | ||
| 014547 | FVB/N-Tg(tetO-Fasl)BDepa/J | Under Development - Now Accepting Orders |
| Mice hemizygous for the (tetOp)7-FasL transgene (TetOp-FasL transgenic mice) are viable and fertile with no reported phenotypic abnormalities. The (tetOp)7-FasL transgene has the Tet response element (TRE or tetO) upstream of a murine Fas ligand (FasL) coding sequence. When bred with other mice expressing tetracycline-controlled transactivator protein (tTA) or reverse tetracycline-controlled transactivator protein (rtTA), FasL overexpression in the resulting double mutant offspring can be regulated with tetracycline or its analog doxycycline (dox). FasL overexpression leads to Fas/FasL receptor-mediated death-signaling pathway activation and results in cell apoptosis.
The donating investigator reports that transgenic mice from founder line B (TetOp-FasL transgenic line B) exhibit very high FasL overexpression levels in the presence of rtTA and 0.01 mg/ml Dox (low FasL levels are achievable by titrating Dox even lower). The donating investigator rep ..... For more information please see the full phenotype on the strain data sheet | ||
| 014180 | STOCK Myocdtm1(cre)Jomm/J | Under Development - Now Accepting Orders |
| This strain expresses Cre recombinase from the endogenous Myocd locus. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs during early development, at embryonic day 7.5, in the developing heart, dorsal aorta, head mesenchyme and in the somites beginning at embryonic day 8.5. Cre activity is also detected in skeletal muscle fibers and vasculature. Homozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 016622 | STOCK Utrntm1Jrs Dmdmdx/J | Under Development - Now Accepting Orders |
| 016572 | STOCK Tg(Myh6/tetO-Gata4)1Jmol/J | Under Development - Now Accepting Orders |
| These Gata4 transgenic mice contain GATA binding protein 4 (Gata4) sequence regulated by a tetracycline operator (tetO), driven by myosin, heavy polypeptide 6, cardiac muscle, alpha (Myh6 or α-MHC) promoter/enhancer elements. Hemizygotes are viable, fertile, and normal in size. α-MHC limits overexpression of Gata4 to the heart. GATA4 is a zinc-finger-containing transcription factor expressed in cardiomyocytes and has a role in regulating the expression of genes involved in cardiac differentiation. When mated to a mutant strain expressing tetracycline-controlled transactivator protein (tTA), expression of GATA4 protein may be controlled by the administration of tetracycline or its analog doxycycline in bi-allelic offspring. For instance, when bred to mice expressing tTA driven by the α-MHC promoter, double transgenic animals exhibit an increase in myocardial capillary densities, coronary flow reserve, and p ..... For more information please see the full phenotype on the strain data sheet | ||
| 014093 | STOCK Tg(tetO-CHRM3*)1Blr/J | Under Development - Now Accepting Orders |
| Hemizygous TRE-hM3Dq transgenic mice are viable and fertile, with no reported phenotypic abnormalities. The TRE-hM3Dq transgene has a modified Tet response element (TRE or tetO) upstream of the mutant G protein-coupled receptor, hM3Dq (a human muscarinic 3 receptor with two amino acid substitutions (Y149C3.33/A239G5.46) that abolish receptor affinity for the native ligand, acetylcholine (ACh), but allow receptor binding and subsequent activation by the small pharmacologically inert molecule clozapine-N-oxide (CNO)). When bred with another mouse expressing tetracycline-controlled transactivator protein (tTA) or reverse tetracycline-controlled transactivator protein (rtTA), hM3Dq expression in the resulting double mutant offspring can be regulated with tetracycline or its analog doxycycline (dox). As designed, TRE-hM3Dq transgenic mice have no reported levels of hM3Dq activity in tTA(+dox) or rtTA(-dox) cell types. In TRE-hM3Dq transgenic tTA(-dox) ..... For more information please see the full phenotype on the strain data sheet | ||
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Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Awaiting Transfer
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New Strains Awaiting TransferThe Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion.
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