Search Criteria: Research Area is "Research Tools: Metabolism 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. | ||
| 006050 | 129-Sirt6tm1Fwa/J | Repository- Live |
| Homozygous neonates are smaller than their wildtype and heterozygous littermates. They develop normally until approximately 21 days of age, when they develop an acute and rapid, aging-like degenerative pathology resulting in death by postnatal day 24. Homozygous mutant mice exhibit subcutaneous fat loss, lordokyphosis (hunchbacked spine) with osteopenia (30% loss of bone mineral density), colitis, and severe lymphopenia due to increased lymphocyte apoptosis. At day 12, mice have reduced insulin-like growth factor I (IGF-1) levels in serum, and develop severe hypoglycemia. Mouse embryonic fibroblasts (MEFs) prepared from homozygous embryos exhibit reduced proliferation, defective base excision repair function, as indicated by increased sensitivity to alkylating agents and ionizing radiation, and increased chromosomal aberrations. The donating investigators report that no gene product (mRNA or protein) is detected by RT-PCR or immuoblot analysis of tissues, MEFs or embryonic stem cells f ..... For more information please see the full 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 | ||
| 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. | ||
| 007741 | B6.129-Arg1tm1Rki/J | Repository- Live |
| Homozygous AI-mutant mice completely lack hepatic arginase (AI) activity, exhibit hyperagrininemia, severe symptoms of hyperammonemia (ncluding decerebrate posture, lethargy, and high-frequency tremor of the extremities, particularly the tail) and die between 10-14 days after birth. Neural stem cells (NCSs) isolated from homozygous mice exhibit abnormal proliferation and differentiation. In addition, haploid germ cells carrying the disrupted AI allele may be less fit/less effective in forming zygotes compared to wild-type spermatozoa. Heterozygotes are viable and fertile. These AI-mutant mice may be useful in studying metabolic defects of arginase I deficiency, urea cycle (excretion of excess nitrogen), and neuronal development and function. | ||
| 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. | ||
| 008227 | B6.129S4-Ppargtm3Yba/J | Repository- Live |
| These mice express tTA (tetracycline regulated transactivator) from the endogenous Pparg locus. A fusion transcript (including the 5' portion of Pparg, IRES and tTA (AF1-IRES-tTA)) and a wild-type Pparg transcript are detected by Northem blot analysis of epididymal fat pads from heterozygotes. Mice that are heterozygous for this targeted mutation exhibit a similar but milder phenotype than that observed in Pparg-Ldi mice (129-Ppargtm2Yba/J, Stock No. 008079). Heterozygotes exhibit mild lipodystrophy with pale, unilocular brown adipocytes, hypertrophy of brown fat, reduced subcutaneous fat, gonadal fat pads smaller than wild-type and mild hepatomegaly. Mutant mice develop insulin resistance and dyslipidemia. Treatment with doxycycline prevents this phenotype. Mice that are homozygous for the targeted mutation are not viable. This mutant mouse strain may be useful in studies of lipodystrophy. | ||
| 012564 | B6.129S5-Dhcr24tm1Fein/SbpaJ | Repository- Live |
| Homozygous mice on the C57BL/6 genetic background die within the first postnatal day with features of lethal restrictive dermopathy; including taut, wrinkle-free, shiny skin, severe defects in epidermal maturation/epidermal barrier function (impaired epidermal development), and increased presence of hyperproliferative immature keratinocytes (defective keratinocyte differentiation). The increased transepidermal water loss/increased epidermal water content is associated with increased aquaporin-3 (AQP3) expression throughout the epidermis. Mice heterozygous for this allele are viable and fertile, with no overt phenotype. As the Dhcr24 protein functions to catalyze the last step of cholesterol biosynthesis (the conversion of desmosterol to cholesterol), homozygous disruption of this locus results in desmosterolosis: almost no cholesterol in plasma and tissues with ~99% of total sterols in the form of desmosterol. lacZ expression from the mutant allele is not characterized.
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| 016238 | B6.129S6-Rbp7tm1Vgl/J | Repository- Live |
| Mice that are homozygous for this knockout mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of heart tissue extracts from homozygous mice. Homozygous lactating females have reduced levels of total retinyl ester in milk, with the largest reduction in retinyl palmitate levels. Total retinol levels in heart tissue are reduced in homozygotes at weaning, but not in homozygotes aged 11 or 17 weeks. Decreased levels of retinol and retinyl ester are detected in the mammary glands of homozygous females 11 weeks of age. At 17 weeks of age, only total retinol levels remain diminished. Postprandial retinoid turnover is not changed in mutant mice. Homozygotes fed a high fat diet have reduced hepatic steatosis, lower hepatic triglyceride levels, and decreased serum free fatty acids and efflux from adipose tissue compared to wildtype controls. On a ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 006966 | B6.Cg-Akt2tm1.1Mbb/J | Repository- Live |
| Mice homozygous for this Akt2 (thymoma viral proto-oncogene 2) mutant allele are viable and fertile. Homozygotes develop insulin resistance, hyperglycemia, impaired glucose tolerance, abnormal glucose uptake in muscle tissue, increased pancreatic beta-cell mass, and diabetes. 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. | ||
| 008599 | B6.Cg-Cyp1a2/Cyp1a1tm2Dwn Ahrd Tg(CYP1A1,CYP1A2)1Dwn/DwnJ | Repository- Live |
| These "humanized" hCYP1A1_1A2_Cyp1a1/1a2(-/-)_Ahrd mice carry the human CYP1A1 and CYP1A2 genes in the absence of functional mouse Cyp1a1 and Cyp1a2 orthologs, and also mimic the human poor-affinity aryl hydrocarbon receptor (AHR) by carrying the poor-affinity Ahrd allele derived from DBA/2J mice (rather than the high-affinity Ahrb1 allele normally present on a C57BL/6J genetic background); all on a C57BL/6J (reported >99.8%) genetic background. Mice homozygous for the Cyp1a2/Cyp1a1 targeted allele [Cyp1a1/1a2(-/-)], homozygous for the Ahrd allele, and carrying the hCYP1A1_1A2 transgene are viable and fertile with normal lifespan. As the Cyp1a2/Cyp1a1(-) targeted allele lacks the coding regions of both Cyp1a1 and Cyp1a2 genes, no mouse CYP1A1 or CYP1A2 mRNA expression is observed in liver, lung or kidney. Transgene expression of the orth ..... | ||
| 014648 | B6.Cg-Gt(ROSA)26Sortm37(H1/tetO-RNAi:Taz)Arte/ZkhuJ | Repository- Live |
| These mutant mice have a tetracycline inducible Taz specific short hair pin RNA (shRNA) driven by the endogenous mouse Gt(ROSA)26Sor promoter.
Expression of the shRNA is controlled by the transcription of the H1 RNA polymerase III promoter, which is coupled to a tet-operator (tetO) sequence. Expression of the shRNA is blocked by codon-optimized version of the tet repressor itetR, which is part of the allelic construct found in this mouse. Doxycycline (dox--a tetracycline analog) treatment decreases the affinity of the itetR for the tetO sequence, allowing transcription of the shRNA.
Dox-induced Taz gene silencing is detected in heart (to ~3.7% of wildtype), skeletal muscle (to ~11.2%), liver (to ~8.9%) and brain (to ~3.4%) by RT-PCR analysis. Gene product (mRNA) in transgenic mice without dox induction is reduced by 35% of wildtype control levels. Withdrawal of dox at 4 weeks partially reverses the reduction of Taz expression. Protein product ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 006417 | B6.FVB-Tg(Npy-hrGFP)1Lowl/J | Repository- Live |
| Hemizygous mice are viable and fertile. These mice express humanized Renilla Green Fluorescent Protein (hrGFP, Stratagene) under control of the mouse neuropeptide Y (Npy) promoter. As such, UV light-exposed transgenic brain tissues show GFP fluorescence patterns consistent with the (Npy) gene. The donating investigator reports that the hrGFP expressed from this transgene is more stable and resistant to signal fading compared to other GFP’s. These transgenic mice may be useful for studies of neurobiology, energy metabolism, obesity, seizures, and epilepsy. | ||
| 008041 | B6;129-Sirt1tm1Ygu/J | Repository- Live |
| Mice homozygous for this targeted allele (SirT1co/co) are viable and fertile. A loxP-flanked neomycin cassette just upstream of exon 4 and a third loxP site downstream of exon 4 were inserted to create this targeted mutant Sirt1 allele. The floxed mutation does not affect SIRT1 protein expression in MEFs or mammary gland tissue in homozygotes. When bred to mice that express Cre recombinase, the resulting offspring have exon 4 (encoding an evolutionarily conserved Sir2 motif) deleted in cre-expressing tissue(s); (the donating investigator reports only one recombination event: complete removal of the neomycin cassette and exon 4, leaving a single loxp). These SirT1co/co mice may be useful in generating conditional mutants for studying transcriptional regulation and the role of estrogen, insulin growth factor-1 (IGF-1), and transcription factors (including NF-kappaB) in mammary gland development, mammary cancer, apoptosis, and metabolic di ..... For more information please see the full phenotype on the strain data sheet | ||
| 006414 | B6;129S4-Mc4rtm1Lowl/J | Repository- Live |
| The mice have a loxp-flanked transcriptional blocking (loxTB) sequence that prevents normal endogenous gene transcription and translation from the endogenous locus. As such, homozygous mice are devoid of functional mRNA in all tested regions of the brain. Homozygous mice exhibit severe early-onset obesity, accompanied by hyperphagia, increased snout-anus length and hyperinsulinemia. The function of this disrupted allele can be restored by the enzymatic activity of Cre-recombinase. These mutant mice may be useful in studies of neurobiology, obesity, diabetes, hunger/appetite, and fat and energy metabolism.
When bred to a strain expressing Cre recombinase in the hypothalamus see Stock No. 006395 for example), this mutant mouse strain exhibits as intermediate phenotype in comparison to homozygous null mice. | ||
| 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 | ||
| 013080 | C57BL/6-Actbtm3.1(Sirt1)Npa/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, exhibit delayed reproduction and lower body weight. No homozygotes are produced from heterozygous crosses. Fewer than expected heterozygotes are produced from heterozygote X wildtype crosses. Overexpression of gene product (protein) is detected by Western blot analysis of white adipose tissue, brown adipose tissue, MEFs, skull calvaria cells and brain tissue. Overexpression of the protein is not detected in liver or muscle tissue. Fusion gene product (mRNA) is detected in white adipose tissue by Northern blot analysis. Beta-actin protein expression is equivalent to wildtype levels. Heterozygote knock-in mice have reduced fat mass (epididymal fat pad weight), circulating free fatty acids, leptin, adiponectin and total cholesterol. Food consumption, glucose tolerance and metabolic rate (with associated higher oxygen consumption) are increased in the mutant mice. In fasted conditions, heterozygotes have lower circul ..... For more information please see the full phenotype on the strain data sheet | ||
| 009062 | C57BL/6-Magel2tm1Stw/J | Repository- Live |
| The mouse locus 7qB4/B5 (syntenic with the Prader-Willi region at chromosome position 15q11-q13 in humans) encompasses the cluster of paternally-expressed imprinted genes Magel2, Ndn, Mkrn3, and Peg12. As maternal imprinting silences the Magel2 allele, only the paternally inherited Magel2 allele is expressed. The Magel2-lacZ knock-in allele abolishes endogenous gene function and expresses a β-galactosidase fusion protein. Under control of the upstream promoter/enhancer elements, lacZ expression is directed to the same tissues as the wildtype gene. For example, β-galactosidase expression during embryogenesis is detected in central nervous system (neural tube, forebrain, midbrain and embryonic hypothalamus), peripheral nervous system (dorsal root ganglia and peripheral neurons innervating limb and trunk muscles), and some non-neuronal tissues (genital tubercle, midgut region and placenta). Adult β-galactosidase ..... For more information please see the full phenotype on the strain data sheet | ||
| 009345 | C57BL/6J-Mstnlean/J | Repository- Live |
| Mice homozygous for this ENU-induced mutation, called the lean (Ln) allele of myostatin (MstnLn), are viable and fertile. The MstnLn allele alters mRNA splicing and results in an additional larger transcript containing a 128 basepair insert at the junction between exons 2 and 3. This insertion encodes an additional 4 amino acids before a premature stop codon (ASDNX), and is predicted to generate a truncated protein containing the Mstn signal sequence and propeptide, but lacking the ligand portion of the molecule. In addition to this abnormal splicing product, the mRNA from mutant males is also reduced in abundance by approximately 60% compared to wildtype males. When maintained on normal diet, homozygous (MstnLn/Ln) mice exhibit increased muscularity. When maintained on a high fat diet, homozygotes exhibit glucose tolerance, protection against overall insulin resistance, improved muscle and liver insulin sensitivity (with decreased ..... For more information please see the full phenotype on the strain data sheet | ||
| 009593 | C57BL/6J-Tg(Pomc-EGFP)1Low/J | Repository- Live |
| Mice hemizygous for this POMC-EGFP transgene are viable and fertile, with EGFP expression directed to POMC-expressing neurons by the mouse Pomc (pro-opiomelanocortin-alpha) promoter/enhancer regions. The donating investigator reports that transcripts from the transgene encode EGFP but do not express any POMC prohormone or peptides. Direct EGFP fluorescence is observed in the arcuate nucleus of the hypothalamus (ARC), in melanotrophs/corticotrophs of the pituitary gland, and (unlike other POMC promoter-driven fluorescent mice) in a subpopulation of newly born granule neurons of the dentate gyrus of the hippocampus. EGFP expression is also observed in the nucleus of the solitary tract of the medulla. EGFP expression is downregulated as neurons mature and migrate deeper into the granule cell layer. These POMC-EGFP mice may be useful in studying neuronal signaling pathways, energy metabolism, leptin activity, obesity, seizures, depression, and epilepsy. | ||
| 006421 | FVB-Tg(Pomc1-hrGFP)1Lowl/J | Repository- Live |
| Hemizygous mice are viable and express humanized Renilla Green Fluorescent Protein (hrGFP, Stratagene) under control of the mouse pro-opiomelanocortin-alpha (Pomc1) promoter. As such, UV light-exposed transgenic brain tissues show GFP fluorescence patterns consistent with the endogenous Pomc1 gene, specifically POMC expressing neurons. The donating investigator reports that hrGFP is more stable and resistant to signal fading compared to other GFP's. The donating investigator reports that transgenic males have smaller seminal vesicles, and breeding transgenic males results in infrequent and very small (<2 pups) litter sizes. When non-transgenic males are crossed with transgenic females, fertility is normal. These POMC-GFP transgenic mice may be useful for studies of neurobiology, energy metabolism, obesity, seizures, and epilepsy. | ||
| 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 | ||
| 005965 | STOCK Tg(Pomc1-cre)16Lowl/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre activity is demonstrable in brain area neurons involved in the control of food intake (arcuate nucleus (hypothalamus) and solitary tract nucleus (hindbrain)). When bred with a mouse containing a loxP site-flanked sequence of interest, Cre-mediated recombination results in deletion of the flanked genome in tissues that normally express Pomc1. The mice may be useful in studies of obesity, food intake, hunger, endocrine and exocrine function, and for tissue specific gene targeting. | ||
| 008079 | 129S-Ppargtm2Yba/J | Cryopreserved - Ready for recovery |
| These mice express tTA (tetracycline regulated transactivator) and a tetO-driven Flag-tagged Pparg from the endogenous Pparg locus. A fusion transcript (including the 5' portion of Pparg, IRES and tTA (AF1-IRES-tTA)), a Flag-Pparg transcript and a wildtype transcript are detected by Northem blot analysis of white adipose tissue from heterozygotes. The fusion transcript of AF1-IRES-tTA is also detected in brown adipose tissue. Expression of tTA is detected in adipose tissue by Western blot analysis. No Flag-PPARG1 protein was detected in adipose tissue. Weak expression of tTA and the Flag-Pparg transcript is observed in placenta and liver. Endogenous PPARG2 protein is reduced in adipose tissues of heterozygotes. Heterozygotes exhibit "buffalo humps" (swollen interscapular fat pads swollen by hypertrophy and unilocular lipid deposition in mutant brown adipocytes), absence of subcutaneous adipocytes, reduced gonadal white adipose tissue, irregularly residual a ..... For more information please see the full phenotype on the strain data sheet | ||
| 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)). | ||
| 008077 | 129S1/Sv-Bchetm1Loc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this BChE mutant allele are viable and fertile with no reported spontaneous abnormalities. All tissues and plasma from homozygous mice are devoid of BChE activity. As BChE (butyrylcholinesterase) is a bioscavenger molecule protecting acetylcholinesterase (AChE) activity against nerve agents and organophosphates, homozygous BChE-deficiency leads to impaired protection from toxic compounds. These BChE mutant mice are a model for human butyrylcholinesterase deficiency and may be useful for studying metabolic effects of organophosphorus toxicants or nerve agents, neurotransmitter function, and anti-Alzheimer's drug therapies.
Of note, the donating investigator has multiple strains available that may be useful for testing toxic compounds, including the AChE-deficient (Stock No. 005987), G117H BChE transgenic (Stock No. 007577), and BChE-deficient (see Stock ..... | ||
| 005358 | 129S6/SvEvTac-Car3tm1Gkim/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted allele are viable, fertile, normal in size and life span and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected. Histological examination of tissues discerns no anomalies. Similarly, gas chromatography-mass spectrometry analysis of the fatty-acid distribution in serum, muscle, liver, and fat reveal no differences between mutant and wildtype mice. When exposed to an atmosphere of 100% oxygen homozygous mice display similar mean survival times as wildtype (~ 70 hours). The contractile properties of soleus muscle derived from mutant mice exhibit some differences from wildtype mice. Mutant mice display shorter relaxation and half-relaxation times for single and tetanic twitches and a minor reduction tetanic force. Microarray analysis detects an increase (~30%) in carbonic anhydrase 13 expression. | ||
| 008149 | B6(Cg)-Snord116tm1.1Uta/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Snord116del (1-loxP or knockout) allele are viable and fertile. As the Snord116 gene cluster is imprinted and expressed only from the paternal allele, mice with paternal inheritance of the deletion lack expression of the targeted Snord116 small nucleolar RNAs (snoRNAs) gene cluster in brain tissues. Similarly, paternal transmission of the mutant allele is required to obtain the mutant phenotype in offspring. Affected heterozygotes (paternal deleted/maternal wildtype) recapitulate a subset of Prader-Willi syndrome (PWS) characteristics, including early-onset postnatal growth retardation, delayed sexual maturation, increased anxiety, motor learning deficit and hyperphagia (but not obesity). Other reported abnormalities include altered metabolic fuel usage, prolonged meal time, and increased levels of circulating ghrelin. These Snord116del mice may be useful in studying growth and feeding regulation, mechanisms of obesity, and pa ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 008763 | B6.129-Abcg8tm1Elk/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Female homozygotes are infertile, and male homozygotes exhibit rare infertility, if not maintained on a plant sterol free diet or with drug treatment to block uptake of plant sterols. No gene product (mRNA) is detected by Northern blot and RT-PCR analysis of total hepatic RNA from homozygous animals. Homozygotes have increased plasma and tissue levels of sitosterol and campesterol (plant sterols) with impaired cholesterol secretion in bile. Expression of Abcg5 (ATP-binding cassette, sub-family G (WHITE), member 5) is unchanged in homozygotes. Liver cholesterol levels in homozygotes is decreased by approximately 50%. Serum cholesterol levels are decreased by 52% in homozygotes and 26% in heterozygotes. Heterozygotes exhibit an intermediate phenotype with decreased biliary sterol secretion but do not become sitosterolemic. This ..... For more information please see the full phenotype on the strain data sheet | ||
| 003509 | B6.129-Blmhtm1Geh/J | Cryopreserved - Ready for recovery |
| Bleomycin (BLM) is a clinically used glycopeptide anticancer agent. It is deaminated in vitro by BLMH. Blmh null mice have decreased viability and fertitility. Only about 65% of the expected number survive the neonatal period. Mice lacking Blmh exhibit variably penetrant tail dermatitis that resembles rodent ringtail. This resembles skin lesions in humans with pellagra, necrolytic migratory erythema, and acrodermatitis enteropathica. Null mice also are more sensitive to acute BLM lethality and develop pulmonary fibrosis following BLM treatment. | ||
| 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 | ||
| 003870 | B6.129-Plin1tm1Chan/J | Cryopreserved - Ready for recovery |
| Homozygous null Plin mice are viable and fertile. At birth they are normal in size and do not display any gross physical or behavioral abnormalities. No transcripts are detected and Western-blot analysis of adipocyte and testes indicate no protein products are present. Although null mice consume more food than wildtype littermates, they have significantly less body fat (30-74%) and exhibit smaller white adipocytes (62%). With diminished fat stores, the mice are cold sensitive under fasting conditions. A greater muscle mass allows them to maintain a normal body weight. Hormone sensitive lipase activity is greatly increased in null mice resulting in elevated levels of basal lipolysis. Null mice are resistant to diet-induced obesity. The inheritance of the null alleles in Leprdb/db mice reverses their obesity phenotype. | ||
| 007453 | B6.129P2(Cg)-Dhcr7tm1Gst/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Dhcr7Ex8 allele lack the exon 8 coding sequence and flanking splice acceptor site of the targeted gene, resulting in the truncated DHCR7 mutation most frequently observed in Smith-Lemli-Opitz/RSH Syndrome (SLOS) patients (IVS8-1G > C). Although a truncated product is transcribed from the targeted gene, no mRNA containing the deleted 3'-coding region is detected in homozygous liver or brain tissue. Homozygous mice exhibit the same biochemical defects as observed with SLOS patients, including markedly reduced tissue cholesterol and total sterol levels, and 30- to 40-fold elevated concentrations of 7-dehydrocholesterol. Newborn homozygotes have difficulty breathing, do not suckle, and die soon after birth with immature lungs, enlarged bladder, and, frequently, cleft palate. These Dhcr7Ex8 mutant mice may be useful in studying Smith-Lemli-Opitz/RSH Syndrome (SLOS; a birth-defect mental-retardation syndrome) or other metabolic disorders invol ..... 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 | ||
| 008087 | B6.129S1-Bchetm1Loc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this BChE mutant allele are viable and fertile with no reported spontaneous abnormalities. All tissues and plasma from homozygous mice are devoid of BChE activity. As BChE (butyrylcholinesterase) is a bioscavenger molecule protecting acetylcholinesterase (AChE) activity against nerve agents and organophosphates, homozygous BChE-deficiency leads to impaired protection from toxic compounds. These BChE mutant mice are a model for human butyrylcholinesterase deficiency and may be useful for studying metabolic effects of organophosphorus toxicants or nerve agents, neurotransmitter function, and anti-Alzheimer's drug therapies.
Of note, the donating investigator has multiple strains available that may be useful for testing toxic compounds, including the AChE-deficient (Stock No. 005987), G117H BChE transgenic (Stock No. 007577), and BChE-deficient (see Stock ..... | ||
| 008841 | B6.129S2-Ccrn4ltm1Bjc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Nocturnin (Ccrn4l or Noc) targeted mutation are viable and fertile, with no detectable Noc protein made from the targeted gene. Homozygotes are resistant to diet-induced obesity and remain lean on high-fat diets, with lower body weight and reduced visceral fat. Unlike lean lipodystrophic mouse models, Noc-deficient mice do not have fatty livers (hepatic steatosis) and do not exhibit increased activity or reduced food intake. In addition to changes in glucose tolerance and insulin sensitivity, homozygous mice may also have deficits in lipid metabolism or lipid uptake. Nocturnin-deficient mice may be useful in studying resistance to diet-induced obesity, physiologic rhythms downstream of the circadian clockwork, and post-transcriptional regulation of genes necessary for nutrient uptake, metabolism, and storage. | ||
| 008439 | B6.129S2-Seletm1Hyn Selltm1Hyn Selptm1Hyn/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Sele, Sell and Selp genes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities at birth. As mice mature, however, they become susceptible to mucocutaneous infections that eventually lead to death. No Sele, Sell or Selp gene products (mRNA or protein) are detected. Leukocytes from these mice exhibit a deficiency in the ability to interact with, and roll along, the venular wall endothelium. This deficiency in the crucial first step of leukocyte recruitment to surrounding tissues in response to infection or injury contributes to an elevated leukocyte count in the peripheral blood. Delays in neutrophil and eosinophil recruitment to the peritoneum in response to thioglycollate and ragweed allergen, respectively, have been observed, specifically. These mice are suitable for use in research applications studying leukocyte homeostasis, infectious diseases and inflam ..... For more information please see the full phenotype on the strain data sheet | ||
| 008437 | B6.129S2-Seletm1Hyn Selptm1Hyn/J | Cryopreserved - Ready for recovery |
| Mice homozygous for both the Seletm1Hyn Selptm1Hyn mutations are viable and fertile. They are characterized by leukocytosis, spontaneous bacterial infections, dermatitis and defective leukocyte recruitment in many models of inflammation. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 008434 | B6.129S2-Seletm2Hyn/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Seletm2Hyn targeted mutation are viable and fertile. Homozygous mutant mice show only subtle defects in leukocyte recruitment, unless P-selectin (Selp) is also ablated or blocked with antibody. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 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 | ||
| 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. | ||
| 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. | ||
| 004185 | B6.129S4-Soat2tm1Far/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for this targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Southern blot analysis and RT-PCR indicated the targeted gene was disrupted. These mice lack cholesterol ester synthesis in liver and intestine and are resistant to diet-induced hypercholesterolemia and cholesterol gallstone formation. In homozygous mice fed regular diet, acyl CoA: cholesterol acyltransferase (ACAT) enzyme activity was reduced by 92% in intestine, and by 99% in liver. Homozygous mice fed high-fat/high cholesterol diet had low ACAT activity. Although ACAT2 deficient mice absorb less cholesterol than wild-type mice when fed a high fat/ high cholesterol diet, histological examination indicated enterocytes in the mutant mice were normal. This mutant mouse strain represents a model that may be useful in studies related to human resistance to diet-induced hypercholesterolemia and cholesterol gallstone formation. | ||
| 003823 | B6.129S4-Ttpatm1Far/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Ttpa gene are viable, normal in size and do not display any gross physical abnormalities. The Ttpa protein product is required for the maintenance of proper alpha-tocopherol levels, the major form of vitamin E in plasma and tissues. The absence of Ttpa protein product in homozygous-null animals results in a corresponding 95% reduction in alpha-tocopherol. Low levels of alpha-tocopherol render female mice infertile, a condition that can be addressed with vitamin E supplements. Male fertility is unimpaired. These mice provide a viable model for studying vitamin E deficiency. | ||
| 004125 | B6.129S6-Abcb11tm1Wng/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Abcb11 gene suffer from lowered rates of viability and fertility. No Abcb11 gene product (mRNA or protein) is detected in liver tissue. Homozygotes display growth retardation with body weights being 80% that of wildtype littermates at weaning. Lower body weights persist throughout life. Ultrastructural changes are noted in the hepatic canaliculi (lumen dilation, microvilli loss, and accumulation of biliary material). Hepatocytes exhibit increased numbers of peroxisomes, lysosomes and lipid droplets with a concomitant decrease in stored glycogen. Although average bile flow is not significantly reduced, secretion of major hydrophobic bile salts is clearly impaired. An increase in the secretion of tetra-hydroxylated bile acids, cholesterol and phospholipids is observed. These mice provide a model for studying intrahepatic cholestasis and the mechanisims associated with lipid homeostasis. | ||
| 009082 | B6.129S6-Ostatm1Pda/J | Cryopreserved - Ready for recovery |
| Homozygous (Osta-/-) mice are viable and fertile, with no mRNA or protein expression from the targeted allele. Homozygotes exhibit a small growth deficit that is ameliorated after weaning, partial impairment of intestinal bile acid absorption (impaired basolateral transport of bile acids out of the ileal epithelial cell), altered regulation of bile acid synthesis, a significantly reduced bile acid pool, intestinal lengthening and intestinal hypertrophy. Homozygous mice also have reduced hepatic Cyp7a1 expression that is inversely correlated with ileal expression of fibroblast growth factor 15 (FGF15). These mutant mice may be useful in studying cholesterol metabolism, intestinal drug absorption, intestinal bile acid absorption, bile acid synthesis, and cholesterol and bile acid homeostasis.
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 ..... | ||
| 004665 | B6.129X1(FVB)-Hnf4atm1.1Gonz/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Similarly oriented loxP sites are positioned in introns 3 and 5 of the targeted gene. When used in conjunction with a Cre recombinase-expressing strain, this mouse can be used to generate tissue-specific mutants. Cre-directed recombination results in the deletion of the loxP-flanked sequence causing a splicing event between exons 3 and exon 6. A frame shift occurs generating a premature stop codon. A putative truncated protein may be translated, but such a protein would lack the A and T box motifs necessary for high-affinity binding to DNA. This mouse mutant may be useful in studies related to lipid homeostasis.
When bred to a strain expressing Cre recombinase in pancreatic beta cells (see Stock No. 003573 for example), this mutant mouse strain may be useful in studies of insulin ..... | ||
| 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 | ||
| 009662 | B6.129X1-Ppargc1atm1Dpk/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable and fertile. During the generation of this allele, a 3' homologous recombination and insertion occurred with a duplication of exon 3 between exons 5 and 6. The exon 3 insertion, which was confirmed by RT-PCR, results in a mutant transcript that encodes a truncated protein due to a stop codon at amino acid 255. Normal gene product (mRNA) containing an exon 5?6 border is not detected. If the truncated protein gene product is stable, it could theoretically have some activity, given that it would contain nuclear receptor-interacting domains and the amino-terminal activation domain. Total body weights for homozygotes are reduced 15-20% for the first week after birth, but become normal by 3 weeks of age. By 18 weeks of age, homozygotes have heavier body weights and increased percent body fat than wildtype controls. Heart and slow twitch skeletal muscle (gastrocnemius, soleus) weights are lower in homozygotes than controls. Electr ..... For more information please see the full phenotype on the strain data sheet | ||
| 006558 | B6.Cg-H2-Kbm1 Tg(GUSB)4Sly/SndsJ | Cryopreserved - Ready for recovery |
| Mice that are homozygous for this transgene and the Gusbmps allele have approximately 20-fold higher beta-glucuronidase enzyme activity than wildtype controls. Distribution of human enzyme activity throughout various tissues mimics the endogenous mouse enzyme activity pattern. Of note, mice homozygous for both the transgene and the Gusbmps allele do not exhibit an accumulation of undegraded glycosaminoglycans. These transgenic mice do not carry the Gusbmps allele. Mice that are hemizygous for this transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of lysomal storage diseases and mucopolysaccharidosis VII (Sly syndrome). | ||
| 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. | ||
| 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. | ||
| 006200 | B6.Cg-Tnks2tm1.1Yjc/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of activated spleen lymphocytes. While neither telomere shortening nor chromosomal abnormalities (even across multiple generations) are observed, homozygous mice have significantly decreased body weight. These mutant mice may be useful in studies of both telomerase function and telomerase-independent pathways which affect development and metabolism. | ||
| 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 | ||
| 006451 | B6.FVB(129X1)-Tg(Sim1-cre)1Lowl/J | Cryopreserved - Ready for recovery |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgene expression is observed in all areas that endogenously express Sim1, including paraventricular hypothalamus and other parts of the brain. When these Sim1-Cre mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the flanked sequences in Sim1-expressing tissues (including hypothalamus). As such, Sim1-Cre transgenic mice may be useful in studying body weight homeostasis, obesity, leptin metabolism, or as a reporter strain for Sim1-transcription factor activity.
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 st ..... | ||
| 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 ..... | ||
| 008333 | B6;129P2-Dldtm1Ptl/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the Dld (dihydrolipoamide dehydrogenase or E3 component) targeted mutation are viable and fertile. Heterozygous mice exhibit approximately half of wild-type enzymatic activity levels for E3 and all affected mitochondrial multienzyme complexes. Heterozygotes (on a C57BL/6;129P2 genetic background) exhibit increased vulnerability to treatments with MPTP (dopaminergic neurotoxin used to induce Parkinson's disease-like lesions), malonate (inhibitor of cellular respiration used to mimic Huntington's disease features), and 3-NP (mitochondrial toxin used to mimic Huntington's disease features). Homozygous mice exhibit normal development and metabolism during the preimplantation period, explained by the persistence of E3 enzyme from the oocyte. Homozygotes exhibit developmental delays shortly after implantation (7.5 to 8.5 days postcoitum (dpc)) and cease development within the subsequent two days. These Dld mutant mice may be useful to study early murine em ..... For more information please see the full phenotype on the strain data sheet | ||
| 003807 | B6;129S-Seletm1Hyn Selltm1Hyn Selptm1Hyn/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Sele, Sell and Selp genes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities at birth. As mice mature, however, they become susceptible to mucocutaneous infections that eventually lead to death. No Sele, Sell or Selp gene products (mRNA or protein) are detected. Leukocytes from these mice exhibit a deficiency in the ability to interact with, and roll along, the venular wall endothelium. This deficiency in the crucial first step of leukocyte recruitment to surrounding tissues in response to infection or injury contributes to an elevated leukocyte count in the peripheral blood. Delays in neutrophil and eosinophil recruitment to the peritoneum in response to thioglycollate and ragweed allergen, respectively, have been observed, specifically. These mice are suitable for use in research applications studying leukocyte homeostasis, infectious diseases and inflam ..... For more information please see the full phenotype on the strain data sheet | ||
| 004858 | B6;129S1-Tshrtm1Rmar/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation exhibit delayed eye opening, are runted by day 21, and will die within 1 week if weaned at day 21. Homozygotes will survive by extending weaning to 28 days but will not reproduce. Homozygotes are viable and fertile when weaned at day 21 and subsequently placed on a hormone replacement therapy diet consisting of a 100ppm desiccated thyroid powder supplement. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis of thyroid membranes. Enhanced Green Fluorescent Protein (EGFP) gene product is detected by RT-PCR and Western blot analysis of thyroid tissue. Hypothyroidism is exhibited by mutant mice that have a longer weaning period and a non-supplemented diet, as indicated by low T4 and T3 serum levels, and high thyrotropin (TSH) serum levels. Treatment with exogenous TSH does not result in a thyroid hormone release response. Mutant mice produce uniodinated thyroglobulin and do not accumulate radioactive iodide in ..... For more information please see the full phenotype on the strain data sheet | ||
| 002916 | B6;129S2-Seletm1Hyn Selptm1Hyn/J | Cryopreserved - Ready for recovery |
| Mice homozygous for both the Seletm1Hyn Selptm1Hyn mutations are viable and fertile. They are characterized by leukocytosis, spontaneous bacterial infections, dermatitis and defective leukocyte recruitment in many models of inflammation. | ||
| 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. | ||
| 005937 | B6;129S4-Ucp3tm1Lowl/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable and fertile and do not express full length mRNA in skeletal muscle and brown adipose tissue. In skeletal muscle mitochondria, endogenous protein was undetectable. Skeletal muscle mitochondria from homozygous mice show decreased state 4 respiration. Further, skeletal muscle, but not liver, mitochondria produce more superoxide anions and reactive oxygen species both in vitro (lucigenin-derived chemiluminescence) and in vivo (aconitase activity). Skeletal muscle ATP synthesis under fasting conditions is approximately 4-fold greater in mutant mice. This mouse may be useful in studies of energy metabolism, thermogenesis, aerobic respiration (including mitochondrial respiration coupling), and age-related progressive deterioration of fatty acid homeostasis. | ||
| 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. | ||
| 005939 | B6;129S6-Insig1tm1Mbjg Insig2tm1Mbjg/J | Cryopreserved - Ready for recovery |
| Mice homozygous for both targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This double mutant has normal expression of Insig1 and no Insig2 gene expression or protein in liver. As the Insig1 mutant locus contains a loxP, frt-flanked exon 1, Cre-mediated deletion of exon 1 (encoding amino acids 1-113) terminates gene function. The resulting double homozygous "knockout" mice die in utero some time after embryonic day 18.5. These mice may be useful in studies of cholesterol synthesis and feedback suppression, sterol regulatory element-binding protein (SREBP) processing pathways, liver metabolism and storage functions, and may have use in insulin-related topics such as diabetes and endocrine/exocrine function. | ||
| 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. | ||
| 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. | ||
| 009685 | B6N.129S1(Cg)-Tnkstm1.1Yjc/J | Cryopreserved - Ready for recovery |
| Homozygous (TANK1-/-) mice are viable and fertile with no reported developmental or gross physical abnormalities. As exon 1 is deleted from the targeted allele, no full length protein (TANK1) is detected in thymus, testis or spleen tissues. Because the deletion does not encompass the potential alternative promoter between exons 4-5, an alternative transcript and subsequent low molecular weight protein (TANK1a) is expressed in testis (but not in other assayed tissues). These TANK1-mutant mice may be useful for studying the post-translational modification of proteins associated with cell cycle, mitosis, telomere length maintenance/aging, DNA replication/repair, cellular senescence, apoptosis, tumorigenesis, vesicle trafficking, and insulin responses. These TANK1-mutant mice may also be used along with TANK2-mutant mice (Stock No. 006200). | ||
| 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 | ||
| 008440 | C.129S2(B6)-Seletm1Hyn Selltm1Hyn Selptm1Hyn/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Sele, Sell and Selp genes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities at birth. As mice mature, however, they become susceptible to mucocutaneous infections that eventually lead to death. No Sele, Sell or Selp gene products (mRNA or protein) are detected. Leukocytes from these mice exhibit a deficiency in the ability to interact with, and roll along, the venular wall endothelium. This deficiency in the crucial first step of leukocyte recruitment to surrounding tissues in response to infection or injury contributes to an elevated leukocyte count in the peripheral blood. Delays in neutrophil and eosinophil recruitment to the peritoneum in response to thioglycollate and ragweed allergen, respectively, have been observed, specifically. These mice are suitable for use in research applications studying leukocyte homeostasis, infectious diseases and inflam ..... For more information please see the full phenotype on the strain data sheet | ||
| 008438 | C.129S2(B6)-Seletm1Hyn Selptm1Hyn/J | Cryopreserved - Ready for recovery |
| Mice homozygous for both the Seletm1Hyn Selptm1Hyn mutations are viable and fertile. They are characterized by leukocytosis, spontaneous bacterial infections, dermatitis and defective leukocyte recruitment in many models of inflammation. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 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 | ||
| 006781 | C57BL/6-Tg(Ckm-DGAT2)10Far/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this MCK-DGAT2 transgene are viable and fertile. Under direction of the mouse muscle creatine kinase (MCK) promoter, these mice overexpress human acyl CoA:diacylglycerol acyltransferase 2 (DGAT2) in striated skeletal muscles, specifically glycolytic (rather than oxidative) muscle. DGAT2 overexpression leads to increased lipid deposition (triacylglycerol, ceramide, and fatty acyl CoA) in glycolytic muscle. This lipid accumulation leads to impaired insulin signaling (insulin resistance), glucose uptake, and glucose tolerance in this tissue, as well as whole-body glucose intolerance. These MCK-DGAT2 transgenic mice may be useful in studying lipid accumulation in skeletal muscle, insulin and glucose metabolism, obesity, and type 2 diabetes. Of note, these mice may also be useful in conjunction with Liv-DGAT2-low transgenic mice (Stock No. 007744) which exhibit DGAT2 overexpression directed to hepatic tissue. | ||
| 008231 | C57BL/6-Tg(Ckm-Ppargc1a)31Brsp/J | Cryopreserved - Ready for recovery |
| These transgenic mice express mouse peroxisome proliferative activated receptor, gamma, coactivator 1 alpha under the direction of the mouse muscle creatine kinase promoter. Transgene expression is specific to skeletal muscle. The increased levels of the transgene product induces expression of energy and mitochondrial oxidative metabolism genes such as cytochrome c oxidase II and IV. Muscle fibers from transgenic mice exhibit a more type II oxidative phenotype than wildtype mice. Isolated extensor digitorum longus muscle from transgenic mice exhibit increased fatigue resistance when compared to wildtype. Muscle fiber diameter loss in response to denervation and fasting is less severe in transgenic animals when compared to controls. Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of muscle physiology and disease, exercise and oxidative capacity, ..... For more information please see the full phenotype on the strain data sheet | ||
| 006699 | C57BL/6J-Pcsk1N222D/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this ENU-induced "Pc1N222D" mutation are viable and fertile, although the donating investigator reports that homozygous breeders have diminished reproductive performance. Unlike mice homozygous for the traditional knockout allele, Pc1N222D homozygotes are not runted. Homozygous mice exhibit obesity, abnormal proinsulin processing and multiple endocrinological defects. Increased energy intake and a more efficient metabolism contribute to the obesity. Defective proinsulin processing leads to glucose intolerance, but neither insulin resistance nor diabetes develop despite obesity. Obesity is associated with impaired autocatalytic and neuropeptide processing. These mutant mice are a model of human PC1 deficiency, and may be useful in studying obesity, fat metabolism, propeptide processing, and neuroendocrinology. | ||
| 007857 | C57BL/6J-Tg(Eno2-YFP/Cox8a)YRwb/J | Cryopreserved - Ready for recovery |
| These transgenic mice express Yellow Fluorescent Protein (YFP) under the control of the neuron specific rat enolase 2, gamma, Eno2, promoter. YFP is specifically localized to the mitochondria by a mouse cytochrome c oxidase, subunit VIIIa, targeting signal fused to the N-terminus. Fluorescence is detected in many neuronal populations. The donating investigator reports that fluorescence is detected in subcortical structures including the thalamus, basal ganglia, and caudate/putamen; interneurons of the cortex and hippocampus; a subset of retinal ganglion cells; cerebellum mossy fiber rosette terminals of the granule cell layer and spinal cord preganglionic autonomic neurons. It is not known if homozygotes are viable. This mutant mouse strain may be useful in studies of mitochondrial transport and neuronal metabolism. | ||
| 008081 | CBy.129(B6)-Sirt1tm1Ygu/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted allele (SirT1co/co) are viable and fertile with a loxP-flanked neomycin cassette just upstream of, and a third loxP site just downstream of exon 4 of the targeted gene. The floxed mutation does not affect the protein expression of the targeted gene in MEF's or mammary tissue from homozygotes. When bred to mice that express Cre recombinase, the resulting offspring have exon 4 (encoding a conserved Sir2 motif) deleted in the cre-expressing tissue(s) (the donating investigator reports that they observe only one recombination event; complete removal of the neomycin cassette and exon 4, leaving a single loxp site remaining). These SirT1co/co mice may be useful in generating conditional mutations for studying the role of estrogen, insulin growth factor-1 (IGF-1), and transcription factors (including NF-kappaB) in mammary gland development, breast cancer, apoptosis, and metabolic diseases.
In an att ..... | ||
| 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 | ||
| 008784 | FVB-Tg(Lactb)74.2Lus/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the mouse Lactb (lactamase, beta) transgene are viable, fertile, normal in size and do not display any gross behavioral abnormalities. The transgene encompasses the entire mouse structural gene and its regulatory sequences. Transgenic mice have a higher fat-mass-to-lean-mass (FMLM) ratio compared to wild-type littermates when fed a 6% fat diet. Over time the FMLM ratio difference between transgenic and wild-type animals increases. This mutant mouse strain may be useful in studies of metabolic syndrome and obesity. | ||
| 012662 | FVB-Tg(Ttr-Igf1)1Sykr/J | Cryopreserved - Ready for recovery |
| These "HIT" transgenic mice overexpress rat IGF1 specifically in the liver, with normal tissue IGF-I but have increased serum IGF-I levels. Mice homozygous 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 there is no difference between the phenotype exhibited by homozygotes compared to hemizygotes. | ||
| 012385 | FVB-Tg(tetO-Ppargc1b)7Dpk/J | Cryopreserved - Ready for recovery |
| These transgenic mice express Ppargc1b (peroxisome proliferative activated receptor, gamma, coactivator 1 beta) 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 Ppargc1b expression may be regulated with the tetracycline analog doxycycline (dox) in the double mutant offspring. This "high expressor" strain may be useful in studies further characterizing the signaling role of the transgene as it pertains to physiology and disease, particularly mitochondrial function. | ||
| 012563 | FVB.129(Cg)-Slc9a3tm1Ges/J | Cryopreserved - Ready for recovery |
| These mice harbor a targeted mutation of the Na+/H+ exchanger isoform 3 locus (Nhe3 or Slc9a3) that abolishes endogenous gene expression. While no full-length mRNA is detected in kidney or intestine of homozygous mice, a truncated mutant mRNA lacking codons 320-831 (encoding sequences required for Na+/H+ exchange) is observed but expected to impart no dominant negative effects. When maintained as congenic on the FVB/N genetic background, homozygous mice exhibit a high mortality rate beginning just after weaning, with ~30% surviving to adulthood. Homozygous females are fertile, but homozygous males are infertile.
Homozygous (Nhe3-null) mice lack Na+/H+ exchanger isoform 3 function, and exhibit impaired intestinal absorption; resulting in severe diarrhea, altered salt and water homeostasis, and increased luminal fluid throughout the intestinal tract. Nhe3-null mice have increased PCNA-positive cells in the cryp ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 007580 | STOCK Cyp1a2/Cyp1a1tm2Dwn Tg(CYP1A1,CYP1A2)1Dwn/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Cyp1a2/Cyp1a1(-) targeted allele and carrying the hCYP1A1_1A2 transgene are viable and fertile with normal lifespan. As the Cyp1a2/Cyp1a1(-) targeted allele lacks the coding regions of both Cyp1a1 and Cyp1a2 genes, no expression of either gene transcript or protein is observed in liver or small intestine by quantitative RT-PCR or Western blot, respectively. Transgene expression of the orthologous human genes is observed in the same tissues. While oral benzo[alpha]pyrene (BaP) treatment of Cyp1a2/Cyp1a1(-/-) mutant mice leads to BaP-induced immunosuppression and sickness, the presence of the human CYP1A orthologs in these mice minimizes/prevents such toxicity. These humanized hCYP1A1_1A2_Cyp1a2/Cyp1a1(-/-) mice may useful in drug or carcinogen metabolism research; specifically as a model for human risk assessment studies involving drug or environmental toxicants that may be substrates for cytochrome P450 family mem ..... 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 | ||
| 008598 | STOCK Galptm1Stei/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis. Homozygotes are indistinguishable from wildtype when maintained on ad libitum diet. After fasting, male homozygotes consume less food than wildtype controls. When fed a high fat diet homozygotes gain less weight than wildtype controls. This mutant mouse strain may be useful in studies of energy homeostasis, nutrition and obesity. | ||
| 005740 | STOCK Ppiftm1.1Mmos/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Brain architecture and cerebrovasculature are normal. No gene product (protein) is detected by immunoblot analysis of mitochondria isolated from liver tissue of mutant mice. Mitochondria from mutant mice have an increased capacity to retain calcium and fail to swell/rupture in response to CaCl2, suggesting abnormal permeability transition pore (PTP) function. Mouse embryonic fibroblasts (MEFs) derived from mutant mice are less susceptible to oxidative stress induced in vitro by exposure to hydrogen peroxide than MEFs derived from wildtype mice. In a model of ischemic brain injury employing a middle cerebral artery occlusion protocol, mutant mice exhibited a reduced infarct volume (37% in heterozygotes, and 62% in homozygotes) when compared to wildtype mice. This mutant mouse strain may be useful in studies investigat ..... For more information please see the full phenotype on the strain data sheet | ||
| 005737 | STOCK Ppiftm1Mmos/J | Cryopreserved - Ready for recovery |
| In this strain loxP sites flank 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. Cre-mediated recombination results in the deletion of the loxP-flanked region. This strain represents an effective tool for generating tissue-specific targeted mutants useful in studies examining the consequences of disrupting Ppif-dependent pathways. | ||
| 007570 | STOCK Sim1tm1.2Az/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this "Sim1-floxed exon 1" (2-loxP) conditional allele are viable and fertile, with loxP sites flanking the translation start site and the first 17 amino acids of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (coding for the basic domain of SIM1) deleted in the cre-expressing tissue(s). These "Sim1-floxed exon 1" (2-loxP) mice may be useful in generating conditional mutations for studying basic helix-loop-helix-Per-ARNT-Sim (bHLH-PAS) transcription factors, central nervous system development, early-onset/hyperphagic obesity, and regulation of appetite and energy balance. | ||
| 007577 | STOCK Tg(Gt(ROSA)26Sor-BCHE*G117H)837Loc/J | Cryopreserved - Ready for recovery |
| Transgenic "G117H BChE" mice are viable and fertile. These mice express a mutant form of human butyrylcholinesterase (BCHE or BChE), harboring a single amino acid change at codon 117 (His for Gly), under the control of the ROSA26 promoter. This mutation has the unusual ability to hydrolyze organophosphorus toxicants (OP), as well as acetylcholine and is resistant to inhibition by OP. All tested tissues show G117H BChE enzymatic activity. In the founder mice and immediate offspring, plasma concentrations of the mutant protein are approximately 25% of endogenous wildtype mouse BChe. No reported abnormalities result from BChE overexpression in homozygous mutant mice. Transgenic mice injected with the OP echothiophate are protected from the severe toxicity and lethality observed in wildtype controls. This is the first transgenic mouse strain that expresses human BChE as well as the first mammal with hereditary OP resistance. These G117H BChE transgenic mice may be useful for biodefe ..... For more information please see the full phenotype on the strain data sheet | ||
| 006395 | STOCK Tg(Sim1-cre)1Lowl/J | Cryopreserved - Ready for recovery |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgene expression is observed in all areas that endogenously express Sim1, including paraventricular hypothalamus and other parts of the brain. When these Sim1-Cre mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the flanked sequences in Sim1-expressing tissues (including hypothalamus). As such, Sim1-Cre transgenic mice may be useful in studying body weight homeostasis, obesity, leptin metabolism, or as a reporter strain for Sim1-transcription factor activity. Of note, Sim1-Cre mice may also available on a C57BL/6J congenic background (see Stock No. 006451). | ||
| 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 | ||
| 017476 | 129S-Ucp1tm1Kz/J | Under Development - Now Accepting Orders |
| Mice that are homozygous for this knockout allele are viable and fertile, but exhibit sensitivity to cold temperatures. The Donating Investigator notes that homozygous offspring have increased survival rates to weaning age when maintained at 25°C to 28°C. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brown adipose tissue from homozygotes. When maintained at 20°C, homozygotes are resistant to diet induced obesity with reduced white fat depot weights, exhibit a 0.1-0.3°C higher body temperature, and a slightly lowered respiratory quotient compared to controls. Notably, when maintained at 27°C, homozygous mutant mice are no longer resistant to diet induced obesity and gain weight at a rate similar to wildtype controls. An increase in the number of brown adipocytes in the inguinal fat depots is observed in mutant mice maintained at 20°C, on either diet. Homozygotes have reduced levels of plasma fatty acids, circula ..... 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 | ||
| 016223 | B6(Cg)-Tg(Phox2b-cre)3Jke/J | Under Development - Now Accepting Orders |
| Phox2b-Cre BAC transgenic mice are viable and fertile, with Cre recombinase expression under control of the Phox2b promoter/enhancer regions within the BAC transgene. cre-expressing neurons co-express PHOX2B (as shown by in situ hybridization). Phox2b-Cre BAC transgenic mice from founder line 3 exhibit cre expression directed primarily to the hindbrain; specifically the dorsal motor nucleus of the vagus (DMV) in parasympathetic visceral and branchial motor neurons, nodose sensory ganglia, and nucleus of the solitary tract (NTS) cells. No transgene expression is reported in hypothalamus or spinal cord. Although endogenous Phox2b expression is reported in peripheral ganglia along with the enteric nervous system, no peripheral transgene expression is reported for these Phox2b-Cre BAC transgenic mice. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequences in the offspr ..... For more information please see the full phenotype on the strain data sheet | ||
| 014137 | B6.129S4-Pmchtm1Emf/J | Under Development - Now Accepting Orders |
| Mice that are homozygous for this knockout are viable, fertile, and exhibit a smaller stature and increased locomotor activity when compared to wildtype controls. No gene product (mRNA or protein) is detected by RT-PCR and in situ hybridization analysis of hypothalamus tissue, RT-PCR of pancreatic islets from homozygotes and immunocytochemical analysis of brain tissue from homozygotes.
Homozygotes appear smaller, are leaner than wildtype controls and when placed on a chow diet, display increased basal metabolic rates and locomotor activity.
When fed a high-fat diet, the oxygen consumption ( by 15.7%) and activity levels are further increased and homozygotes do not gain as much weight as controls. The lean phenotype persists in homozygous mice more than 12 months of age. Homozygotes, 12-19 months of age, are more sensitive to insulin, have reduced aging-associated weight and visceral adiposity gain, maintain increased locomotor activity, and are resistant to aging-associated glu ..... 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 | ||
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How to Register Interest
Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Awaiting Transfer
Select the strain name to link to the strain data sheet.
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.
- Receive periodic updates on the status of the colony AWAITING TRANSFER
- Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available
- Provide input affecting speed and quantity of availability
It is VERY IMPORTANT that you register interest in strains Awaiting Transfer. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.
Send questions to our Technical Support team using the Express Technical Support Form.
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