Search Criteria: Research Area is "Research Tools: Diabetes and Obesity Research"
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 004545 | 129S-Npytm1Rpa/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brain or adrenal gland tissue. Beta-galactosidase activity assays and in situ hybridization demonstrate similar expression patterns for the lacZ gene and the endogenous wildtype gene. Spontaneous seizures are exhibited by some mice at age 6 to 8 weeks. Homozygous mice are susceptible to seizures induced by GABA antagonist treatment. Mutant mice have an increased sensitivity to leptin treatment which results in a greater initial reduction of food intake and weight loss when compared to wildtype mice. This mutant mouse strain may be useful in studies related to the role of neuropeptide Y in obesity. | ||
| 007005 | 129S-Scg5tm1Led/J | Repository- Live |
| The following text reflects the phenotype reported by the donating investigator on a "129Sv" genetic background (probably "Taconic Sv129" (129S6/SvEvJ)). While heterozygotes are viable and fertile, mice homozygous for this mutation (7B2-null) die in prepubertal or pubertal ages (5 weeks) with severe cardio-respiratory failure, convulsions, and hypothermia. No transcripts are detected in brain tissue from the targeted gene. 7B2 null mice are unable to make an active form of prohormone convertase 2 (PC2) and have high circulating corticosterone. Homozygotes on the 129S genetic background exhibit Cushing's-like disease pathologies of liver, pancreas, and pituitary; including pituitary-dependent hyperadrenocorticosteronism, severe hypoglycemia, hyperproinsulinemia, adrenal hypertrophy, pituitary hypotrophy, and altered islet cell morphology. 7B2-null mice develop the disease from intermediate lobe ACTH hypersecretion (rather than from pituitary adenomas). Other abnormalities include thinni
..... For more information please see the full phenotype on the strain data sheet | ||
| 001673 | AXB1/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001681 | AXB10/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001683 | AXB12/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001826 | AXB13/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB13/PgnJ and AXB14/PgnJ are considered ?sister strains? being identical throughout much of the genome but differing in large regions of Chromosomes 11, 12, 13, and in small regions of a few other Chromosomes. Because these two strains are "near congenics" a nomenclature change has been made to update AXB14/PgnJ to AXB13a/PgnJ. In general, 'sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a ?near congenic? for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their suscepti
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| 001685 | AXB15/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001687 | AXB19/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB18/Pgn, AXB19/Pgn, and AXB20/Pgn were found to be highly similar in their overall genomes, but with particular Chromosomes differing between them. Two of these "sister" strains were renamed. AXB19/Pgn was designated the primary strain since it has the best traceable history, and therefore its name remained unchanged. AXB18/Pgn was renamed AXB19a/Pgn and AXB20/Pgn was renamed AXB19b/Pgn. In general, the "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalu ..... For more information please see the full phenotype on the strain data sheet | ||
| 001686 | AXB19a/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB18/Pgn, AXB19/Pgn, and AXB20/Pgn were found to be highly similar in their overall genomes, but with particular Chromosomes differing between them. Two of these "sister" strains were renamed. AXB19/Pgn was designated the primary strain since it has the best traceable history, and therefore its name remained unchanged. AXB18/Pgn was renamed AXB19a/Pgn and AXB20/Pgn was renamed AXB19b/Pgn. In general, the "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalu ..... For more information please see the full phenotype on the strain data sheet | ||
| 001688 | AXB19b/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB18/Pgn, AXB19/Pgn, and AXB20/Pgn were found to be highly similar in their overall genomes, but with particular Chromosomes differing between them. Two of these "sister" strains were renamed. AXB19/Pgn was designated the primary strain since it has the best traceable history, and therefore its name remained unchanged. AXB18/Pgn was renamed AXB19a/Pgn and AXB20/Pgn was renamed AXB19b/Pgn. In general, the "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalu ..... For more information please see the full phenotype on the strain data sheet | ||
| 001674 | AXB2/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001690 | AXB23/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001691 | AXB24/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001676 | AXB4/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001677 | AXB5/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001678 | AXB6/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001679 | AXB8/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 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. | ||
| 006201 | B6.129-Scd1tm1Ntam/J | Repository- Live |
| Homozygous mice are viable and fertile. Transcripts from the targeted gene are absent in homozygous liver, eyelid, skin, and white adipose tissues. In addition, the endogenous protein and enzyme activity are absent from homozygous liver tissue. Homozygous mice exhibit cutaneous abnormalities and narrow eye fissure with atrophic sebaceous and meibomian glands. Mutant mice also have reduced body adiposity, increased insulin sensitivity, increased basal and insulin-mediated glucose uptake, and are resistant to diet-induced weight gain. Homozygotes have altered hepatic glycerophospholipid profiles. Homozygous mice are not recommended for breeding as skin lesion severity may prohibit colony success. These mutant mice may be useful in studies of monounsaturated fatty acid synthesis, cholesterol homeostasis, skin disease, obesity, and diabetes. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background differ
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| 006879 | B6.129-Scd2tm1Myz/J | Repository- Live |
| While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die within 24 hours of birth. Brain tissues from homozygous mice show no expression from the targeted gene. Homozygotes exhibit neonatal lethality with 100% penetrance on this genetic background (less penetrant on 129SvEv genetic background) likely due to severe skin permeability barrier abnormalities. Null mice also have abnormal epidermal morphology and abnormal lipid homeostasis in the skin and liver. These mutant mice may be useful in studying monounsaturated fatty acid synthesis, lipid biosynthesis and metabolism, cholesterol homeostasis, and skin disease, as well as obesity and diabetes. | ||
| 007668 | B6.129S4(Cg)-Arntltm1Weit/J | Repository- Live |
| Mice homozygous for this conditional (floxed) allele possess loxP sites flanking exon 8 of the targeted gene and are viable and fertile, with circadian behavioral rhythms indistinguishable from wildtype littermates. When bred to mice that express Cre recombinase, the resulting offspring will have the exon encoding the ARNTL (BMAL1) basic helix-loop-helix (bHLH) domain deleted in the cre-expressing tissue(s). These Bmal1-floxed mutant mice may be useful in generating conditional mutations (whole-mouse or tissue-specific) to study the role of circadian clock/circadian rhythm in physiological and behavioral regulation.
For example, when crossed to a strain expressing Cre recombinase in the retina (see Stock No. 005105), this mutant mouse strain may be useful in studies of the circadian clock of the retina. | ||
| 006503 | B6.129S4-Lpltm1Ijg/J | Repository- Live |
| These mice possess loxP sites on either side of exon 1 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When 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. | ||
| 005897 | B6.129S4-Ppardtm1Rev/J | Repository- Live |
| These mice possess loxP sites on either side of exon 4 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice with a cre recombinase gene under the control of a promoter of interest, exon 4 of the targeted gene is deleted in the tissue of interest, leading to premature termination of the translation product upstream of the DNA binding domain. This strain may be useful in generating tissue-specific mutants of the floxed allele for use in studies including embryo development, adipocyte physiology, fat metabolism and storage, inflammation, and cancer. | ||
| 007682 | B6.129X1-Apobtm1.1Zc/J | Repository- Live |
| 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 | ||
| 006952 | B6.Cg-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. | ||
| 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. | ||
| 006580 | B6.Cg-Ins2Akita Ldlrtm1Her/J | Repository- Live |
| Mice homozygous for the Akita spontaneous mutation die postnatally, typically by 12 weeks of age. Independently, heterozygous Akita mutant mice are a model of insulin dependent diabetes mellitus (IDDM) with severe hyperglycemia (see the datasheet for Stock No. 003548 for additional information). LDLR-null homozygotes have elevated serum cholesterol levels (200-400 mg/dl) which can escalate to very high levels (> 2000 mg/dl) when the mice are fed a high fat diet. LDLR-deficient mice also are predisposed to develop atherosclerosis. These double mutant mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, hypercholesterolemia, and diabetes-related macrovascular complications. | ||
| 006883 | B6.Cg-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. | ||
| 006877 | B6.Cg-Ldlrtm1Her Tg(H2-K-AKR1B1)1Tj/J | Repository- Live |
| 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 | Repository- Live |
| 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 | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of activated spleen lymphocytes. While neither telomere shortening nor chromosomal abnormalities (even across multiple generations) are observed, homozygous mice have significantly decreased body weight. These mutant mice may be useful in studies of both telomerase function and telomerase-independent pathways which affect development and metabolism. | ||
| 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. | ||
| 006872 | B6.Cg-Tg(Ins1-DsRed*T4)32Hara/J | Repository- Live |
| Mice hemizygous for this "MIP-RFP" transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the DsRed.T4 variant of Enhanced Red Fluorescent Protein under the control of mouse insulin 1 promoter. Fluorescence is detected in tissues where insulin I is normally expressed; fluorescent protein expression in pancreatic beta-cells is evident from embryonic day (E)13.5 through adult. Transgenic mice exhibit normal glucose tolerance and pancreatic insulin levels. While the human growth hormone sequence in the transgene is designed to enhance expression of the fluorescent protein and is not expressed in a similarly constructed transgene (see Stock No. 006864), whether or not it is expressed for this strain was not characterized. This mutant mouse strain may be useful in studies of pancreatic development and pancreatic beta islet cell biology. In an a
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| 006864 | B6.Cg-Tg(Ins1-EGFP)1Hara/J | Repository- Live |
| Mice hemizygous for this "MIP-GFP" transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Enhanced Green Fluorescent Protein (EGFP) under the control of the mouse insulin 1 promoter. Fluorescence is detected in tissues where insulin I is normally expressed; fluorescent protein expression in pancreatic beta-cells is evident from embryonic day (E)13.5 through adulthood. The fluorescence expression pattern is similar to the patterns seen in other stocks (see Stock No. 006784 and Stock No. 006866). MIP-GFP transgenic mice exhibit normal glucose tolerance and pancreatic insulin levels. The human growth hormone (hGH) sequence in the transgenic insert enhances expression of the EGFP, but hGH is not expressed. This mutant mouse strain may be useful in studies of diabetes and pancreatic beta islet
..... For more information please see the full phenotype on the strain data sheet | ||
| 003573 | B6.Cg-Tg(Ins2-cre)25Mgn/J | Repository- Live |
| This strain carries the "RIP-Cre" transgene construct (containing a 668 bp fragment of the rat insulin II promoter, Cre recombinase with a nuclear localization sequence, and a 2.1 kb fragment from the human growth hormone gene). Hemizygous mice carrying this transgene are phenotypically normal and overexpresss cre specifically in pancreatic beta cells. This transgene strain is used in combination with mice carrying floxed targeted mutations to create various pancreatic beta cell-specific gene knockouts using the "Cre-lox" system. Results from several different laboratories have shown that this transgenic strain is at least 85% efficient in achieving pancreatic beta cell-specific recombination. It should also be noted that the transgene in this line has been found to be expressed at a low level in the hypothalamus. In some cases this has resulted in a phenotype due to deletion of the floxed allele in this region of the brain. It has also been shown that these transgenic mice may
..... For more information please see the full phenotype on the strain data sheet | ||
| 006475 | B6.FVB(129S4)-Tg(Ckmm-cre)5Khn/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice have the Cre recombinase gene driven by the muscle creatine kinase (MCK or Ckm) promoter. Cre activity is observed in skeletal and cardiac muscle. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in skeletal and cardiac muscle deletion of the flanked genome. | ||
| 006451 | B6.FVB(129X1)-Tg(Sim1-cre)1Lowl/J | Repository- Live |
| 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
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| 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. | ||
| 006410 | B6;129S6-Chattm1(cre)Lowl/J | Repository- Live |
| Homozygous mice maintained at The Jackson Laboratory are viable and fertile. An "IRES-Cre" sequence is inserted downstream of the stop codon such that cre expression is controlled by the endogenous Chat gene promoter. Chat gene expression, however, is unaffected. Cre recombinase activity is reported in all cholinergic neurons. These mice may be useful for "Cre-lox" technology applications in neurobiology, including studies of motor function, learning and memory, Alzheimer's disease, and Down syndrome, and in obesity and diabetes research. | ||
| 006907 | B6;CBA-Tg(APOC3)3707Bres/J | Repository- Live |
| 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. | ||
| 001692 | BXA1/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin.The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001699 | BXA11/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001700 | BXA12/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001701 | BXA13/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001702 | BXA14/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. In 2004 a phenotype of small body size was found to be segregating in this colony after recovery from cryopreservation. It appears that this phenotype is segregating recessively in this strain and is present in the cryopreserved bank stock. The expressed phenotype is small size relative to littermates and mice with this diminished body size often catch up to their littermantes in body size af ..... For more information please see the full phenotype on the strain data sheet | ||
| 001703 | BXA16/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001693 | BXA2/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001710 | BXA24/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001711 | BXA25/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001999 | BXA26/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001694 | BXA4/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001696 | BXA7/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001697 | BXA8/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. BXA17/Pgn was found to be a replica of BXA8/Pgn. BXA17/Pgn was lost in 1989 or 1990. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 006781 | C57BL/6-Tg(Ckm-DGAT2)10Far/J | Repository- Live |
| 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. | ||
| 005432 | C57BL/6-Tg(Ins2-OVA)307Wehi/WehiJ | Repository- Live |
| Immunohistochemistry does not detect ovalbumin in the islet beta cells of the pancreas. The double transgenic resulting from a cross of this transgenic stock with C57BL/6-Tg(Tcra Tcrb)1100MjbJ (OT-1) mice have early onset of spontaneous diabetes with islet infiltration; implying that the beta cells express OVA. One of 60 irradiated Tg(Ins2-OV)307 mice receiving a 1:4 mixture (OT-1 transgenic mice:C57BL/6-Thy1.1 congenic) of bone marrow become diabetic when followed for 10 weeks post transfer. Histolocigal evaluation indicates 22% of the islets are mildly infiltrated 15-21 weeks post transfer. This stock only show antigen presentation in the draining lymph node when the pancreatic islets have been damaged. This ovalbumin expressing model is a tool for assessing antigen ignorance and is used in tumor immunity studies and tissue damage studies. | ||
| 005433 | C57BL/6-Tg(Ins2-OVA)59Wehi/WehiJ | Repository- Live |
| Transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The pancreatic islets exhibit weak ovalbumin- (OV-) specific immunohistologic staining and OV is detectable in the islets by Western blot analysis. These mice develop diabetes following adoptive transfer of activated, but not naive, CD8+ T lymphocytes from mice bearing Tg(TcraTcrb)1100Mjb (OT-1). Both CD8+ T-cells and CD4+ T cells from these transgenic animals are tolerant to ovalbumin. This model provides a tool for assessing the requirements of peripheral T-cell deletion. | ||
| 005431 | C57BL/6-Tg(Ins2-TFRC/OVA)296Wehi/WehiJ | Repository- Live |
| Ins2-TFRC/OVA (commonly referred to as RIP-mOVA) line 296-1B hemizygote transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Immunohistochemical analysis detects strong expression in pancreatic beta cells and kidney proximal tubular cells and weak expression in testes. When C57BL/6-Tg(Ins2-TFRC/OVA)296Wehi/WehiJ is mated to C57BL/6-Tg(TcraTcrb)1100Mjb/J (commonly referred to as OT-1 and recognizes OVA specific T-cells, Stock No. 003831) thymic deletion of OT-1 cells is observed in double transgenic mice, suggesting very low levels of thymic expression. OVA specific CD-8+ T-cells activated by cross presentation infiltrate the pancreas causing beta cell destruction resulting in diabetes. However, these cells do not infiltrate the kidney. Proliferating OT-1 T-cells appeared specifically in the lymph nodes draining the pancreas (PLN's) and kidney (RLN's) on day
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| 006699 | C57BL/6J-Pcsk1N222D/J | Repository- Live |
| 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. | ||
| 005307 | CBy.Cg-Thy1a Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ | Repository- Live |
| Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities.The TCR expressed from this transgene is specific for influenza virus A/PR/8 hemagglutinin (HA) in the context of the MHC class I moleculeH2-Kd. Both thymic and peripheral T-cell populations are skewed toward CD8+ cells. The majority of thymocytes and virtually all CD8+ T cells in lymph nodes express the transgenic TCR beta chain. About 40% of peripheral blood CD8+ T cells react with the HA peptide presented by H2-Kd. When mated with Tg(Ins2-HA)165Bri, double transgenic neonates have similar levels of V-beta 8 and total number of thymocytes as Tg(TcraCl4,TcrbCl4) mice however the double transgenics become spontaneously diabetic after birth and die within 10 days. This mouse is further modified with the Thy1.1 allele, rather than the alternate allele present in C57BL/10, DBA/2, and BALB/c mice. T
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| 007683 | CByJ.129X1(Cg)-Apobtm1.1Zc/J | Repository- Live |
| 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 | ||
| 006405 | FVB-Tg(Ckmm-cre)5Khn/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice have the Cre recombinase gene driven by the muscle creatine kinase (MCK or Ckm) promoter. Cre activity is observed in skeletal and cardiac muscle. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in skeletal and cardiac muscle deletion of the flanked genome. | ||
| 006364 | FVB-Tg(Nr5a1-cre)2Lowl/J | Repository- Live |
| Mice hemizygous for the "Sf1-Cre" transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgene expression mimics the mRNA pattern of Nr5a1; with Cre activity observed in steroidogenic factor-1 (SF1)-positive neurons in the ventromedial hypothalamic nucleus (VMH) as well as pituitary, gonad, and adrenal tissue. Expression is also noted in the cerebral cortex and in a few scattered cells in the caudal brainstem of mice derived from line 2 (but not line 7). If bred with mice containing a loxP-flanked sequence of interest, tissue-specific deletion of that genome results in the offspring. Specifically, these cre-expressing mice may be useful in studies involving the hypothalamus, such as body weight homeostasis, obesity, leptin metabolism, or as a reporter strain for SF1-transcription factor activity. | ||
| 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. | ||
| 006654 | FVB.BKS(D)-Leprdb/ChuaJ | Repository- Live |
| The phenotype of this congenic "FVB-db" strain varies from that previously published on other genetic backgrounds. Specifically, obese FVB-db mice show long-term hyperglycemia that is primarily due to severe insulin resistance. The hyperglycemia in the fed state persists despite escalating insulin secretion and a massive increase in pancreatic beta-cell mass. Obese FVB-db mice show evidence of mesangial matrix expansion, a hallmark of diabetic nephropathy. Whereas the original C57BLKS/J-db mice are hyperglycemic due to the development of hypoinsulinemia and loss of beta-cell mass, the hyperglycemia of FVB-db appears to be due to severe insulin resistance with continual increases in insulin secretory capacity from beta-cell mass expansion. As the phenotype varies by genetic background, these mutant mice, along with db mutants on other genetic backgrounds (see Stock No. 000642, For more information please see the full phenotype on the strain data sheet | ||
| 004947 | NOD.129S2(B6)-Casp1tm1Sesh/LtJ | Repository- Live |
| Casp1tm1Sesh homozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. There is no detectable expression of Casp1 in spleen by northern blot analysis or by RT-PCR of peritoneal exudate cells, brain, lung, heart, liver, adrenal gland, kidney, testis, and thymus (Li et al, 1995). Cultured LPS stimulated bone marrow derived macrophages from homozygous NOD.129S2(B6)- Casp1tm1Sesh /LtJ animals secrete 4-fold less IL1 beta, 30% less IL1 alpha, and IL18 is undetectable when compared with hemizygous and wild-type controls. Diabetes frequency of Casp1tm1Sesh deficient animals is equivalent to NOD/Lt, heterozygote and wild-type controls. Weanling Casp1tm1Sesh homozygous animals injected with Complete Freund's adjuvant and young pre-diabetic males treated with multiple low dose streptozotocin behave similarly to control (wild type, heterozygote, or NOD/Lt) a
..... For more information please see the full phenotype on the strain data sheet | ||
| 005868 | NOD.Cg-Tg(TcraTcrbNY8.3)1Pesa/DvsJ | Repository- Live |
| NOD.Cg-Tg(TcraTcrbNY8.3)1Pesa/DvsJ, commonly called 8.3-NOD, express rearranged Tcra and Tcrb transgenes derived from the pancreatic beta cell-cytotoxic CD8+ T cell clone NY8.3. CD4-CD8+ thymocytes and lymph derived T cells are skewed toward VB8.1/2+ expression when compared to wild type controls. Although, transgenic mice exhibit dramatically accelerated diabetes, the cumulative diabetes incidence and kinetics of disease are remarkably similar to their wild type cohorts. Insulitis scores of 3 week old transgene+ mice was significantly lower, while insulitis scores of 6 week olds were significantly more severe than in wild types controls, Verdaguer J et al, 1997, J. Exp Med 186, 1663-1676.
Transgenic animals bearing both TCR transgenes offer a source of CTL precursors useful in examining the diversity of beta cell peptides recognized by the autoreactive CD8+ T lymphocytes contributing to th ..... For more information please see the full phenotype on the strain data sheet | ||
| 005328 | NOD/ShiLt-Tg(Cd4-DsRed)4Lt/J | Repository- Live |
| The donating investigator reports that hemizygous transgenic mice are viable, fertile and normal in size. FACS analysis of splenic lymphocytes shows transgenic expression in 36% of CD4+ and 6% of CD8+ T-cells and minimal expression (background levels) in B cells and macrophages. When compared to wild-type NOD/ShiLt mice, the diabetes incidence is lower (50%) and diabetes onset is delayed. Adoptive transfer experiments with splenocytes and bone marrow from hemizygous CD4-DsRed transgenic mice does not confer diabetes protection on NOD inbred mice, suggesting that the agent of protection is not dependent on hematopoietic cells. No homozygous transgenic mice have been identified in litters produced from hemizygote intercrosses, suggesting that homozygotes are not viable. This strain is useful for tracking resting and activated T cells in vivo and in vitro. | ||
| 005334 | NOD/ShiLt-Tg(Cd4-EGFP)1Lt/J | Repository- Live |
| Homozygous transgenic mice are viable, fertile, normal in size and do not exhibit any gross physical or behavioral abnormalities. The donating investigator reports uniform transgenic expression, about 81% of inactivated or resting CD8+ T cells and CD4+ T cells, with minimal expression in B cells (2.3%) and macrophages (1.5%). Over a three day period following activation in vitro with anti-CD3, gating on live populations of CD4+ and CD8+ subsets show continued GFP expression in both. However, there is a greater diminution of GFP fluorescence in the activated CD8+ T population by day three in vitro. Diabetes onset is similar to wild-type NOD/ShiLt mice. These CD4-GFP transgenic mice may be useful for fluorescent monitoring of T cells both in vivo and in vitro. | ||
| 004339 | STOCK Bdnftm3Jae/J | Repository- Live |
| These mice possess loxP sites on either side of exon 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 bred to a strain expressing Cre recombinase under the control of a tetracycline-responsive promoter element (see Stock No. 006224, 006234, 006244) and a strain expressing a tetracycline-controlled activator protein in brain tissues (see Stock No. 003763), this mutant mouse strain may be useful in studies of hippocampal-dependent learning and long-term potentiation. When bred to a strain expressing Cre recombinase in neuronal cells (see Stock No. 003966 for example), this
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| 007603 | STOCK Isl2tm1Arbr/J | Repository- Live |
| Mice homozygous for the Isl2DTA targeted mutation are viable and fertile. These mice have the diphtheria toxin (DTA) gene inserted into the Isl2 (insulin related protein 2 (islet 2)) locus. Expression of DTA in Isl2-expressing cells is blocked by an upstream loxP-flanked STOP sequence. When bred to Cre recombinase-expressing mice, the STOP sequence is deleted in tissues where Cre is present, permitting DTA expression and subsequent cell ablation.
When bred to a strain expressing Cre recombinase in motor neurons (see Stock No. 006600 for example), this mutant mouse strain may be useful in neurodevelopmental studies. These Isl2DTA mutant mice are available on a STOCK genetic background (Stock No. 007603), as well as a C57BL/6J-backcrossed background (Stock No. 007942
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| 007570 | STOCK Sim1tm1.2Az/J | Repository- Live |
| 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. | ||
| 006866 | STOCK Tg(Ins1-DsRed*T4)32Hara/J | Repository- Live |
| Mice hemizygous for this "MIP-RFP" transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the DsRed.T4 variant of Enhanced Red Fluorescent Protein under the control of mouse insulin I promoter (MIP). Fluorescence is detected in tissues where insulin I is normally expressed; fluorescent protein expression in pancreatic beta-cells is evident from embryonic day (E)13.5 through adulthood. Transgenic mice exhibit normal glucose tolerance and pancreatic insulin levels. The human growth hormone sequence in the transgene is designed to enhance expression of the fluorescent protein. Although the expression of this sequence in this strain has not been characterized, the sequence is not expressed in a similarly constructed transgenic strain (see Stock No. 006864). This mutant mouse strain may be useful in studies of pancreatic development and pancreatic b
..... For more information please see the full phenotype on the strain data sheet | ||
| 006784 | STOCK Tg(Ins1-ECFP)24Hara/J | Repository- Live |
| Mice hemizygous for this "MIP-CFP" transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the Cerulean variant of Enhanced Cyan Fluorescent Protein under the control of mouse insulin 1 promoter (MIP). Fluorescence is detected in tissues where insulin I is normally expressed; fluorescent protein expression in pancreatic beta-cells is evident from embryonic day (E)13.5 through adult. The fluorescence expression pattern observed in this strain is similar to the patterns seen in other stocks that express fluorescent proteins from the MIP promoter (see Stock No. 006864 and Stock No. 006866). The human growth hormone sequence in the transgene is designed to enhance expression of the fluorescent protein. Although the expression of this sequence in this strain has not been characterized, the seque
..... For more information please see the full phenotype on the strain data sheet | ||
| 006395 | STOCK Tg(Sim1-cre)1Lowl/J | Repository- Live |
| 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 | Repository- Live |
| 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 | ||
| 001684 | AXB13a/PgnJ | Repository-Cryopreserved |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB13/PgnJ and AXB14/PgnJ are considered “sister strains” being identical throughout much of the genome but differing in large regions of Chromosomes 11, 12, 13, and in small regions of a few other Chromosomes. Because these two strains are “near congenics” a nomenclature change has been made to update AXB14/PgnJ to AXB13a/PgnJ. In general, “sister” strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a “near congenic” for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their sus ..... For more information please see the full phenotype on the strain data sheet | ||
| 005308 | B10.Cg-H2d Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ | Repository-Cryopreserved |
| Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities.The TCR expressed from this transgene is specific for influenza virus A/PR/8 hemagglutinin (HA) in the context of the MHC class I molecule H2-Kd. Both thymic and peripheral T-cell populations are skewed toward CD8+ cells. The majority of thymocytes and virtually all CD8+ T cells in lymph nodes express the transgenic TCR beta chain. About 40% of peripheral blood CD8+ T cells react with the HA peptide presented by H2-Kd. When mated with Tg(Ins2-HA)165Bri, double transgenic neonates have similar levels of V-beta 8 and total number of thymocytes as Tg(TcraCl4,TcrbCl4) mice however the double transgenics become spontaneously diabetic after birth and die within 10 days. This transgenic model is useful in the study of T-cell activation, cross presentation of antigens, process of thymic selection, peripheral tolerance and
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| 005534 | B10.Cg-H2d Tg(Ins2-HA)165Bri/ShrmJ | Repository-Cryopreserved |
| Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. Mice homozygote for the transgene have silver grey fur color. Hemizygous and wildtype mice are black. Immunohistochemistry reveals pancreatic islet cell expression of the transgene and no expression in the spleen, kidney or thymus. Isolated islets stain normally for insulin and are morphologically indistinguishable from control islets. Additional functional studies found no expression in bone marrow. Histology revealed no insulitis and the single transgenic mice do not become diabetic. T-cell proliferation assays, Cytotoxic Lymphocyte (CTL) assays, and adoptive transfer studies performed using transgenic mice indicate significantly reduced class 1 and class II T-cell responses compared to controls. Hemagglutination inhibition assays of sera from HA primed transgenic mice indicate antibody titers slightly lower but nearly equivalent to HA primed control m
..... For more information please see the full phenotype on the strain data sheet | ||
| 003870 | B6.129-Plintm1Chan/J | Repository-Cryopreserved |
| 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. | ||
| 005711 | B6.129P2-Prkcqtm1Litt/J | Repository-Cryopreserved |
| Mice homozygous for the targeted allele are viable, fertile, normal in size, and do not display any behavioral abnormalities. No endogenous or truncated protein product was detected in thymocytes or T cells. Mature T lymphocytes from null mice have blunted proliferative responses with decreased levels of both IL-2 and IL-2 receptor, and defective T cell receptor-initiated IkappaB-degradation/NF-kappaB activation. Homozygous mice exhibit severely impaired Th2, but normal Th1, immune responses as well as abnormal insulin signaling and glucose transport. Mutant mice also have defective regulatory T cell development (very low CD25 expression). This mutant may be suitable for use in studies related to T cell proliferation/signal transduction/immunodeficiency, Th2-mediated disease, asthma, and diabetes. | ||
| 006142 | B6.129S4-Ppargtm1Rev/J | Repository-Cryopreserved |
| 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. | ||
| 005500 | B6.C-Tg(Ins2-GP)34-20Olds/MvhJ | Repository-Cryopreserved |
| Transgenic mice were created with the Lymphocytic choriomeningitis virus (LCMV) glycoprotein(GP) or nucleoprotein (NP) under the control of the rat insulin promoter. Ins2-GP expression was determined only in the pancreas by RT-PCR (von Herrath et al 1994). Tg(Ins2-GP)34-20Olds untreated mice rarely develop insulin-dependent diabetes mellitus (IDDM). When challenged with LCMV they develop IDDM. The B6.C -Tg(Ins2-GP)34-20Olds mice (H2b) exhibit a rapid (10-14 days) onset of IDDM compared to C.B6-Tg(Ins2-NP)25-3Olds mice (H2d) (10-21 days) or B6.C -Tg(Ins2-NP)25-3Olds mice (H2b) (30-120 days) (Oldstone et al.,1991; von Herrath et al.,1994). Thymic expression of nucleoprotein has been shown to be responsible for this delayed onset of IDDM. Thymi from newborn B6.C -Tg(Ins2-GP)34-20Olds transplanted into nude hosts produce a primary CTL response when challenged with LCMV. CD8 T cells are required for IDDM development in both glycoprotein
..... For more information please see the full phenotype on the strain data sheet | ||
| 005715 | B6.Cg H2g7-Tg(Ins2-CD80)3B7Flv/LwnJ | Repository-Cryopreserved |
| Transgenic mice are characterized by pancreatic beta cells that express a rat insulin promoter (Ins2) regulated transgene encoding the human CD80 T cell co-stimulatory molecule. These mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Better than 70% of the B6.H2g7 transgenic mice become diabetic by 30 weeks of age compared the control B6.H2g7 which does not develop insulitis or diabetes. Spleens of diabetic B6.H2g7 transgenic mice used in adoptive transfer experiments transfer diabetes to NOD.scid/RIP-B7.1 and irradiated non-diabetic B6.Cg H2g7-Tg(Ins2-CD80)3B7Flv/LwnJ mice, yet failed to transfer disease to NOD.scid, B6.scid, CB17.scid, or irradiated B6/RIP-B7.1. B6.Cg H2g7-Tg(Ins2-CD80)3B7Flv/LwnJ provides a tool for studying mechanisms of loss of tolerance in potentially diabetogenic CD8 T-cells. | ||
| 004826 | B6.Cg-Tg(Ins2-NP)25-3Olds/MhvJ | Repository-Cryopreserved |
| Transgenic mice were created with the Lymphocytic choriomeningitis virus (LCMV) nucleoprotein(NP) or glycoprotein(GP) under the control of the rat insulin promoter. Northern blot analysis identifies a 3kb band expected of the transgene and SV40 processing signals in the pancreas (Oldstone et al., 1991). Ins2-NP expression was determined in the pancreas and thymus by RT-PCR (von Herrath et al 1994). Tg(Ins2-NP)25-3Olds untreated mice rarely develop insulin-dependent diabetes mellitus (IDDM). When challenged with LCMV they develop IDDM. The B6.Cg -Tg(Ins2-NP)25-3Olds mice (H2b) exhibit a slower (30-120 days) onset of IDDM than the C.Cg-Tg(Ins2-NP)25-3Olds mice (H2d) (10-21 days) or the B6.Cg -Tg(Ins2-GP) 34-20Olds mice (H2b) (10-14 days) (Oldstone et al.,1991, Homann et al.,1999). Thymic expression of nucleoprotein has been shown to be responsible for this delayed onset of IDDM. Thymi from newborn B6.Cg-Tg(Ins2-NP)25-3Olds transplante
..... For more information please see the full phenotype on the strain data sheet | ||
| 005713 | C.Cg-Tg(Ins2-CD80)3B7Flv/LwnJ | Repository-Cryopreserved |
| Transgenic mice are characterized by pancreatic beta cells that express a rat insulin promoter (Ins2) regulated transgene encoding the human CD80 T cell co-stimulatory molecule. These mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Approximately 10% of the BALB transgenic mice become diabetic by 30 weeks of age compared the control BALBs which are diabetes resistant. Spleens of diabetic BALB transgenic mice used in adoptive transfer experiments do not transfer diabetes to NOD.scid/RIP-B7.1. C.Cg-Tg(Ins2-CD80)3B7Flv/FswJ provides a tool for studying mechanisms for loss of tolerance in potentially diabetogenic CD8 T-cells. | ||
| 005533 | C.Cg-Tg(Ins2-HA)165Bri/ShrmJ | Repository-Cryopreserved |
| Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. Immunohistochemistry reveals pancreatic islet cell expression of the transgene and no expression in the spleen, kidney or thymus. Isolated islets stain normally for insulin and are morphologically indistinguishable from control islets. Additional functional studies found no expression in bone marrow. Histology revealed no insulitis and the single transgenic mice do not become diabetic. T-cell proliferation assays, Cytotoxic Lymphocyte (CTL) assays, and adoptive transfer studies performed using transgenic mice indicate significantly reduced class 1 and class II T-cell responses compared to controls. Hemagglutination inhibition assays of sera from HA primed transgenic mice indicate antibody titers slightly lower but nearly equivalent to HA primed control mice. Antibody titers of all transgenic mice tested were significantly higher than preimmune levels. Wh
..... For more information please see the full phenotype on the strain data sheet | ||
| 004827 | C.Cg-Tg(Ins2-NP)25-3Olds/MvhJ | Repository-Cryopreserved |
| Transgenic mice were created with the Lymphocytic choriomeningitis virus (LCMV) nucleoprotein(NP) or glycoprotein(GP) under the control of the rat insulin promoter. Northern blot analysis identifies a 3kb band expected of the transgene and SV40 processing signals in the pancreas (Oldstone et al., 1991). Ins2-NP expression was determined in the pancreas and thymus by RT-PCR (von Herrath et al 1994). Tg(Ins2-NP)25-3Olds untreated mice rarely develop insulin-dependent diabetes mellitus (IDDM). When challenged with LCMV they develop IDDM. The B6.Cg -Tg(Ins2-NP)25-3Olds mice (H2b) exhibit a slower (30-120 days) onset of IDDM than the C.Cg-Tg(Ins2-NP)25-3Olds mice (H2d) (10-21 days) or the B6.Cg-Tg(Ins2-GP) 34-20Olds mice (H2b) (10-14 days) (Oldstone et al.,1991, Homann et al.,1999). Thymic expression of nucleoprotein has been shown to be responsible for this delayed onset of IDDM. Thymi from newborn B6.Cg-Tg(Ins2-NP)25-3Olds transplanted
..... For more information please see the full phenotype on the strain data sheet | ||
| 006402 | FVB/N-Adrb3tm1Lowl/J | Repository-Cryopreserved |
| 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. | ||
| 005739 | NOD-Tg(H2-Ea-Ins2)1Wehi/WehiJ | Repository-Cryopreserved |
| Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. RT/PCR indicates transgene expression in the spleen and thymus. Blood glucose levels of transgenic and non-transgenic littermates are identical. 90-98 % of the transgenic islets of females and males are insulitis free. Transgenic mice do not develop spontaneous diabetes and are resistant to cyclophosphamide-induced diabetes. Sialitis is not statistically different between transgenic and littermate controls (French MB, Diabetes 1997 46:34-9). Transgenic bone marrow transplanted into 4-week-old irradiated NOD female’s almost entirely prevented diabetes compared to control NOD to irradiated NOD transplants, which have an overall diabetes incidence similar to untreated controls. Thymoma incidence was similar in both irradiated groups.(Steptoe RJ, J Clin Invest 2003 111:1357-63) This model may be helpful for looking at antigen speci ..... For more information please see the full phenotype on the strain data sheet | ||
| 005020 | NOD-Tg(Igh-6/Igh-V281)3Jwt/JwtJ | Repository-Cryopreserved |
| The double transgenic produced by crossing this stock with Stock No. 005018 serves as a control to the double transgenic which results from crossing Stock No. 005018 with Stock No. 005019. | ||
| 005522 | NOD-Tg(Ins2*Y16A)1Ell/GseJ | Repository-Cryopreserved |
| Expression has been reported in the pancreatic islets and thymus of NOD mice carrying the Tg(Ins2*Y16A)1Ell mutation. Approximately 75% of line B female transgenic mice become diabetic in the presence of native insulin genes by 35 weeks of age. NOD female transgenic mice lacking both Ins1 and Ins2 fail to produce insulin autoantibodies, and there is no diabetes or insulitis at 26 weeks of age, but sialitis is present. Donating investigator reports male transgenics lacking both Ins1 and Ins2 develop metabolic diabetes before 10 weeks of age. In contrast, transgenic female mice in the presence of Ins1 and lacking Ins2 develop diabetes in 75% of the animals by 25 weeks of age (Nakayama et al, 2004, 2005). Donating investigator reports line B transgenics have lower expression levels than line F and that male transgenics lacking both Ins1 and Ins2 develop metabolic diabetes before 10 weeks of age. NOD-Tg(Ins2*Y16A)1Ell/GseJ is usefu
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| 005523 | NOD-Tg(Ins2*Y16A)3Ell/GseJ | Repository-Cryopreserved |
| Expression has been reported in the pancreatic islets and thymus of NOD mice carrying the Tg(Ins2*Y16A)3Ell mutation. Approximately 15% of line F female transgenic mice become diabetic in the presence of native insulin genes by 35 weeks of age. NOD female transgenic mice lacking both Ins1 and Ins2 fail to produce insulin autoantibodies, and there is no diabetes or insulitis at 26 weeks of age, but sialitis is present. In contrast, transgenic mice in the presence of Ins1 and lacking Ins2 develop diabetes in 75% of the animals by 25 weeks of age (Nakayama et al, 2004, 2005). NOD-Tg(Ins2*Y16A)3Ell/GseJ is useful to study insulin-reactive autoimmunity. | ||
| 004308 | NOD.ALR-(D17Mit16-H2-D)/LtJ | Repository-Cryopreserved |
| This allelic congenic strain commonly called D.R2, carries a defined segment of Chr 17 that includes the ALR H2gx complex and insulin dependent diabetes susceptibility locus 16, Idd16aALR. At 35 weeks of age diabetes incidence in this NOD.ALR strain is significantly suppressed with 50% of the females and almost 15% the males diabetic as compared to NOD/ShiLt in which 100% of the females and nearly 70% of the males were diabetic. Similar to Stock No. 004309 pancreatic histological examination of pre-diabetic 8-week old males show lower mean insulitis scores than controls. This strain is useful for identifying candidate genes and dissecting the role of Idd16a in autoimmune diabetes. | ||
| 003585 | NOD.B6-(Gpi1-D7Mit346)/LtJ | Repository-Cryopreserved |
| NOD.B6-(Gpi1-D7Mit346)/LtJ mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Congenic NOD Gpib mice become diabetic at a similar rate and onset as NOD/Lt (Chen et al, 2005). Gpi1b in these mice can be used as a marker for transplant studies. | ||
| 005616 | NOD.C-(Ptprc-D1Mit262)/WehiJ | Repository-Cryopreserved |
| This NOD/LtJWehi congenic strain is carrying Chr 1alleles derived from BALB/cWehi including Ptprcb. Diabetes onset and incidence is similar between NOD.C-(Ptprc-D1Mit262)/WehiJ congenic mice (6/8 by 300 days of age) and NOD/LtJWehi (17/24 by 300 days of age). NOD.C-(Ptprc-D1Mit262)/WehiJ bone marrow transplanted into irradiated NOD/LtJWehi recipients yielded incomplete replacement of donor leukocytes at 16 weeks post transfer versus nearly complete replacement of donor leucocytes in C57BL/6Wehi and B6.SJL/Wehi irradiated mice (Steptoe, et al., 2004, Journal of AutoImmunity, Vol 22, p131-138). This strain provides a unique cell surface marker that can be used to track lineage and phenotype of all hematopoietic donor derived or transferred cells making it useful in studies monitoring diabetes progression. | ||
| 004306 | NOD.CBALs-Hc1/LtJ | Repository-Cryopreserved |
| This NOD/Lt congenic strain is carrying Chr 2 alleles derived from CBA/Ls including Hc1. Diabetes onset and incidence is the same as NOD/Lt. | ||
| 005346 | NOD.Cg-Il10tm1Cgn Casp1tm1Sesh/LtJ | Repository-Cryopreserved |
| Mice homozygous for the Il10 and Casp1 targeted mutations are viable and fertile when housed under SPF conditions. NOD/Lt mice deficient for both of these genes develop type 1 diabetes at a rate equivalent to the parental strains. The Il10 targeted mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions. | ||
| 005686 | NOD.Cg-Thy1a Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ | Repository-Cryopreserved |
| Transgenic mice, commonly referred to as NOD.clone-4 TCR, are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. The TCR expressed from this transgene is specific for influenza virus A/PR/8 hemagglutinin (HA) in the context of the MHC class I molecule H2-Kd. FACS analysis of pancreatic lymph node indicates CFSE treated NOD clone-4 T cells adoptively transferred into NOD.InsHA (Stock No. 005685) proliferate vigorously and there is a 2-3-fold increase in the percentage of dividing clone-4 TCR, CD8+ T cells when compared to BALB/cBy (Stock Nos. 005307 and 005533) or B10.D2 (Stock Nos. 005308 and 005534). HA specific reactivity not tolerance is observed.
This mouse is further modified with the Thy1a allele, rather than the alternate allele Thy1b present in C57BL/10, DBA/2, BALB/c and NOD/Lt mice. Thus, cell populations derived from these transgenic mice c
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| 005019 | NOD.Cg-Tg(Igh-6/Igh-V125)2Jwt/JwtJ | Repository-Cryopreserved |
| 005018 | NOD.Cg-Tg(Igk-C/Igk-V125)1Jwt/JwtJ | Repository-Cryopreserved |
| 005524 | NOD.Cg-Tg(Ins2*Y16A)1Ell Ins1tm1Jja Ins2tm1Jja/GseJ | Repository-Cryopreserved |
| Transgenic mice reportedly express the mutant Ins2*Y16A protein in the pancreatic islets and thymus. The donating investigator reports approximately 75% of female transgenic mice (founder line B) become diabetic in the presence of native insulin genes by 35 weeks of age. In contrast, NOD female transgenic mice lacking both Ins1 and Ins2 fail to produce insulin autoantibodies, and neither diabetes nor insulitis develops by 26 weeks of age. Sialitis does occur, however. Line B transgenics have lower expression levels than line F (see Stock No. 005525), and 50% of the line B male transgenics lacking both Ins1 and Ins2 develop metabolic diabetes, with little to no insulitis, before 10 weeks of age. This strain is useful to study insulin-reactive autoimmunity. | ||
| 005525 | NOD.Cg-Tg(Ins2*Y16A)3Ell Ins1tm1Jja Ins2tm1Jja/GseJ | Repository-Cryopreserved |
| Expression has been reported in the pancreatic islets and thymus of NOD mice carrying the Tg(Ins2*Y16A)3Ell mutation. Approximately 15% of line F female transgenic mice become diabetic in the presence of native insulin genes by 35 weeks of age. NOD female transgenic mice lacking both Ins1 and Ins2 fail to produce insulin autoantibodies, and there is no diabetes or insulitis at 26 weeks of age, but sialitis is present. In contrast, transgenic mice in the presence of Ins1 and lacking Ins2 develop diabetes in 75% of the animals by 25 weeks of age (Nakayama et al, 2004, 2005). This stock is useful to study insulin-reactive autoimmunity. | ||
| 005685 | NOD.Cg-Tg(Ins2-HA)165Bri/ShrmJ | Repository-Cryopreserved |
| Transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The diabetes rate in transgenic females is similar to NOD females. FACS analysis using anti-HA antibodies indicates similar levels of HA expression on pancreatic beta cells as BALB-InsHA (Stock No. 005533). Tetramer (KdHA) binding and dose titration analysis indicate CD8+ T cells obtained from transgenic mice exhibit high avidity for HA. Irradiated transgenic females adoptively transferred with transgenic CTL's exhibit rapid diabetes onset, whereas irradiated, non-transgenic NOD females do not become diabetic indicating HA antigen specificity. This model is useful for studying CD8+ T cell peripheral tolerance deficiency (Kreuwel et al, 2001). | ||
| 004937 | NOD.Cg-Tg(Ins2-tTA)1Doi/DoiJ | Repository-Cryopreserved |
| Tg(Ins2-tTA)1Doi encodes the tetracycline regulatable transactivator (tTA) regulated by the rat insulin promoter (Ins2, commonly designated RIP), and is expressed in the pancreatic beta cells. Mice hemizygous for this transgenic insert are viable, fertile, normal in size, display normal NOD diabetes onset, but do not display any other gross physical or behavioral abnormalities. When transgenic mice are mated to a second transgenic strain carrying the target gene regulated by the tetO responsive elements, expression of the target gene is turned off by the tetracycline analog, doxycycline (dox). Dox can be administered orally in the food or water. This strain provides a Tet-Off tool that permits the inducible expression of genes in the pancreatic beta cells during various stages of diabetes development. | ||
| 005076 | NOD.Cg-Tg(tetO-EGFP/FADD)1Doi/DoiJ | Repository-Cryopreserved |
| Mice hemizygous for this transgenic insert are viable, fertile, normal in size. Diabetes incidence and onset is similar to that observed in NOD inbred mice, but otherwise, the mice do not display any gross physical or behavioral abnormalities. These transgenic mutant mice may be mated to strains carrying either rtTA (reverse tetracycline trans-activator protein) or tTA (the tetracycline trans-activator) transgenes regulated by tissue specific promoters. In the bi-transgenic offspring of such crosses, tissue-specific expression of the EGFP/FADD fusion protein can be either induced (in rtTA transgenic mice) or suppressed (in tTA transgenice mice) by administration of the tetracycline analog, doxycycline (dox). Dox may be administered in the animals? water supply. Double transgenic mice generated by intercrossing Tg(tetO-EGFP/FADD)1Doi transgenic mice with NOD.Cg-Tg(Ins2-rtTA)2Doi/DoiJ (Stock No. 004602) transgenic mice express
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| 003855 | NOD/ShiLt-Tg(Ins2-cre)5Lt/LtJ | Repository-Cryopreserved |
| This strain expresses Cre recombinase under the control of the rat insulin II promoter. Hemizygous mice carrying this transgene are phenotypically normal and overexpresss cre specifically in pancreatic beta cells. Homozygous transgenic mice experience delayed onset diabetes compared to wildtype controls. This transgenic strain is used in combination with mice carrying floxed targeted mutations to create various pancreatic beta cell-specific gene knockouts using the Cre/loxP system. | ||
| 005282 | NOD/ShiLtJ-Tg(Ins1-EGFP/GH1)14Hara/HaraJ | Repository-Cryopreserved |
| Donating investigator reports transgenic mice develop normally and behave similarly to controls with respect to glucose tolerence and and pancreatic insulin content. Histology confirms transgenic mice have normal islet architecture with coexpression of insulin and GFP. The enhanced GFP reporter allows the beta cells to be easily identified and purified for further studies. Studies completed at The Jackson Laboratory indicate there is strong non-mosaic expression of green fluorescent protein in NOD/LtJ-Tg(Ins1-EGFP/GH1)14Hara/HaraJ islets. 100% of homozygous Ins1-EGFP transgenic males and females, identified by qPCR, become diabetic by 9 weeks of age. Pancreatic histopathology of homozygous mice shows beta cell loss without insulitis. | ||
| 005714 | NOR.Cg-Tg(Ins2-CD80)3B7Flv/LwnJ | Repository-Cryopreserved |
| Transgenic mice are characterized by pancreatic beta cells that express a rat insulin promoter (Ins2) regulated transgene encoding the human CD80 T cell co-stimulatory molecule. These mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Approximately 50% of the NOR (backcross 5) transgenic mice become diabetic by 30 weeks of age compared the control NOR which is diabetes resistant. Spleens of diabetic NOR transgenic mice used in adoptive transfer experiments transfer diabetes to NOD.scid/RIP-B7.1 and irradiated non-diabetic NOR.Cg-Tg(Ins2-CD80)3B7Flv/FswJ mice, yet failed to transfer disease to NOD.scid, B6.scid, or CB17.scid. NOR.-Tg(Ins2-CD80)3B7Flv/FswJ provides a tool for studying mechanisms for loss of tolerance in potentially diabetogenic CD8 T-cells. | ||
| 005994 | STOCK Mbtps1tm1Jdh/J | Repository-Cryopreserved |
| These mice carry a targeted mutation in which exon 2 of the targeted gene is flanked by loxP sites. A loxP-flanked ("floxed") neomycin resistance cassette also is inserted downstream in intron 2. Homozygotes are viable and fertile, and the floxed gene appears to function normally. When homozygotes are crossed with transgenic strains expressing Cre-recombinase, cre-mediated recombination of the loxP-flanked sequences can result in one of three genotypes: a) deletion of the neo cassette only, leaving a loxP-flanked second exon and unimpaired endogenous gene function. b) Deletion of exon 2 only, leaving a loxP-flanked neo cassette and no endogenous gene function. c) Deletion of both the neo cassette and exon 2, leaving a single loxP site and no endogenous gene function. When these floxed mutant mice are bred to mice carrying the Mx1-cre transgene (for example, Stock No. 003556), liver-
..... For more information please see the full phenotype on the strain data sheet | ||
| 005728 | STOCK Tg(tetO-Ipf1,lacZ)958.1Macd/J | Repository-Cryopreserved |
| Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Expression of the bicistronic transgene is under the regulation of a tetracycline-responsive promoter element (TRE; tetO). When transgenic mice are bred to a second transgenic strain expressing tetracycline-transactivator (tTA) protein under the control of a tissue-specific promoter, the bitransgenic offspring express Ipf1 and lacZ in the appropriate target tissue. Further, Ipf1 and lacZ expression in bitransgenic mice can be suppressed by administration of the tetracycline analog, doxycycline. All cells expressing Ipf1 coexpress the reporter, and mRNA levels of the transgenic and endogenous Ipf1 fluctuate in concert during development. This mouse was designed originally to be mated to an pancreatic targeted mutant with tTAoff in place of the Ipf1 gene (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
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