Search Criteria: Research Area is "Endocrine Deficiency Research: Pancreas Defects"
Additional Register Interest Strains
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000697 | B6.BKS(D)-Leprdb/J | Level 2 |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) become identifiably obese around 3 to 4 weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at four to eight weeks. Affected mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. On the C57BL/6 background there is compensatory hyperplasia of the islet B cells, and continued hyperinsulinemia throughout an 18- to 20-month life span. Wound healing is delayed and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Leprdb/+) also have increased metabolic efficiency and can survive a prolonged fast longer than controls. Experiments involving destruction of the ventromedial nucleus of the hypothalamus suggest that Leprdb may cause a defect in the hypothalamus. Steroid sulfotransferase enzymes, aberrantly expressed in ..... For more information please see the full phenotype on the strain data sheet | ||
| 000632 | B6.V-Lepob/J | Level 2 |
| Mice homozygous for the obese spontaneous mutation, (Lepob; commonly referred to as ob or ob/ob), are first recognizable at about four weeks of age. Homozygous mutant mice gain weight rapidly and may reach three times the normal weight of wild-type controls. In addition to obesity, mutant mice exhibit hyperphagia, a diabetes-like syndrome of hyperglycemia, glucose intolerance, elevated plasma insulin, subfertility, impaired wound healing, and an increase in hormone production from both pituitary and adrenal glands. They are also hypometabolic and hypothermic. The obesity is characterized by an increase in both adipocyte number and size. Adipose tissue transplants in Lepob homozygotes protect them from obesity, normalize insulin sensitivity, and restore fertility. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight mainte ..... For more information please see the full phenotype on the strain data sheet | ||
| 000642 | BKS.Cg-Dock7m +/+ Leprdb/J | Level 2 |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) become identifiably obese around three to four weeks of age. Elevations of plasma insulin begin at 10 to 14 days of age and of blood sugar at four to eight weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. A number of features are observed on the C57BLKS background, including an uncontrolled rise in blood sugar, severe depletion of the insulin-producing beta-cells of the pancreatic islets, and death by 10 months of age. Exogenous insulin fails to control blood glucose levels and gluconeogenic enzyme activity increases. Peripheral neuropathy and myocardial disease are seen in C57BLKS-Leprdb homozygotes. Wound healing is delayed, and metabolic efficiency is increased. Female homozygotes exhibit decreased uterine and ovarian weights, decreased ovarian hormone production and hypercytolipidemia in fol ..... For more information please see the full phenotype on the strain data sheet | ||
| 012888 | 129-Wlstm1.1Lan/J | Repository- Live |
| These Wls floxed mutant mice possess loxP site before the ATG start site in the 5' untranslated region of exon 1 and another upstream of exon 2 of the wntless homolog (Drosophila) (Wls) gene. Mice that are homozygous for this allele are viable, fertile, and normal in size. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 1 deleted in cre-expressing tissues, abolishing gene function. When bred to a strain expressing Cre recombinase in the germline, homozygotes fail to develop mesoderm and are embryonic lethal by E8.5. When bred to a strain expressing Cre recombinase in pancreatic precursors, the mutant mice develop pancreatic hypoplasia. When bred to a strain expressing Cre recombinase in neural crest cells, the mutant mouse strain has severe brain malformations and exhibit postnatal lethality. This mutant mouse strain is useful to study Wnt signaling in any organ or tissue that can be targeted ..... For more information please see the full phenotype on the strain data sheet | ||
| 007688 | 129S6.B6-Ins2Akita/CofJ | Repository- Live |
| Congenic 129S6/SvEvTac mice heterozygous for the Ins2 Akita (Akita) spontaneous mutation are viable and fertile. Mice carrying the Akita mutation exhibit hyperglycemia, polydipsia, polyuria and elevated systolic blood pressure when compared to wild-type controls. The diabetic phenotype is more severe and progressive in the male than in the female. Heterozygous males exhibit significantly increased albuminuria and albumin-to-creatine ratios compared to wild-type controls. The absolute level of 129S6-Akita albumin excretion is intermediate when compared to C57BL/6-Ins2Akita/J (Stock No. 003548) being the lowest and D2.B6-Ins2Akita/MatbJ (Stock No. 007562) being the highest. At six months of age, glomerular filtration rates (GFR) are significantly higher in the 129S6-Ins2Akita mice than either ..... For more information please see the full phenotype on the strain data sheet | ||
| 004369 | B6.Cg-Rag1tm1Mom Ins2Akita/J | Repository- Live |
| Mice homozygous for the Rag1 targeted mutation and heterozygous for the Akita spontaneous display the diabetes phenotype in the absence of B and T cells and unlike single Akita mice, double mutants do not reject allografts. Mice heterozygous for only the Akita spontaneous mutation are viable and fertile. (Homozygotes typically die by 12 weeks of age from extreme hyperglycemia.) Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. The diabetic phenotype is more severe and progressive in heterozygous males than in females. Obesity and insulitis do not accompany diabetes. This double mutant strain is ideally suited for use in allogeneic or xenogeneic islet or stem cell transplantation protocols because the mice are severely immunocompromised and spontaneously develop diabetes at a young age. | ||
| 006333 | B6.FVB(Cg)-Tg(Neurog3-cre)C1Able/J | Repository- Live |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Expression of the transgene is directed by a neurogenin 3 promoter. Tissues where Cre recombinase expression is detected include the small intestine (base of intestinal crypts) and fetal pancreatic epithelial cells. Cre activity has been shown in islets of the adult pancreas, small intestine enteroendocrine cells, endocrine portions of the stomach, all pancreatic endocrine cells, and in some non-endocrine intestinal cells. When bred with a mouse containing a loxP site-flanked sequence of interest, Cre-mediated recombination results in deletion of the flanked gene in the tissues that normally express neurogenin 3.
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 not ..... | ||
| 003923 | B6.HRS(BKS)-Cpefat/J | Repository- Live |
| Mice homozygous for the fat spontaneous mutation (Cpefat) on a C57BL/6J genetic background (N10) become noticeably obese by 14-15 weeks of age. There is also some sexual dimorphism; female homozygous mutant mice develop obesity at a later age than males. Cpefat mice actually weigh less than wildtype controls prior to weaning age. Homozygous mutant mice develop a diabetic phenotype characterized by hyperglycemia and insulin resistance. Cpefat mice appear healthier on the C57BL/6J genetic background, avoiding the hereditary hydronephrosis present in C57BLKS/J and a lower incidence of malocclusion. | ||
| 008340 | BKS.Cg-Leprdb Nos3tm1Unc/RhrsJ | Repository- Live |
| These double mutant mice harbor both the Leprdb spontaneous mutation and the Nos3 (eNOS) targeted mutation and are congenic on C57BLKS/J genetic background. Mice homozygous for both mutations (called eNOS-/- C57BLKS/J db/db, eNOS-/- db/db, or db/db/eNOS-/- double mutant mice) are viable with development of type II diabetes and diabetic nephropathy. The eNOS-/- C57BLKS/J db/db mice develop type II diabetes with significant obesity and hypertension: while both mutations are associated with insulin resistance, the mutated leptin receptor in db/db mice chiefly accounts for the observed hyperglycemia and defective leptin signaling (leading to persistent hyperphagia and obesity), and the eNOS-deficiency accounts for the moderate systemic hypertension. In addition, eNOS-/- C57BLKS/J db/db mice exhibit rapid onset and progression of pathologic ..... For more information please see the full phenotype on the strain data sheet | ||
| 004824 | BTBR.V(B6)-Lepob/WiscJ | Repository- Live |
| Mice homozygous for the obese spontaneous mutation, (Lepob commonly referred to as ob or ob/ob) exhibit obesity hyperphagia, a diabetes-like syndrome of hyperglycemia, glucose intolerance, elevated plasma insulin, subfertility, impaired wound healing, and an increase in hormone production from both pituitary and adrenal glands. They are also hypometabolic and hypothermic. The obesity is characterized by an increase in both number and size of adipocytes. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase body weight and is probably the result of it. Homozygotes do have an abnormally low threshold for stimulation of pancreatic islet insulin secretion even in very young preobese animals. As is the case with mice carrying the diabetes mutation (Leprdb ..... For more information please see the full phenotype on the strain data sheet | ||
| 003548 | C57BL/6-Ins2Akita/J | Repository- Live |
| Mice heterozygous for the Akita spontaneous mutation (Ins2Akita) are viable and fertile. Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning around 3-4 weeks of age. The diabetic phenotype is more severe and progressive in the male than in the female. Obesity or insulitis does not accompany diabetes. Expression of glutathione S-transferase mRNA is increased in epithelial cells in proximal tubules of hyperglycemic mutants (Fujita et al., 2001). As well, plasma concentrations of valine, leucine, isoleucine, as well as the total branched chain amino acids, alanine, citrulline and proline, were significantly higher in the Akita mice (Mochida et al., 2011). Sphingosine-1-phosphate is elevated and diabetic animals demonstrated reductions in plasma levels of omega-9 24:1 (nervonic acid)-containing ceramide, sphingomyelin, and cerebrosides. Reduction of 24:1-esterfied sphi ..... For more information please see the full phenotype on the strain data sheet | ||
| 007562 | D2.B6-Ins2Akita/MatbJ | Repository- Live |
| DBA/2J mice heterozygous for the Akita spontaneous mutation are viable and fertile. The donating investigator reports that the symptoms in heterozygous mutant mice are more severe and progressive in the males than in the females and include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. Obesity and insulitis do not accompany diabetes. Litter sizes range from 2-8 pups. Heterozygous Akita males develop albuminuria at two months of age. The albuminuria is progressive such that by 6 months of age albumin/creatine levels are approximately 600ug/mg. Additionally, it has been reported that DBA/2J heterozygous mutant mice develop diabetic nephropathy.
Although not studied in the DBA/2J heterozygotes, C57BL/6 heterozygous mutant mice exhibit gait disturbance and decreased sensory nerve conduction velocity, but do not exhibit learning or memory deficits (Choeiri C et al., 2005). Progressive retinal abnormalities begin as early as ..... | ||
| 006654 | FVB.BKS(D)-Leprdb/ChuaJ | Repository- Live |
| The congenic "FVB-db" strain differs from that previously published on other genetic backgrounds in that it presents a marked obesity/diabetes phenotype intermediate between the severe uncompensated hyperglycemia observed in C57BLKS/J and DBA2/J backgrounds and the mild, compensated syndrome reported on the C57BL/6J and 129/J backgrounds. The literature reports that obese FVB-db mice of both sexes show long-term hyperglycemia primarily due to severe insulin resistance. The hyperglycemia in the fed state persists despite continued extreme hyperinsulinemia correlated with a marked pancreatic cell hypertrophy and hyperplasia. These phenotypes have been replicated in the stock at The Jackson Laboratory. However, the diabetic nephropathy (glomerulosclerosis) reported in the literature was not evident in the stock imported to JAX at the age evaluated (24 weeks).
As the phenotype varies by genetic background, these mutant mice, along with db mutants on other ge ..... | ||
| 008659 | NOD.Cg-Rag1tm1Mom Ins2Akita Prf1tm1Sdz/SzJ | Repository- Live |
| Like NOD.Cg-Rag1tm1Mom Prf1tm1Sdz/J (004848), this strain lacks mature T and B cells. NK cells, although present, lack cytotoxic activity. Both sexes develop spontaneous hyperglycemia as early as three weeks of age, however, the phenotype is predominantly exhibited by males. Pancreatic islets have reduced insulin staining and exhibit an altered morphology with age. Human islet transplantation at doses of 4000 IEQ is successful in returning hyperglycemic males to a euglycemic state. This strain may useful in studies of human islet and beta stem and progenitor cell function. | ||
| 014568 | NOD.Cg-Rag1tm1Mom Ins2Akita Il2rgtm1Wjl/SzJ | Repository- Live |
| NRG-Akita mice, which are homozygous for the Rag1tm1Mom and the Il2rgtm1Wjl alleles (males are hemizygous for the X-linked Il2rgtm1Wjl allele) and heterozygous for the Ins2Akita allele, develop spontaneous hyperglycermia. No mature T, B or NK cells are detected in flow cytometric analysis of splenocytes from NRG-Akita mutant mice. Granulocyte and macrophage populations are similar to those seen in NRG mice (Stock No. 7799). NRG-Akita mice develop hyperglycemia between 3 and 5 weeks of age. Histological examination at 3 weeks of age reveals normal pancreas morphology, and routine insulin and glucagon staining. By approximately 32 weeks of age, NRG-Akita mice display disorganized, condensed pancreatic islet architecture, with loss of insulin-positive cells. Euglycemia is restored by subrenal transplantation of mouse or human islets or intrapancreatic transplantation of dissociated mouse islet cells. NRG-Akita ..... For more information please see the full phenotype on the strain data sheet | ||
| 009340 | STOCK Eif2ak3tm1Dron/HotaJ | Repository- Live |
| These mice harbor a targeted mutation of the Eif2ak3 (eukaryotic translation initiation factor 2 alpha kinase 3 [also called Perk]) locus that abolishes endogenous gene expression. To date (Feb 2010), the donating investigator has not been able to generate homozygous mice on a C57BL/6J congenic background. The following phenotype describes mice on a mixed albino Swiss Webster;129/SvEv genetic background. Heterozygous mice are viable and fertile. Homozygous (Perk-/-) mice appear runty within a few days of birth and develop a rapid and progressive decline in endocrine and exocrine pancreatic function. This results in a complex pleiotropic phenotype including hyperglycemia, exocrine pancreatic insufficiency, diabetes, growth retardation, inability to breed, and early mortality. The phenotype of the Perk-/- mice is very similar to that observed in humans with Wolcott-Rallison syndrome; the consistent feature of which is severe diabetes mellitus developing in infancy. Heterozygous mi ..... For more information please see the full phenotype on the strain data sheet | ||
| 008755 | STOCK Tg(Ins2-rtTA)2Efr Tg(teto-DTA)1Gfi/J | Repository- Live |
| This strain was generated by breeding Stock No. 008168 and Stock No. 008250 together at The Jackson Laboratory. The resulting double transgenic colony was established as Stock No. 008755. The Ins2-rtTA (or RIP7-rtTA) transgene expresses the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the rat insulin 2 (Ins2) promoter. The tet-DTA (or tetO-DTA) (transgene expresses diphtheria toxin A (DTA) under the control of a tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator) and a cytomegalovirus minimal promoter. Mice harboring both of these transgenes has doxycycline-inducible expression of DTA in pancreatic beta cells; i.e. addition of the tetracycline analogue doxycycline (dox) results in ablation of pancreatic beta cells. | ||
| 014158 | STOCK Tg(Pax4-cre)1Dam/J | Repository- Live |
| Pax4-cre transgenic mice have the mouse paired box gene 4 (Pax4) promoter directing expression of an enhanced green fluorescent protein fused to a Tet-off cassette (EGFP/tTA). The transgene also contains a tetracycline-responsive element with a CMV minimal promoter (tetO-CMVmin) driving expression of a Cre-recombinase gene. In the absence of tetracycline/doxycycline, Cre recombinase expression is observed in Pax4-expressing cells (pancreatic progenitor cells). While designed to concomitantly allow tetracycline/doxycycline-dependant inhibition of Cre recombinase expression, the donating investigator confirms no such inhibition is observed. Also, no GFP expression is observed with or without tetracycline/doxycycline administration. Therefore, Pax4-cre transgenic mice function only for Cre recombinase expression in Pax4-expressing cells. When bred with mice containing a loxP-flanked sequence, Cre-mediated recombination will result in deletion of ..... For more information please see the full phenotype on the strain data sheet | ||
| 017601 | B6.129-Eif2s1tm1Rjk/J | Under Development - Now Accepting Orders |
| The Eif2aS51A mutation in these mice prevents phosphorylation of the α subunit of eIF2. Phosphorylation of eIF2α in the endoplasmic reticulum (ER) is required for translational regulation, transcriptional induction, and survival in response to ER stress. EIF2α translational regulation is also required for the maintenance of blood glucose and pancreatic insulin content. Homozygotes die within 18 hr after birth due to hypoglycemia associated with defective gluconeogenesis. Homozygous mutant embryos and neonates displayed a deficiency in pancreatic β cells and an increase in circulating insulin. Heterozygotes are viable and fertile. On a high fat diet, heterozygous mice develop diabetes due to unregulated proinsulin translation. These mice also exhibit defective ER cargo trafficking, increased oxidative damage, reduced expression of stress response and beta-cell-specific genes, and apoptosis. | ||
| 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 | ||
| 000709 | 129P3/J-Leprdb-3J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the diabetes 3J spontaneous mutation (Leprdb-3J) become identifiably obese around three to four weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at four to eight weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. Homozygous mutant mice on the 129P3/J background exhibit severe obesity but the diabetes phenotype is much reduced. | ||
| 002048 | B6 x C57BLKS-Dock7m Leprdb Myo15sh2-J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the shaker 2 Jackson spontaneous mutation (Myo15sh2-J) are viable and fertile, showing only a slight reduction in both compared to wild-type mice. The shaker 2 Jackson remutation is not visibly different from the original shaker 2 (Myo15sh2, Stock No. 000109). Homozygous mutant mice of both alleles display a phenotype very similar to the behavior and pathology to shaker-1 (Myo7ash1) with the exception that the abnormalities are observed a little earlier in shaker 2 mice. This strain is also carrying the misty (Dock7m) and diabetes (Leprdb) spontaneous mutations. | ||
| 000562 | B6(Cg)-Tubtub/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the tubby spontaneous mutation experience maturity-onset obesity. Homozygous mutant mice are recognizable by increased body weight at 3 to 4 months in males and at 4 to 6 months in females. Both sexes are fertile. The increased weight is composed of excess adipose tissue. Blood glucose is normal, but plasma insulin is increased prior to obvious signs of obesity and may rise to 20 times normal by 6 months. Despite elevated plasma total cholesterol, triglycerides, and high-density lipoprotein cholesterol, homozygous mutant mice do not exhibit atherosclerotic fatty streak blood vessel lesions. Tubby mutant mice also exhibit retinal degeneration, initially believed due to the presence of another mutation which was called rd5, but since demonstrated to be a pleiotropic effect of the Tubtub mutation (Ohlemiller et al., 1997); the retinal phenotype is moderated by a QTL on Chromosome 11 (Ikeda et al., 2002). Tubby homozygotes additionally exhibit p ..... 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 | ||
| 006411 | B6.129-Gasttm1(INS)Ez/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for this "G-InsKi" allele are viable and fertile. Human insulin expressed from this mutant allele retains full biological activity. Expression of human insulin is specific to gastrin-expressing cells (G cells of the antral stomach and some duodenum cells), and is released into portal circulation in response to the same meal-associated stimuli that control gastrin release. Heterozygous mice exhibit normal blood glucose levels, and toxic hypoglycemia is not observed. The donating investigators report that human insulin levels are sufficient to activate insulin signaling cascades in the liver but not in skeletal muscle. These mutant mice may be useful for diabetes and obesity research, specifically for studying the molecular and physiological mechanisms by which the hepatic action of transgenic insulin prolongs the survival of diabetic mice (e.g. Ins2Akita mutant mice). | ||
| 006860 | B6.129-Ins2Akita Bdkrb2tm1Jfh/SmiJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation and heterozygous for the Ins2Akita spontaneous mutation are viable and fertile. Similar to mice only heterozygous for the Ins2Akita mutation, the double mutant mice are severely diabetic: their body weights are 70% of wildtype, they consume over 3-fold the normal amount of food, and their urinary output is approximately 20-fold more than that of wildtype mice. Double mutant mice have markedly enlarged kidneys. Urinary albumin excretion in double mutants is almost 4-fold that of either single mutant, and double mutants experience more severe nephropathy than mice that are heterozygous for the Akita mutation alone. Megsin and nephrin expression is markedly increased in double mutant mice when compared to wildtype or to mice with either single mutation alone. By 12 months of age, double mutant mice experience hair loss due to a reduction in hair follicle numbers and thinning of the dermis. Double mutants ..... For more information please see the full phenotype on the strain data sheet | ||
| 003316 | B6.129P2-Gcktm1Efr/J | Cryopreserved - Ready for recovery |
| Glucokinase catalyzes a rate-limiting step in glucose metabolism in hepatocytes and pancreatic beta cells and is considered the "glucose sensor" for regulation of insulin secretion. Patients with maturity-onset diabetes of the young (MODY) have heterozygous point mutations in the glucokinase gene that result in reduced enzymatic activity and decreased insulin secretion. Disruption of the glucokinase gene results in a phenotype similar to MODY in heterozygous mice. These mice manifest a decreased insulin secretory response to glucose. | ||
| 003142 | B6.129P2-Prlrtm1Cnp/J | Cryopreserved - Ready for recovery |
| There is complete female sterility due to abberant estrous cycles, abnormal preimplantation development of eggs, no implantation of blastocysts, lack of pseudopregnancy. Males show slightly delayed fertility. Mammary development is markedly affected. Homozygotes have no mammary development and do not lactate. Heterozygotes are unable to lactate after the first pregnancies, but attain some degree of lactation as they age or after multiple pregnancies. Serum prolactin levels are increased 60 - 100 fold in both males and females. Maternal behavior is diminished in pimiparous and nulliparous animals. Bone remodelling is decreased in homozygote mutants. | ||
| 005517 | B6.129S4-Cyb5r4tm1Hfb/HfbJ | Cryopreserved - Ready for recovery |
| Mice heterozygous for the targeted mutation are viable and fertile, glucose tolerant, have normal blood sugar levels, serum lipid profiles and white adipose tissue mass. No protein from the targeted gene was detected by Western Blot analysis of mice homozygous for the allele. Homozygous mice consume more food, have decreased adipose tissue mass and are hyperlipidemic compared to wildtype controls post-weaning. At 4 weeks of age glucose levels are normal but insulin levels are 40% of wildtype controls. At 7 weeks of age clinical diabetes is present in both male and female of homozygous mice. Histological evaluation of pancreas from 21 week old homozygote animals revealed a significant reduction in the number of islets and decreased cytoplasmic to nuclear ratio in the islet cells and there was no insulitis nor phagocytosis of necrotic beta cell fragments. While there is a progressive loss of beta cells in aging homozygous mice, there is no loss of alpha, delta or PP cells. Electron m ..... | ||
| 003264 | B6.129S7-Gcktm1Ts/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Gcktm1Ts targeted mutation die perinatally with severe hyperglycemia. Heterozygous mutant mice exhibit elevated blood glucose levels and reduced insulin secretion. | ||
| 003126 | B6.129X1-Grprtm1Jfb/J | Cryopreserved - Ready for recovery |
| Mice homozygous (females) or hemizygous (males) for the X-linked Grprtm1Jfb targeted mutation are viable with no gross phenotypic abnormalities observed. There is a deficiency in bombesin-induced mediation of satiety as measured by glucose intake. A modest increase in body weight is observed in older animals. At 18-20 months of age, hemizygous males (N = 8) are 44.5g ± 5.1 (mean ± std dev) and wildtype littermates (N = 8) are 38.3g ± 5.1 (L. Hampton, unpublished observation). We have recently observed head tilts and bobbing in the hemizygous males in our production colony. The donating investigator of this strain has also observed this phenotype and considers it a mutation not related to the gene. We are working to remove this phenotype, but we will continue to ship from the colony while we finish this process. | ||
| 013040 | B6.Cg-Apoetm1Unc Ins2Akita/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Akita spontaneous mutation are stunted and typically die postnatally 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). Apoe-null homozygotes have marked increase in total plasma cholesterol levels that are unaffected by age or sex (see the datasheet for Stock No. 002052 for additional information). These double mutant mice (Apoe-null, Akita heterozygous) may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, hypercholesterolemia, and diabetes-related macrovascular complications. | ||
| 000699 | B6.Cg-Dock7m Leprdb/+ +/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) become identifiably obese around 3 to 4 weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at 4 to 8 weeks. Affected mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. On the C57BL/6 background there is compensatory hyperplasia of the islet B-cells, and continued hyperinsulinemia throughout an 18- to 20-month life span. Wound healing is delayed, and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Leprdb/+) also have increased metabolic efficiency, and can survive a prolonged fast longer than controls. Experiments involving destruction of the ventromedial nucleus of the hypothalamus suggest that Leprdb may cause a defect in the hypothalamus. Steroid sulfotransferase enzymes, aberrantly expressed in diabe ..... For more information please see the full phenotype on the strain data sheet | ||
| 006580 | B6.Cg-Ins2Akita Ldlrtm1Her/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Akita spontaneous mutation die postnatally, typically by 12 weeks of age. Independently, heterozygous Akita mutant mice are a model of insulin dependent diabetes mellitus (IDDM) with severe hyperglycemia (see the datasheet for Stock No. 003548 for additional information). LDLR-null homozygotes have elevated serum cholesterol levels (200-400 mg/dl) which can escalate to very high levels (> 2000 mg/dl) when the mice are fed a high fat diet. LDLR-deficient mice also are predisposed to develop atherosclerosis. These double mutant mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, hypercholesterolemia, and diabetes-related macrovascular complications. | ||
| 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. | ||
| 008247 | B6.Cg-Tg(Ela1-TAg*)289Mjt/J | Cryopreserved - Ready for recovery |
| Hemizygous T1-147 transgenic mice (harboring the E1-T147 transgene) are viable and fertile, with high-level expression of an N-terminal, truncated (1-147 amino acid), and mutant (does not express the small t antigen) form of simian virus 40 large T antigen (TAg) directed to pancreatic acinar cells by the rat elastase 1 (Ela1 or E1) upstream control region. Hemizygous T1-147 transgenic mice exhibit pancreatic dysplasia in the embryonic pancreas, with cancer progression after birth to primary pancreatic acinar cell tumor formation (100% penetrance). These mice have microadenomas and acinar cell carcinomas present as early as 10 weeks of age, and become moribund or show clear evidence of abdominal distention around 20-30 weeks of age. T1-147 transgenic mice with large tumors develop metastatic disease to the liver and mesenteric lymph nodes. The donating investigator reports that the cancer phenotype of these T1-147 transgenic mice is identical to that of their similar T1-127 trans ..... For more information please see the full phenotype on the strain data sheet | ||
| 002963 | B6;129-Pcsk2tm1Dfs/J | Cryopreserved - Ready for recovery |
| 004176 | BKS.B6-Tubtub/Jng | Cryopreserved - Ready for recovery |
| Mice homozygous for the tubby spontaneous mutation experience maturity-onset obesity. Homozygous mutant mice are recognizable by increased body weight at 3 to 4 months in males and at 4 to 6 months in females. Both sexes are fertile. The increased weight is composed of excess adipose tissue. Blood glucose is normal, but plasma insulin is increased prior to obvious signs of obesity and may rise to 20 times normal by 6 months on the C57BL/6 background. Despite elevated plasma total cholesterol, triglycerides, and high-density lipoprotein cholesterol, homozygous mutant mice do not exhibit atherosclerotic fatty streak blood vessel lesions. Tubby mutant mice also exhibit retinal degeneration, initially believed due to the presence of another mutation which was called rd5, but since demonstrated to be a pleiotropic effect of the Tubtub mutation (Ohlemiller et al., 1997); the retinal phenotype is moderated by a QTL on Chromosome 11 (Ikeda et al., 2002). ..... For more information please see the full phenotype on the strain data sheet | ||
| 000700 | BKS.Cg-Dock7m Leprdb/+ +/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) become identifiably obese around three to four weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at four to eight weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. A number of features are observed on the C57BLKS background, including an uncontrolled rise in blood sugar, severe depletion of the insulin-producing beta-cells of the pancreatic islets, and death by 10 months of age. Exogenous insulin fails to control blood glucose levels and gluconeogenic enzyme activity increases. Peripheral neuropathy and myocardial disease are seen in C57BLKS Leprdb homozygotes. Wound healing is delayed and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Leprdb/+) also have increased metabolic ..... For more information please see the full phenotype on the strain data sheet | ||
| 001192 | BKS.Cg-meaJ Leprdb +/+ + Dock7m/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the meander tail-J spontaneous mutation (meaJ) have variably shortened and kinked tails. At about two weeks an unsteadiness of gait, often amounting to a tremor, appears. Homozygous mutant mice are smaller and less vigorous than wild-type controls but are fertile. The anterior lobe of the cerebellum is disorganized. Purkinje cells are scattered, some cellular layers never form, and Bergmann glial processes are absent. The cytoarchitecture of the posterior lobe is normal, and the transition from normal to disorganized areas is sharply demarcated. This mutation occurred in the BKS.Cg-Leprdb +/+ Dock7m strain so it is also segregating for the diabetes (Leprdb) and misty (Dock7m) mutations. See strain description for Stock No. 000642 for more information. | ||
| 000696 | BKS.V-Lepob/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the obese spontaneous mutation (Lepob, commonly referred to as ob or ob/ob) are first recognizable at about 4 weeks old. Homozygous mutant mice increase in weight rapidly and may reach three times the normal weight of wildtype controls. In addition to obesity, mutant mice exhibit hyperphagia; a diabetes-like syndrome of hyperglycemia, glucose intolerance, and elevated plasma insulin; subfertility; and increased hormone production from both pituitary and adrenal. They are also hypometabolic and hypothermic. The obesity is characterized by both an increased number and size of adipocytes. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase body weight and is probably the result of it. Homozygotes do have an abnormally low threshold for stimulati ..... For more information please see the full phenotype on the strain data sheet | ||
| 002391 | BKSChpLt.HRS-Cpefat/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the fat spontaneous mutation (Cpefat) on a C57BLKS/J genetic background (N10) have a diabetes phenotype that is primarily restricted to males and is more severe than what is seen on the original HRS/J or C57BLKS/J (N5) genetic backgrounds. At weaning both males and female homozygous mutant mice were significantly lighter than wildtype or heterozygous littermates. Obesity develops between 6 and 8 weeks of age and mutant mice can be distinguished from wildtype littermates between 8 and 12 weeks of age. By 18 weeks fat mutant mice will reach 45-55 g and may reach 60-70 g by 6 months of age. Thus, the obesity is thus slower to develop than in the obese (Lepob) and diabetes (Leprdb) mutant mice. The excess adiposity is distributed throughout the body's fat stores, in contrast to the largely axial and inguinal fat deposition of the obese and diabetes mutant mice. Hyperinsulinemia is severe by 4 weeks of age and contin ..... For more information please see the full phenotype on the strain data sheet | ||
| 005516 | C.129S4-Cyb5r4tm1Hfb/HfbJ | Cryopreserved - Ready for recovery |
| Mice heterozygous for the targeted mutation are viable and fertile, glucose tolerant, have normal blood sugar levels, serum lipid profiles and white adipose tissue mass. No protein from the targeted gene was detected by Western Blot analysis of mice homozygous for the allele. Homozygous mice consume more food, have decreased adipose tissue mass and are hyperlipidemic compared to wildtype controls post-weaning. At 4 weeks of age glucose levels are normal but insulin levels are 40% of wildtype controls. At 7 weeks of age clinical diabetes is present in both male and female of homozygous mice. Histological evaluation of pancreas from 21 week old homozygote animals revealed a significant reduction in the number of islets and decreased cytoplasmic to nuclear ratio in the islet cells and there was no insulitis nor phagocytosis of necrotic beta cell fragments. While there is a progressive loss of beta cells in aging homozygous mice, there is no loss of alpha, delta or PP cells. Electron m ..... | ||
| 013633 | C57BL/6J-Bicc1b2b222Clo/J | Cryopreserved - Ready for recovery |
| This c.10048T->C Bicc1 (bicaudal C homolog 1 (Drosophila)) recessive mutation was identified in an ENU screen for recessive cardiovascular development phenotypes in Dr. Cecilia Lo's laboratory, NHLBI Cardiovascular Development Consortium (CvDC). It was recovered from G1 sperm and associated with the phenotype described described here. Because G1 sperm were cryopreserved, additional ENU mutations are also segregating in this strain.
Homozygotes demonstrate laterality defects, including situs inversus totalis, and heterotaxy. Congenital heart disease (CHD) is marked by double outlet right ventricle (DORV)/transposition of the great arteries (TGA), atrioventricular septal defects (AVSD), and an interrupted aortic arch (IAA). Polycystic kidney disease, as well as pancreatic, choleductal, and gonadal cysts are also found. | ||
| 003711 | CAST.B6-Tubtub/Jng | Cryopreserved - Ready for recovery |
| Mice homozygous for the tubby spontaneous mutation experience maturity-onset obesity. Homozygous mutant mice are recognizable by increased body weight at 3 to 4 months in males and at 4 to 6 months in females. Both sexes are fertile. The increased weight is composed of excess adipose tissue. Blood glucose is normal, but plasma insulin is increased prior to obvious signs of obesity and may rise to 20 times normal by 6 months on the C57BL/6 background. Despite elevated plasma total cholesterol, triglycerides, and high-density lipoprotein cholesterol, homozygous mutant mice do not exhibit atherosclerotic fatty streak blood vessel lesions. Tubby mutant mice also exhibit retinal degeneration, initially believed due to the presence of another mutation which was called rd5, but since demonstrated to be a pleiotropic effect of the Tubtub mutation (Ohlemiller et al., 1997); the retinal phenotype is moderated by a QTL on Chromosome 11 (Ikeda et al., 2002). ..... For more information please see the full phenotype on the strain data sheet | ||
| 000707 | CBA.Cg-Dock7m Leprdb/+ +/J | Cryopreserved - Ready for recovery |
| Leprdb/Leprdb mice on the CBA strain background are characterized by exocrine pancreatic necrosis and kidney lesions in aging mice. In contrast to the obesity observed in other strain backgrounds, five month old homozygous males exhibit weight loss in comparison to controls. Homozygous males develop severe hyperglycemia exhibiting blood sugar levels of +/-475 mg/dl by three months of age and increasing to +/- 517 mg/dl by five months. Five month old homozygous males do not exhibit hyperinsulinemia, however homozygous females reach levels of +/-540 uU/ml. Homozygous males do not survive beyond six months (Leiter EH et al, 1981).
Because of the sterility of Leprdb homozygotes, misty has been incorporated into stocks for maintenance of the diabetes mutation. The repulsion double heterozygote (Leprdb +/+ Dock7m) facilitates identification of heterozygotes for breeding, while the coupling ..... | ||
| 013719 | D2.Cg-Apoetm1Unc Ins2Akita/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Akita spontaneous mutation typically die postnatally 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. 007562 for additional information). Apoe-null homozygotes have marked increase in total plasma cholesterol levels that are unaffected by age or sex (see the datasheet for Stock No. 007067 for additional information). These double mutant mice (Apoe-null, Akita heterozygous) may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, hypercholesterolemia, and diabetes-related macrovascular complications. | ||
| 006867 | FVB.B6-Ins2Akita/MlnJ | Cryopreserved - Ready for recovery |
| FVB/NJ mice heterozygous for the Akita spontaneous mutation are viable and fertile. The donating investigator reports that the symptoms in heterozygous mutant mice are more severe than those observed in C57BL/6-Ins2Akita mice (Stock No. 003548). These symptoms include hyperglycemia (females > 600mg/dl, males ~560 mg/dl), hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. In contrast to Akita heterozygotes on a C57BL/6 background, FVB/NJ adult heterozygous females are more hyperglycemic than heterozygous males. Obesity and insulitis do not accompany diabetes. Ins2 is expressed in the fetal yolk sac and is maternally imprinted. Heterozygous mutant females become more hyperglycemic during pregnancy, and are susceptible to embryo malformations leading to reabsorption, even with insulin therapy. Heterozygous mutant males do not produce mutant and wild-type o ..... For more information please see the full phenotype on the strain data sheet | ||
| 006241 | STOCK Hhiptm1Amc/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for this targeted mutation are viable and fertile. Homozygotes die from respiratory failure shortly after birth. Expression of the "knocked-in" lacZ gene is detected in a pattern similar to the endogenous transcript (in lung, skeleton, stomach, duodenum, spleen, and pancreas), and serves as a faithful reporter for Hedgehog (Hh) signaling. Because Hh and fibroblast growth factor (Fgf) signaling are abnormal, homozygous mice have defects in many Hh target tissues. Although the primary lung buds form in homozygotes, lung branching morphogenesis is defect beginning at 10.5 days postcoitus (dpc), and fails to generate a complete respiratory tree. The single left lobe also is significantly reduced, and total lung size at birth is diminished 67-75% compared to wildtype. In addition, homozygous mice have delayed mineralization of the endochondral skeleton, as well as impaired pancreas morphogenesis, islet formation and endocrine cell proliferation. These mutant mice ma ..... For more information please see the full phenotype on the strain data sheet | ||
| 005701 | STOCK Pdx1tm1Macd/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation fail to develop a pancreas. Heterozygous mice have normal pancreas development but partially impaired glucose tolerance in adulthood. The substitution of the targeted gene with tTAoff inactivates the endogenous allele and places tTAoff expression under the control of the endogenous transcriptional regulatory sequences. tTA expression from the modified locus is identical to that of the normal allele; tTA mRNA is detectable in the pancreas but not in other visceral organs or salivary glands. This mutant may be useful in studies of pancreatic endocrine/exocrine function and diabetes. Heterozygotes also can be bred with transgenic mice that express a target gene under the regulation of a tetracycline-responsive element (TRE; tetO) for pancreas-specific applications.
This mutant was originally designed to be mated with mutant mice with a TRE-controlled transgene coding for the endogenous Pdx1 (Ipf1) gene alon ..... | ||
| 005667 | STOCK Tg(Neurog3-cre)C1Able/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Expression of the transgene is directed by a neurogenin 3 promoter. Tissues where Cre recombinase expression is detected include the small intestine (base of intestinal crypts) and fetal pancreatic epithelial cells. Cre activity has been shown in islets of the adult pancreas, small intestine enteroendocrine cells, endocrine portions of the stomach, all pancreatic endocrine cells, and in some non-endocrine intestinal cells. When bred with a mouse containing a loxP site-flanked sequence of interest, Cre-mediated recombination results in deletion of the flanked gene in the tissues that normally express neurogenin 3. | ||
| 005699 | STOCK Tg(tetO-Ipf1,EGFP)956.6Macd/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the transgene are viable, fertile, normal in size, and do not display any behavioral abnormalities. At the Jackson Laboratory, no homozygous mice were produced from mating hemizygotes together, suggesting that homozygous transgenic animals die in utero. Expression of the bicistronic transgene is under the regulation of a tetracycline promoter element (TRE; tetO). By themselves, these transgenic mice do not express EGFP, but when these mice are mated with a second transgenic strain expressing tetracycline-transactivator (tTA) protein under the control of a tissue-specific promoter, Ipf1 and EGFP are highly expressed in the appropriate tissue of bitransgenic offspring.
This mouse was originally designed to be mated to an apancreatic targeted mutant with tTAoff in place of the endogenous Ipf1 gene (see Stock No. 005701). The combined mutations allow normal pancreatic dev ..... | ||
| 005728 | STOCK Tg(tetO-Ipf1,lacZ)958.1Macd/J | Cryopreserved - Ready for recovery |
| 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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