Search Criteria: Research Area is "Internal/Organ Research: Adipose Defects"
New Strains Awaiting Transfer from the Donor
| 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 | ||
| 002468 | KK.Cg-Ay/J | Level 3 |
| Ay and other mutations at the a locus conferring a completely yellow coat color are dominant to all a alleles that produce a darker coat. Hair pigment of Ay heterozygotes is yellow, but eyes are black. Heterozygotes usually become obese and infertile within a few months after birth. Increased adipose tissue mass is due to fat cell hypertrophy, and it has been hypothesized that the obesity results from the observed reduction in hypothalamic norepinephrine and dopamine. Heterozygotes are more susceptible to several kinds of tumors than are normal mice, possibly due, at least in part, to a general increase in cell proliferation that also manifests as a slight increase in lean body mass and skeletal length. Further spleen cells from heterozygotes cause a significantly lower graft vs. host reaction. Mice homozygous for the yellow spontaneous mutation (Ay) die before implantation, or shortly thereafter. The time of death and ..... For more information please see the full phenotype on the strain data sheet | ||
| 001934 | B6(D2)-LmnaDhe/TyGrsrJ | Repository- Live |
| Heterozygotes are slightly smaller than normal and develop a sparse, graying, scruffy coat. They have short ear pinnae, an underdeveloped lower jaw, malocclusion, protruding eyes, and low bone mineral density. The skulls are small and disproportionate, and the cranial sutures fail to close. Females can have decreased fertility, but males do not. Males have diminished total body fat. Homozygotes die by approximately 10 days of age, have dysplastic, ulcerated skin and oral mucosae, and a more severe deficiency in skull growth and mineralization. | ||
| 003124 | B6.129-Ucp1tm1Kz/J | Repository- Live |
| Mice that are homozygous for this knockout allele are viable and fertile, but exhibit sensitivity to cold temperatures. The Donating Investigator notes that homozygous offspring have increased survival rates to weaning age when maintained at 25°C to 28°C. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brown adipose tissue from homozygotes. When maintained at 20°C, homozygotes are resistant to diet induced obesity with reduced white fat depot weights, exhibit a 0.1-0.3°C higher body temperature, and a slightly lowered respiratory quotient compared to controls. Notably, when maintained at 27°C, homozygous mutant mice are no longer resistant to diet induced obesity and gain weight at a rate similar to wildtype controls. An increase in the number of brown adipocytes in the inguinal fat depots is observed in mutant mice maintained at 20°C, on either diet. Homozygotes have reduced levels of plasma fatty acids, circula ..... For more information please see the full phenotype on the strain data sheet | ||
| 010537 | B6.129S6-Mlxipltm1Kuy/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. Mutant mice exhibit increased glucose and insulin levels, decreased free fatty acids, reduced epididymal and brown fat weight, and reductions in liver glycolysis and lipogenic enzymes. Mice fed diets high in sucrose or fructose died within one week most likely as a result of inhibited glycolysis. On a high starch diet, mice developed moderate insulin resistance and increased liver weight. This mutant mouse strain may be useful in studies of lipogenesis and glucose metabolism. | ||
| 000021 | B6.Cg-Ay/J | Repository- Live |
| Mice homozygous for the yellow spontaneous mutation (Ay) die before implantation or shortly thereafter. The time of death and type of abnormality is, in part, determined by the genetic background on which the mutation is placed. Hair pigment in heterozygous mice is yellow, but eyes are black. Heterozygotes usually become obese and infertile after the first few months. Increased adipose tissue mass is due to fat-cell hypertrophy. It has been hypothesized that the obesity results from the observed reduction in hypothalamic norepinephrine and dopamine levels. Insulin resistance and hyperglycemia follow development of hyperinsulinemia in early adulthood, although the degree is less severe than on the KK/UpJ genetic background (Stock No. 002468). Heterozygotes are also more susceptible to several kinds of tumors than normal mice, and their spleen cells cause a significantly lower graft vs. host reaction. The level of ..... For more information please see the full phenotype on the strain data sheet | ||
| 007083 | B6.Cg-Cav1tm1Mls/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical abnormalities. Mutant mice exhibit exercise intolerance when challenged and are slightly hyperphagic. No gene product (protein) is detected by Western blot analysis in adipose, lung and heart tissues or in cultured mouse embryonic fibroblasts (MEFs). A decrease in the level of co-expressed caveolin-2 protein is immunodetected. At age 4-5 months, mutant mice are often smaller than their wildtype littermates. By one year of age, mutant mice weigh 5 to 7 grams less than wildtype, and are resistant to diet-induced obesity. Progressive adipose pathology results in reduced white adipose tissue with abnormally small adipocytes and enlarged, hyperplastic brown adipose tissue. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Isolated aortic tissue segments have a diminished vasoconstriction ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 005956 | B6;D1Lac-Scd1ab-2J/J | Repository- Live |
| The overall appearance of mice homozygous for either the Scd1ab-J allele or the Scd1ab-2J allele (Stock No. 002304 or 005956) includes slightly hunched posture, dry, scaly skin, thin fur sometimes detectable by 7 days of age, and small eyes with encrusted eyelids stuck shut. They have hypoplasia of the sebaceous glands and other hair follicle abnormalities that result in scarring alopecia. These mice have a paucity of adipose tissue, thin subcutis, and a distinctive odor. Hepatic cholesterol ester and triglyceride synthesis has been shown to be deficient in Scd1ab-J homozygotes and could not be restored through diet. Early studies of skin lipids in the original asebia mutant (Scd1ab) revealed a deficiency in wax esters, wax diesters, and sterols esterified with very long-chain fatty acids along with an in ..... For more information please see the full phenotype on the strain data sheet | ||
| 010803 | B6;FVB-Tg(Adipoq-cre)1Evdr/J | Repository- Live |
| Mice hemizygous for this Adipoq-Cre BAC transgene are viable and fertile, with expression of a Cre recombinase directed to adipose tissue by the promoter/regulatory regions of the mouse adiponectin (Adipoq) locus on the BAC transgene. Transcription/translation from the BAC Adipoq locus is disabled, and Cre recombinase expression levels are similar to that of endogenous Adipoq expression. These mice express Cre recombinase effectively in white adipose tissue (WAT) and brown adipose tissue (BAT), but not in macrophages (including adipose-tissue resident macrophages, alveolar macrophages, or thioglycollate-stimulated peritoneal macrophages). The donating investigator reports highly efficient Cre recombinase activity, with no ectopic expression. The phenotype of homozygous mice was not determined by the donating investigator. These Adipoq-Cre BAC transgenic mice may be useful in generating conditional mutations for studying adipose tissue function and storage, obesity, ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 013080 | C57BL/6-Actbtm3.1(Sirt1)Npa/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, exhibit delayed reproduction and lower body weight. No homozygotes are produced from heterozygous crosses. Fewer than expected heterozygotes are produced from heterozygote X wildtype crosses. Overexpression of gene product (protein) is detected by Western blot analysis of white adipose tissue, brown adipose tissue, MEFs, skull calvaria cells and brain tissue. Overexpression of the protein is not detected in liver or muscle tissue. Fusion gene product (mRNA) is detected in white adipose tissue by Northern blot analysis. Beta-actin protein expression is equivalent to wildtype levels. Heterozygote knock-in mice have reduced fat mass (epididymal fat pad weight), circulating free fatty acids, leptin, adiponectin and total cholesterol. Food consumption, glucose tolerance and metabolic rate (with associated higher oxygen consumption) are increased in the mutant mice. In fasted conditions, heterozygotes have lower circul ..... For more information please see the full phenotype on the strain data sheet | ||
| 009345 | C57BL/6J-Mstnlean/J | Repository- Live |
| Mice homozygous for this ENU-induced mutation, called the lean (Ln) allele of myostatin (MstnLn), are viable and fertile. The MstnLn allele alters mRNA splicing and results in an additional larger transcript containing a 128 basepair insert at the junction between exons 2 and 3. This insertion encodes an additional 4 amino acids before a premature stop codon (ASDNX), and is predicted to generate a truncated protein containing the Mstn signal sequence and propeptide, but lacking the ligand portion of the molecule. In addition to this abnormal splicing product, the mRNA from mutant males is also reduced in abundance by approximately 60% compared to wildtype males. When maintained on normal diet, homozygous (MstnLn/Ln) mice exhibit increased muscularity. When maintained on a high fat diet, homozygotes exhibit glucose tolerance, protection against overall insulin resistance, improved muscle and liver insulin sensitivity (with decreased ..... For more information please see the full phenotype on the strain data sheet | ||
| 016131 | C57BL/6J-Sec61a1m1Gek/J | Repository- Live |
| Mice homozygous for the ENU-induced missense mutation, called Sec61a1Y344H, are viable and fertile. By ~4 weeks of age, homozygous males and females maintained on a high-fat diet (~58% kcal from fat) become diabetic (hyperglycemic) with hypoinsulinemia; the result of endoplasmic reticulum (ER) stress-induced apoptosis of pancreatic β-cells. In addition to diabetes, these mice exhibit other metabolic, endocrinological, and growth abnormalities (including hyperlipidemia, hepatosteatosis, hypercholesterolemia, hypertriglyceridemia, and, in older mice, hepatic cirrhosis). Homozygous mice maintained on a chow diet (~5% kcal from fat) become diabetic by ~10 weeks of age; exhibiting hyperglycemia, hypoinsulinemia, glucose intolerance, and pancreatic β-cell loss. Heterozygous mice have an intermediate hypoinsulinemic phenotype on high-fat diet. These Sec61a1Y344H mutant mice may be useful in studying diabetes, ER protein trafficking/processing/sec ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 ..... | ||
| 004585 | STOCK Cav1tm1Mls/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical abnormalities. Mutant mice exhibit exercise intolerance when challenged and are slightly hyperphagic. No gene product (protein) is detected by Western blot analysis in adipose, lung and heart tissues or in cultured mouse embryonic fibroblasts (MEFs). A decrease in the level of co-expressed caveolin-2 protein is immunodetected. At age 4-5 months, mutant mice are often smaller than their wildtype littermates. By one year of age, mutant mice weigh 5 to 7 grams less than wildtype, and are resistant to diet-induced obesity. Progressive adipose pathology results in reduced white adipose tissue with abnormally small adipocytes and enlarged, hyperplastic brown adipose tissue. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Isolated aortic tissue segments have a diminished vasoconstriction ..... For more information please see the full phenotype on the strain data sheet | ||
| 017476 | 129S-Ucp1tm1Kz/J | Under Development - Now Accepting Orders |
| Mice that are homozygous for this knockout allele are viable and fertile, but exhibit sensitivity to cold temperatures. The Donating Investigator notes that homozygous offspring have increased survival rates to weaning age when maintained at 25°C to 28°C. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brown adipose tissue from homozygotes. When maintained at 20°C, homozygotes are resistant to diet induced obesity with reduced white fat depot weights, exhibit a 0.1-0.3°C higher body temperature, and a slightly lowered respiratory quotient compared to controls. Notably, when maintained at 27°C, homozygous mutant mice are no longer resistant to diet induced obesity and gain weight at a rate similar to wildtype controls. An increase in the number of brown adipocytes in the inguinal fat depots is observed in mutant mice maintained at 20°C, on either diet. Homozygotes have reduced levels of plasma fatty acids, circula ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 017560 | B6.FVB-Tg(Fabp4-IKBKB*)49Hxu/J | Under Development - Now Accepting Orders |
| These aP2-hIKKbeta SE transgenic mice express a constitutively active form of the human inhibitor of kappaB kinase beta (IKBKB) gene in adipose tissue under direction of the mouse fatty acid binding protein 4 (Fabp4) promoter. Hemizygous mice are viable and fertile. IKBKB gene product, IKKβ, is a master kinase involved in obesity-related inflammation and insulin resistance. These mice exhibit increased food intake, reduced weight of white adipose tissue, increased energy expenditure, and reduced triglyceride contents in adipose tissue, liver and muscle. They also exhibit reduced plasma free fatty acid (FFA) levels, increased systemic and tissue inflammation, decreased blood glucose levels, and improved glucose and insulin tolerance. These aP2-hIKKbeta SE mice show a decrease in hepatosteatosis even on a high fat diet. These mice may be useful for studying the effects of inflammation on adipose tissue and metabolism. | ||
| 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. | ||
| 011120 | 129S-Wwtr1tm1Benj/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, small in size and less active than wildtype controls. Only 10-25% of the expected homozygotes are born. The Donating Investigator reports that breeding homozygous females successfully is uncommon and homozygotes usually succumb before breeding age. No gene product (protein) is detected by Western blot analysis. Homozygotes develop severe polycystic renal disease, with an onset as early as a few weeks of age, and emphysema, with swollen alveoli and breakdown of alveolar walls. Kidney size increases with age. Intestinal and pulmonary inflammation is observed in some homozygotes. Levels of protein polycystin 2 (PC2) is increased in kidney epithelial cells of homozygotes. Histological analysis reveals adipocytes are smaller than wildtype control. | ||
| 006446 | B10.Cg-H2h4 Sh3pxd2bnee/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the nose eyes ear mutation are runted, with proportionally smaller skeletons, shortened noses, shortened and domed skulls, reduced areal bone mineral density, diminished visceral and subcutaneous white adipose tissue, but not brown adipose tissue, and abnormal eyes and middle ears. The eyes have an enlarged anterior chamber, cloudy cornea, and severe peripheral anterior synechia of the irideocorneal angle. The middle ear shows inflammation as serous fluid with diffuse neutrophils with thickened epithelium. Elevated ABR thresholds are found in all homozygotes and homozygotes are infertile. | ||
| 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. | ||
| 000061 | B6 x STOCK Nox3het/J | Cryopreserved - Ready for recovery |
| Head tilt (Nox3het) is an autosomal recessive mutation that can cause abnormal circling behavior and hyperactivity in affected mice. Homozygotes also exhibit a subtle head tilt. Together, the abnormal behavioral phenotype is consistent with that of a vestibular disorder. Evoked auditory brainstem response profiles are normal indicating that the mutants are not deaf. Nox3het/Nox3het mutants are unable to sense orientation under water and therefore, cannot swim properly. If held by the tail, Nox3het/Nox3het mice retract, rather than extend, their limbs; they also flex ventrally, instead of dorsally as wild type mice do. When lowered quickly by the tail, Nox3het/Nox3het mice fail to extend their forelimbs in a normal manner and have difficulty righting themselves if dropped vertically from a short distance. Morphological assessment of the inner ear of homozygotes r ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 006620 | B6.129P2-Scp2tm1Usee/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. No protein product from the targeted gene is detected in liver tissue. Northern blot experiments show a low-intensity signal from a non-functional truncated transcript, however. Histologically, greater numbers of peroxisomes are observed in the livers of these mice. Liver function appears normal based on liver enzyme levels, but cholesterol and triglyceride storage pools are depleted. Hepatic gene expression is altered. Higher expression levels of liver fatty acid binding protein and multiple peroxisomal beta-oxidation enzymes are observed. Whereas plasma insulin and cholesterol concentrations are normal, triglycerides are slightly higher and free fatty acid and glucose concentrations are moderately lower in homozygous mice. Food intake is significantly higher in homozygotes as compared to control animals. A prononounced accumulation of phytanic acid is o ..... For more information please see the full phenotype on the strain data sheet | ||
| 005429 | B6.129S-Gpamtm1Rcol/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, and do not display any gross behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis. Enzyme activity levels in liver tissue are negligible. Residual activity is due to the inactivated microsomal isoform. Homozygotes exhibit reduced body weight. Female homozygotes weigh 20% less than wildtype controls at age 10 months. Male homozygotes do not exhibit as significant a weight reduction. Gonadal fat pad mass is reduced. Liver triacylglycerol and plasma lipid levels are reduced by 37% and 15% respectively. Very low density lipoprotein (VLDL) triacylglycerol level and secretion are decreased. Hepatic triacylglycerol fatty acid and phospholipid fatty acid compositions are abnormal with diminished palmitate content. F2 mice on a 50% C57BL/6J and 50% 129SvEv genetic background were used in all of the experiments described in the primary reference. This mutant mouse strain may be useful in stu ..... For more information please see the full phenotype on the strain data sheet | ||
| 012768 | B6.129S1-Gnai2tm1.1Rneu/J | Cryopreserved - Ready for recovery |
| A G184S point mutation was created in the Gnai2 (guanine nucleotide binding protein (G protein), alpha inhibiting 2; also called Gαi2) gene which disrupts interactions with regulator of G protein signaling (RGS) proteins that normally deactivate Gα G protein signals. A complex phenotype affecting multiple organ systems (heart, myeloid, skeletal, and central nervous system) can be observed. Homozygous mice and their cardiocytes exhibit enhanced muscarinic (M2) but not adenosine (A1) receptor-mediated responses. Isoproterenol-stimulated beating rates of heterozygous and homozygous hearts are significantly more sensitive to inhibition to carbachol than are those of wildtype mice.
Homozygous mice show slightly reduced adiposity. Unlike females, males placed on a high-fat diet are resistant to weight gain and have decreased body fat as compared to wildtype mice. Both males and females exhibit enhanced insulin sensitivity (protected f ..... | ||
| 008841 | B6.129S2-Ccrn4ltm1Bjc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Nocturnin (Ccrn4l or Noc) targeted mutation are viable and fertile, with no detectable Noc protein made from the targeted gene. Homozygotes are resistant to diet-induced obesity and remain lean on high-fat diets, with lower body weight and reduced visceral fat. Unlike lean lipodystrophic mouse models, Noc-deficient mice do not have fatty livers (hepatic steatosis) and do not exhibit increased activity or reduced food intake. In addition to changes in glucose tolerance and insulin sensitivity, homozygous mice may also have deficits in lipid metabolism or lipid uptake. Nocturnin-deficient mice may be useful in studying resistance to diet-induced obesity, physiologic rhythms downstream of the circadian clockwork, and post-transcriptional regulation of genes necessary for nutrient uptake, metabolism, and storage. | ||
| 003824 | B6.129S4-Dgat1tm1Far/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Dgat1tm1Far targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities however, homozygous mutant females exhibit a complete absence of milk production, necessitating the use of foster mothers. Dgat1 mRNA is undetectable by Northern blot analysis, and DGAT enzyme activity in a variety of tissues is either absent or shows only residual levels. Surprisingly, in DGAT deficient mice triglyceride levels and fasting serum triglycerides levels are similar to wildtype controls. Although homozygotes do not differ in body weight compared to age- and sex-matched controls, total fat pad weight is reduced. Tissue triglyceride levels are reduced 30-40% in white adipose tissue and muscle. Liver triglyceride levels tend to be lower in chow-fed DGAT-deficient mice, but high-fat feeding leads to significantly lower liver triglycerides. Changes in tissue triglyceride levels are associated with in ..... For more information please see the full phenotype on the strain data sheet | ||
| 002939 | B6.129S4-Insrtm1Dac/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Insrtm1Dac targeted mutation die 48-72 hours after birth due to diabetic keto-acidosis which causes weight loss by dehydration and protein wasting. There are no apparent gross anatomical or morphological changes. Embryonic growth is unaffected. Heterozygotes exhibit a form of mild insulin resistance. | ||
| 005897 | B6.129S4-Ppardtm1Rev/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exon 4 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice with a cre recombinase gene under the control of a promoter of interest, exon 4 of the targeted gene is deleted in the tissue of interest, leading to premature termination of the translation product upstream of the DNA binding domain. This strain may be useful in generating tissue-specific mutants of the floxed allele for use in studies including embryo development, adipocyte physiology, fat metabolism and storage, inflammation, and cancer. | ||
| 005901 | B6.129S4-Ppardtm2Rev/J | Cryopreserved - Ready for recovery |
| Heterozygous mice are viable and fertile. All homozygous mice die in utero. Macrophages homozygous for this mutation have no transcriptional response to very low-density lipoprotein treatment. No evaluation of lacZ expression is published. The donating investigator reports homozygous mice on this background have a similar, albeit earlier, embryonic phenotype as the exon 4 deleted mutants described in other publications (Barak PNAS 2002 99:303-8, Chawla PNAS 2003 100:1268-73, and Lee Science 2003 302:453-7). Heterozygous mice or homozygous embryo-derived cells may be useful in studies of embryo development, adipocyte physiology, fat metabolism and storage, inflammation, and cancer. | ||
| 000017 | B6.C3-Avy/J | Cryopreserved - Ready for recovery |
| Homozygous (Avy/Avy) and heterozygotes (Avy/A and Avy/a) show considerable variation in appearance, ranging from clear yellow, to mottling with dark patches, to a completely agouti-like coat. The variation is strongly influenced by the agouti-locus genotype and strain genome of the dam. Homozygotes and heterozygotes tend to become obese, and the degree of obesity is correlated with the amount of yellow in the coat. Avy resembles Ay in causing greater tumor susceptibility and lower graft vs. host reactivity and higher hepatic malic enzyme activity. Homozygotes have a reduced humoral response to tetanus toxoid and decreased rates of carbon clearance as well as impaired mononuclear phagocyte function. The greater tumor susceptibility as well as several altered immune responses occur in Avy/a mice of mottled phenotype but not in those of agouti phenotype. | ||
| 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 | ||
| 006906 | B6.Cg-Lepob Ldlrtm1Her/J | Cryopreserved - Ready for recovery |
| Independently, the C57BL/6-Lepob homozygotes (Stock No. 000632) model the increasingly prevalent metabolic disorder seen in humans (hyperglycemia, hyperinsulinemia, and hyperlipidemia), while LDLR-deficient mice (Stock No. 002207) are predisposed to atherosclerosis. When mutant mice are homozygous for both mutant alleles, they exhibit exacerbated hyperlipidemia and extensive atherosclerotic lesions in the aorta. The mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, and hypercholesterolemia. | ||
| 006200 | B6.Cg-Tnks2tm1.1Yjc/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of activated spleen lymphocytes. While neither telomere shortening nor chromosomal abnormalities (even across multiple generations) are observed, homozygous mice have significantly decreased body weight. These mutant mice may be useful in studies of both telomerase function and telomerase-independent pathways which affect development and metabolism. | ||
| 007032 | B6;129S-Wnt4tm1.1Bhr/BhrEiJ | Cryopreserved - Ready for recovery |
| This strain contains loxP sites flanking exon 2 of Wnt4 resulting in a Cre-dependent conditional null allele. Homozygotes are normal. Studies by Kobayashi et al., determined that when this conditional allele is exposed to Cre expression by Amhr2tm3(cre)Bhr Mullerian duct regression proceeds normally. | ||
| 004858 | B6;129S1-Tshrtm1Rmar/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation exhibit delayed eye opening, are runted by day 21, and will die within 1 week if weaned at day 21. Homozygotes will survive by extending weaning to 28 days but will not reproduce. Homozygotes are viable and fertile when weaned at day 21 and subsequently placed on a hormone replacement therapy diet consisting of a 100ppm desiccated thyroid powder supplement. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis of thyroid membranes. Enhanced Green Fluorescent Protein (EGFP) gene product is detected by RT-PCR and Western blot analysis of thyroid tissue. Hypothyroidism is exhibited by mutant mice that have a longer weaning period and a non-supplemented diet, as indicated by low T4 and T3 serum levels, and high thyrotropin (TSH) serum levels. Treatment with exogenous TSH does not result in a thyroid hormone release response. Mutant mice produce uniodinated thyroglobulin and do not accumulate radioactive iodide in ..... For more information please see the full phenotype on the strain data sheet | ||
| 002426 | B6;129S4-Insrtm1Dac/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Insrtm1Dac targeted mutation die 48-72 hours after birth due to diabetic keto-acidosis which causes weight loss by dehydration and protein wasting. There are no apparent gross anatomical or morphological changes. Embryonic growth is unaffected. Heterozygotes exhibit a form of mild insulin resistance. | ||
| 003393 | B6;SJL-Tg(aP2-SREBF1c)9884Reh/J | Cryopreserved - Ready for recovery |
| This transgenic mouse strain overexpresses human nuclear sterol regulatory element binding protein-1c in adipose tissue under the control of the adipocyte-specific aP2 promoter. The phenotype of transgenic mice resembles congenital generalized lipodystrophy (CGL), a rare autosomal recessive disorder in humans. CGL is characterized by an insufficiency of adipose tissue which is evident at birth and is accompanied by a severe insulin resistance leading to symptoms of type II diabetes mellitis, (hyperinsulinemia and hyperglycemia), and an enlarged fatty liver. Transgenic mice exhibit these symptoms showing defects in differentiation of white fat accompanied by an hypertrophy of brown fat that resembles immature white fat. | ||
| 002557 | B6Ei.GL-Nox3het/J | Cryopreserved - Ready for recovery |
| Head tilt (het) is an autosomal recessive mutation that can cause abnormal circling behavior and hyperactivity in affected mice. Homozygotes also exhibit a subtle head tilt. Together, the abnormal behavioral phenotype is consistent with that of a vestibular disorder. Evoked auditory brainstem response profiles are normal indicating that the mutants are not deaf. het/het mutants are unable to sense orientation under water and therefore, cannot swim properly. If held by the tail, het/het mice retract, rather than extend, their limbs; they also flex ventrally, instead of dorsally as wild type mice do. When lowered quickly by the tail, het/het mice fail to extend their forelimbs in a normal manner and have difficulty righting themselves if dropped vertically from a short distance. Morphological assessment of the inner ear of homozygotes reveals an abnormal appearance of the saccule and utricle owing to a complete absence of otoliths. Otoliths are tiny cal ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 001768 | C3.Cg-Irs1Sml H2b/GrsrJ | Cryopreserved - Ready for recovery |
| The small mutation causes hyperinsulinemia with only mild insulin resistance, a paucity of body fat, deficiencies in bone development and homeostasis, and hearing loss. Homozygotes can be distinguished by 2 weeks of age by their smaller body size and thin short tails, and adult homozygotes are visibly smaller with a tail that is 20% shorter than in wild-type controls. Hearing loss was shown through increased ABR threshold values when assessed between 8 and 12 weeks of age. The skeletal defects include shortened femurs with smaller growth plates, decreased cortical and trabecular thickness and abnormal trabecular number, with an increase in the number of osteoclasts and osteoblasts per bone perimeter but impaired osteoblast proliferation and differentiation in culture. This spontaneous point mutation is semidominant in some aspects of phenotype, unlike targeted mutations of this gene. Heterozygotes are statistically smaller than wild-type controls, but the severity of dwarfing is not ..... For more information please see the full phenotype on the strain data sheet | ||
| 003401 | C3H/HeJ-Lpin1fld-2J/J | Cryopreserved - Ready for recovery |
| Homozygous fatty liver dystrophy (fld) mice have an enlarged, fatty liver and hypertriglyceridemia which resolve to normal during the weaning transition. However, decreased overall size, decreased lipid in the fat pads, and a peripheral neuropathy persist throughout the lifespan. This peripheral neuropathy manifests as a tremor and an unsteady gait shortly after 10 days of age and worsens with age. The fld neuropathy is specific to the peripheral nervous system. Electron microscopy of sciatic nerves revealed thin, poorly compacted myelin sheaths, hypertrophic Schwann cells, myelin debris, degenerating axons, bands of Bugner, and regenerative clusters, but no evidence of inflammation (Langner et al, 1991). Western blot analysis of sciatic nerve from two-to-three month old fld/fld mice showed a 7-13-fold reduction in myelin P0, a vast increase in apoE, an increase in GAP-43, and no detectable myelin P2. It was also noted that a ..... For more information please see the full phenotype on the strain data sheet | ||
| 000099 | C3HeB/FeJ-Avy/J | Cryopreserved - Ready for recovery |
| Homozygotes (Avy/Avy) and heterozygotes (Avy/A and Avy/a) show considerable variation in appearance, ranging from clear yellow, to mottling with dark patches, to a completely agouti-like coat. The variation is strongly influenced by the agouti-locus genotype and strain genome of the dam. Homozygotes and heterozygotes tend to become obese, and the degree of obesity is correlated with the amount of yellow in the coat. Avy resembles APy in causing greater tumor susceptibility and lower graft vs. host reactivity and higher hepatic malic enzyme activity. Homozygotes have a reduced humoral response to tetanus toxoid and decreased rates of carbon clearance as well as impaired mononuclear phagocyte function. The greater tumor susceptibility as well as several altered immune responses occur in Avy/a mice of mottled phenotype but not in those of agout ..... For more information please see the full phenotype on the strain data sheet | ||
| 004109 | C57BL/6J-Glra1nmf11/J | Cryopreserved - Ready for recovery |
| Early onset visible phenotype characterized by small size and severely impaired gait that becomes detectable between 18-21 days (mean 18.6 +/- 1.7 days). Gently dropping the animals from a height of 10-15cm onto a soft surface frequently induces intense seizure-like behavior that may last several minutes (generalized seizure-like episodes, including front and hind limb contractions, hind limb extensions); however the animals recover and continue to move around. Electroretinograms (ERG) showed abnormal b-waves in three (2 males, 1 female) of four mutants examined. Mutants of either gender have been produced; homozygotes are not viable.
For more information please see the full phenotype on the strain data sheet | ||
| 002244 | C57BL/6J-Tg(Apoa2)1Lus/J | Cryopreserved - Ready for recovery |
| This strain carryies the mouse apolipoprotein A-II transgene. Fasting plasma APOA2 concentrations in transgenic mice are on average about 3-fold higher than normal wildtype siblings with males showing a 1.5-fold higher level than females. ApoA-I concentraions are normal. These mice show a 3-fold increase in plasma triglyceride levels, as well as a predisposition to atherosclerotic fatty streak lesions even on a low fat diet. | ||
| 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 ..... | ||
| 002304 | DBA/1LacJ-Scd1ab-2J/J | Cryopreserved - Ready for recovery |
| The overall appearance of mice homozygous for either the Scd1ab-J allele or the Scd1ab-2J allele (Stock No. 002304
or 005956) includes slightly hunched posture, dry, scaly skin, thin fur sometimes detectable by 7 days of age, and small eyes with encrusted eyelids stuck shut. They have hypoplasia of the sebaceous glands and other hair follicle abnormalities that result in scarring alopecia. These mice have a paucity of adipose tissue, thin subcutis, and a distinctive odor. Hepatic cholesterol ester and triglyceride synthesis has been shown to be deficient in Scd1ab-J homozygotes and could not be restored through diet. Early studies of skin lipids in the original asebia mutant (Scd1ab) revealed a deficiency in wax esters, wax diesters, and sterols esterified with very long-chain fatty acids along with an i ..... For more information please see the full phenotype on the strain data sheet | ||
(58 stocks) Back to Top
How to Register Interest
Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Awaiting Transfer
Select the strain name to link to the strain data sheet.
Send questions to our Technical Support team using the Express Technical Support Form.
(5.3)